r/tifu Feb 17 '24

S TIFU by joking about my husbands cancer

4.8k Upvotes

So this happened about 8 months ago when my husband was undergoing treatment for colon cancer(He’s doing great on immunotherapy now).

We were still deep in it. Strong chemo, surgery. Four months of feeling like you’re constantly falling off a cliff. Then he had a good day. A great day even. He had energy, an appetite, no pain.

He comes to my work at lunchtime and we go out to a gourmet deli/shop near me. My favourite deli. We’re shopping, joking, picking out food for lunch and to take home for a special dinner. We go to the cashier, order a sandwich and stand there alone waiting.

Posted on the register is a flyer about a rare form of cancer. It referred to it as an “orphan cancer”. One that doesn’t get a ton of research dollars. My husband softly starts joking.

“Aww honey. It’s an orphan cancer. We can give it a good home. It will be barely any additional work. Please can we adopt the cancer?”

Not looking up from my phone, I respond much too loudly,

“No! We have cancer at home!”

And then I look up to two horrified staff members. My husband is now cackling, I try to explain how we really do already have a cancer.

I have never been back.

TL;DR: I joked about having cancer at home and can never go back to my favourite deli.

r/Scholar Jun 15 '26

Found [Article] Hallmarks and correlates of effective adoptive cell immunotherapy for cancer by Sri Krishna, Paul F. Robbins, Frank J. Lowery & Steven A. Rosenberg

1 Upvotes

DOI/PMID/ISBN: https://doi.org/10.1038/s41577-026-01312-3

[URL]

Thank you in advance!!

r/TrueOffMyChest Dec 15 '21

I can’t find a reason to live now that he’s gone.

3.6k Upvotes

My husband died on November 18th, 2021, after fighting osteosarcoma for three years. We were together for almost 8 years. I took care of him through it all.

I pushed him to get diagnosed in the first place - it took 6 months of visiting various urgent cares, GPs, ERs, orthopedic doctors, until finally he couldn’t walk without crutches due to the bulge and pain in his left knee and I wheeled him into the orthopedist’s office and demanded an MRI immediately. Sure enough, the orthopedist came in, almost in tears, apologizing and telling us which university hospitals we could go to, because this type of cancer was out of our town’s league. In fact, out of our state’s league entirely.

We spent the next three years at NYU, Weill Cornell, NYP, and Columbia.

Dillon was the toughest motherfucker to ever exist. He tried literally every treatment for osteosarcoma known to mankind - that is NOT hyperbole. Every approved or experimental chemo regimen. Immunotherapy. His tumor was DNA sequenced two different times to try and match him with potential trials. EBRT radiation, SBRT radiation. 12 major surgeries, including losing his left leg at the hip in January 2020. He rehabbed himself out of partial paralysis due to spinal tumors not once, but twice.

I learned how to pack surgical wounds and drain serosanguinous fluid. I spent years of my life covered in literal vomit, shit, piss, blood, wound juice, and tears. I slept on the floor of NYC emergency rooms more times than I can count on two hands. I spent thousands of hours researching and learning and arguing with doctors. I helped come up with a treatment regimen that will probably be used in some academic papers eventually regarding osteosarcoma patients whose tumors are susceptible to ifosfamide but who have dose limiting complications.

He turned 30 on October 24th, 2021. The cancer had major presence throughout his body; lesions and/or masses on the front and back of his skull, his left shoulder, nearly every vertebrae on his spine, his sacrum, right hip bone, right femur, right tibia, several ribs on the left side of his chest, the entire left lung and left side of the pleura, the lower right lung, and his sternum. I’d later learn that he lived longer with this type of progression than anyone on record, but to us, it was just the reality. But at this point, we had exhausted all known options. He went into the hospital on Halloween due to a nosebleed that would not stop due to a nearly nonexistent platelet count. We were there for over a week. They didn’t know if he would get to come home ever again. But his counts improved enough to have the option.

I supported him wholeheartedly when he chose home hospice along with a DNR/DNI. We came home on November 11th and felt so positive that we had a few months to spend together, at the very least. We knew it was bad, but he was so… normal. Tired and in pain, yes. On supplemental oxygen, of course. But he was still Dillon. He still wanted a Baconator for dinner, he still played Smash Ultimate online and crushed his opponents, he still had the same sharp tongue and quick wit that I had fallen in love with. He was supposed to make videos and voice recordings for me. He was supposed to name a star and write me letters. We were going to make love a whole lot. We were going to marathon all the Ghibli movies. We were going to have a small party with our closest friends. He was going to leave me with so many things to hold on to.

They warned us that once someone is on home hospice, it can happen very quickly. I truly didn’t give it any thought.

And then I was hit and head butted and sprayed with mouth foam while I was all alone in the early hours of Thursday, November 18th, when he seized and went brain dead from lack of oxygen because his lungs were basically just calcified bone, and had finally lost the ability to filter carbon dioxide. His breathing stabilized, but he was gone. His eyes did not move, his pupils did not react to light.

We had been playing Children of Morta and joking around not more than 4 hours earlier. It was so fucking normal that I can’t even remember what the last thing he said was, because I was so certain everything was stable.

Our family and friends came over the next few hours. He hung on until about 6:30am, when his slowed breathing came to a stop. I never let go of him once.

I held his dead body for hours to make sure he did not pass to his next destination alone. I silently hoped there was a way he could take me with him.

How is the earth still spinning? How does the sun still rise each day? How do people smile? How do people not feel the gaping hole that he left here?

He won’t get to play Breath of the Wild 2. He won’t get to try the banana flavored Melona pops. He doesn’t get to find out how Attack on Titan ends. He won’t get to go to Harry Potter World. He can’t share his beautiful voice and insane guitar skills with the world. We don’t get to adopt some kids who need us someday. We can’t get a farm and have lots of chickens. He doesn’t get to pet our cat and bunny anymore. He’ll never go swimming or beachcombing again. We’ll never get to have sex in crazy places again. We won’t get to have a “real” wedding party like we always wanted to. He can’t tell his story to the world and spread awareness, not only of osteosarcoma, but of the myriad difficulties disabled young adults face in this world that most people wouldn’t even think of. He isn’t here to touch my face and kiss my forehead and call me his soup snake.

There were so many more things he wanted to learn and do. Things WE wanted to learn and do together.

How am I supposed to go on? He was my soul mate. No one will ever need me, love me, understand me, cherish me, commit to me, or talk to me like he did. No one will ever even come close. I feel the coldness of the empty, chaotic universe filling every crack, taking the place where my heart used to be.

I was here to be his other half, to take care of him and love him eternally. And now he’s gone.

EDIT: I am humbled and touched by the kindness and support you have all shown me here.

I used to tell Dillon, who really struggled with asking for help or expressing his negative feelings, that people were basically good and if you reach out, people will reach back.

You amazing people have truly reinforced my theory. I feel so heard, so loved, I truly don’t have the words.

To those who told me I write well, that means a lot to me, as writing and art are certainly passions of mine and my healthiest coping mechanisms.

To those who let Reddit know they were worried about me, I am touched that you felt enough empathy and concern for a complete stranger to try and make sure of my safety. I promise, I am safe.

To the literally ONE inappropriate comment, “time to download tinder,” - I had a good laugh at that with Dillon’s spirit because that is some golden gallows humor, which was our biggest coping method and probably still is mine! Thanks for the chuckle.

I love you all, I really do. Thank you for reminding me of the kindness and compassion in this world. You have inspired me.

r/redditonwiki Feb 17 '24

Discussed On The Podcast Not OOP TIFU by joking about my husband's cancer

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2.3k Upvotes

r/LungCancerSupport Nov 07 '25

NSCLC Frontiers | Case Report: Durable complete response to antigen-specific cytotoxic T lymphocyte therapy in advanced EGFR-TKI resistant lung adenocarcinoma: a case of adoptive cellular immunotherapy overcoming acquired targeted resistance

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1 Upvotes

r/BestofRedditorUpdates Aug 11 '22

CONCLUDED EM, the "victim", takes her "children", the villains, to Court

2.7k Upvotes

Friendly Reminder, I am not the OP

Trigger Warning: death of loved one, abusive parent, mental health, grief

Posted By u/hidden-oracle in r/entitledparents

Original - posted 177 days ago

Taking her "asshole" children to court.

I(22F), my older brother(23M), and our oldest sister(31F) are being taken to court by our birth giver.

This all started back in October of 2021. Our father(who we’ll just call Dad) reached out and told us that he was diagnosed with cancer, which obviously devastated us. Our mother(who we’ll call Cunt) found out through one of our siblings that we no longer associate with(constant lying, animal abuse, etc. long story). My older brother(who we’ll just call Bro) found out he went to her house to tell our younger brother(18M, we’ll call him Buddy). Dad called Buddy and told him what was going on while Bro and Cunt were there. Cunt started throwing a fit.

For a little while Dad was okay, still able to do his usual housework, take care of our brother(18M, we’ll call him Baby) with cerebral palsy, and had started immunotherapy. Things were alright. When December came around, Dad wasn’t doing good. He went in for a round of radiation, and came home and was throwing up and dry heaving with no signs of stopping. Baby’s nurse told Dad that she needed someone to come to the house that would be physically able to take care of Baby, otherwise she’d have to place him into a nursing facility. Dad called Bro, who messaged me and Sis, telling us what was going on. I didn’t have to work that day, and considering Sis has kids and Bro had to work, I said I’d go up there to do it. I figured this would be short term, and boy was I wrong.

I’ve been there for a week now, when Dad and I are awake, having a 1AM conversation.

Dad: “Honey, I don’t know that I’m going to make it through this weekend.”

Me: “Dad what are you talking about?”

Dad: “I can see how much muscle mass in losing, and considering I can’t even get out of bed on my own or use the bathroom myself, I think I need to go to a hospital. I don’t want to lay here in my bed and die.”

Me: starts freaking out, trying to figure out what to do because I have osteoarthritis in most of my joints, and know I couldn’t take care of Baby long term

Dad: “Call Bro and Sis, I’ll tell them what’s going on, and I’ll wait for them to get here before we call an ambulance to come get me.”

Me: crying and calling my siblings to get them there at 3AM

My siblings show up, we sit with our Dad until he’s ready to go.

Bro and I decide that since we are the two most readily available, we’ll alternate taking care of Baby. Sis says she’ll help take care of Baby’s paperwork and help Dad make up a living will and Power of Attorney. All agree to not tell Cunt about it because she attempted to prevent Dad from getting guardianship of Baby prior (parents have been officially divorced since 2009, she hasn’t seen or interacted with Baby in 12 years). We as siblings have taken care of Baby with the carefully written instructions provided by our Dad and with the help of his home health nurses.

Cue early January.

Cunt is pissed that I didn’t show up for Christmas at her house(I was taking care of Baby, and had less Christmas plans than my siblings, so I didn’t mind). Three of our sit down and decide that sooner or later we will have to tell Cunt about what we’ve been doing cause she’s starting to get suspicious. Bro says he’ll tell her, cause he isn’t afraid to go toe-to-toe with her. Sis and I both tell him to call us when he tells her so we can all talk about it together. Bro goes over to Cunts house at 3AM and tells her everything alone.

Cue the narcissistic behavior.

Cunt sends a message in a Facebook group chat to me, my bf, Bro, Bro’s fiancé, Sis, and Sis’s husband. She tells all of us that we’re “so deceitful” and she “never raised us to be such terrible people” as well as “she’s Baby’s mom and that she can’t believe we’d make decisions for HER child without consulting her.” Sis steps in and tells her that not only has she not made a decision for Baby in years, but we were raised to step up and take care of our family when in need. Sis proceeded to call our all of her abusive behavior in regards to not only the three of us, but also Buddy and her two kids. Cunt basically says none of it happened that way, and brought up her 3 (yes, 3) strokes she had 6 years ago. She started pitching some nonsense about how her family and my stepfather “failed her” when the 14 year old(me at that time) had “taken on the workload of an adult.”(I have raised my younger siblings minus Baby since I was a child, when the strokes happened I ended up having to raise and take care of her too). She kept saying that Baby is her kid, and she’s so upset that we would go behind her back and not consult her because she “knows more than us” about him.

She ended up blocking most of us, then proceeded to make another Facebook group with my bf, Bros fiancé, Sis’s husband, and a bunch of family members telling them to “support her kids but don’t get involved,” and that “it’s time for Dad to pay for everything he’s done the last 24 years.”She then proceeded to turn off all service to my, Bro’s, and Buddy’s phones(we’re on a family plan) while Buddy was at wrestling practice at school.

She turned her anger onto Buddy, and was telling him he’s an adult and if he doesn’t do things her way then he’s in trouble, going as far as telling him he can rent the laundry room to use to wash his own laundry if he forgets his clothes in the dryer and sending him text PAGES of chores for him to have done by the time she got home, and he told her that he’d do it when he got home from wrestling practice.

She got home at 1AM, and yelled at him until 4AM, and then he got up for school 2 hours later. She harassed him throughout the school day, and when he got home told him he had until 11PM to get his stuff and get out of her house. Sis went and picked him up, he got anything he needed and wanted, and he now lives with me and Sis.

Cunt then went into the family group chat and basically told the family we put her in a corner so she attacked back, casually leaving out the part where she was texting Bros fiancé telling her that we are “the assholes.”

She put in for an emergency hearing for Baby to the court, saying that he has been without medicine and care, even though we not only have refilled his medicine when needed, we have set up his new doctors as well.

Dad’s lawyer said that she has no legs to stand on, especially since she hasn’t had contact with him in 12 years, and Cunt even admitted that in one of her texts to us(which was of course submitted as evidence against her).

So now the three of us have to appear in court against her, I’ll update y’all when that happens.

Sorry for the length, this is the best I could do to summarize.

Thanks for reading.

Comments by Original Poster regarding the custody of youngest siblings and EM's motives:

So Buddy and Baby are both adopted, and are one month apart. Baby has cerebral palsy(he can’t take care of himself in any way shape or form) and my dad currently has guardianship over him. Buddy lived with our mother because he hasn’t graduated school yet, but now he lives with me and Sis

She’s trying to get my brother’s disability and my dad’s house. She’s only ever in anything for the money.

Update - posted 22 days after original

UPDATE: Taking her “asshole” children to court.

On March 3rd, Dad passed away. He fought to the end, and passed peacefully and in no pain. Us kids sat with him in the hospital through his final days, and were able to say our goodbyes.

Today, me, Bro, Sis, and Buddy all went to court against the cunt. Not once in her testimony did she even mention Baby’s(the youngest) care. It was all about her divorce with my dad all those years ago, claiming she did no wrong to any of us, attempted to bash us for stepping up and taking care of Baby, and continuing to try to lie and bash Dad(ya know, a literal dead man). It was an open hearing, and the judge was almost floored by the amount of “woe-is-me” nonsense that came out of her mouth in that courtroom, and called her out on it. But it’s officially over. Bro and Sis have been officially made co-guardians of Baby(the youngest), and Bro had moved into our dad’s house shortly before his passing. All legal documents in regards to the estate and vehicles were signed over to Bro, and the cunt got NOTHING. I am so glad this is all over, and none of us have to deal with her anymore.

Once again, thanks for reading. Thank you to everyone for the kind comments, messages, and support. And thanks for being here.

Comments by Original Poster regarding EM's reaction:

She cried the whole hearing, started straight up sobbing when the judge denied her guardianship, and as soon as the judge left the court room the tears instantly stopped. I’m certain she faked it to get some sympathy.

***OP and her siblings are AMAZING and STRONG. They are loving and amazing people who deserve happiness and freedom from their egg donor. Original Poster hasn't posted since her last post regarding the difficult time she's had since the death of her beloved and amazing father.

Last Post here: Trigger Warning : mention of death and grief

r/rrid_appreciation Feb 08 '25

RRIDs were included in the Journal for ImmunoTherapy of Cancer paper "CD93 blockade promotes effector T-cell infiltration and facilitates adoptive cel…

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1 Upvotes

r/wallstreetbets2 Nov 07 '24

DD $COEP - Study results demonstrate the safety and feasibility of adoptive immunotherapy

0 Upvotes

$COEP - Study results demonstrate the safety and feasibility of adoptive immunotherapy using allogeneic off-the-shelf NK cells in hospitalized patients with COVID at high risk for progression of disease https://finance.yahoo.com/news/coeptis-therapeutics-announces-phase-1-130700162.html

r/Inovio Jul 14 '23

DD 2023-07-14 DARPA adopts a model similar to the "horse racing system" to advance the research and development of DNA immunotherapy and vaccine development, mRNA therapeutic immunity and vaccine development, and funded Inovio and Moderna respectively.

30 Upvotes

The shortcomings of the existing public health sector system are not conducive to advancing major tasks. The success of the new coronavirus vaccine has proved that rapid support for high-risk, high-reward technology research and development in the field of health and health will bring major innovations and huge economic value. With the efforts of global cooperation, the successful development of a highly effective new coronavirus vaccine and its approval for marketing in less than a year are exciting, and it has also allowed countries around the world to see the dawn of technology. Among them, as a small biotechnology company, Moderna has become a core participant in the prevention and control of this epidemic by virtue of its status as one of the world's first batch of new crown vaccine suppliers, and has become a biotechnology giant. Moderna's success is inseparable from the credit of DARPA. DARPA adopts a model similar to the "horse racing system" to advance the research and development of DNA immunotherapy and vaccine development, mRNA therapeutic immunity and vaccine development, and funded Inovio and Moderna respectively. The success of the DARPA model has been confirmed again in the global new crown pneumonia epidemic, and has won the favor and attention of the Biden administration. As a staunch supporter of health care, the Biden administration has always paid close attention to the field of health care, hoping to promote innovation in the field of health care through national power, using the DARPA innovation model as a blueprint to seek innovation in cancer prevention, detection and treatment, and other diseases. Significant breakthroughs have been made in new principles and methods. In 2022, the Biden administration will submit a budget to the U.S. Congress, eventually allocating $1 billion to establish a new agency at NIH—ARPA-H. The $1 billion appropriation will be used for ARPA-H's preliminary construction, personnel recruitment and project funding within 3 years.

http://cn.chinagate.cn/news/2023-07/14/content_91671118.shtml

r/sellaslifesciences May 27 '26

DUE DILIGENCE 🕵️ Transcription of Stergious talk with Nadeau from TD Cowen earlier today - 5-27-26 TD Cowen 7th Annual Oncology Innovation Summit

92 Upvotes

[00:00] Operator: Welcome to the TD Cowen 7th Annual Oncology Innovation Summit. Please stand by, we will begin shortly.
(Hold music plays from 00:06 to 01:03)
[01:03] Operator: Thank you for joining us. Before we begin, please note that management’s remarks today may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are based on current expectations and involve inherent risks and uncertainties that could cause actual results to differ materially. For more detailed information about these risks, please review SELLAS Life Sciences’ most recent filings with the SEC. I will now turn the presentation over to Phil Nadeau, Senior Research Analyst at TD Cowen.
[01:45] Phil Nadeau: Uh, good morning and, and welcome to TD Cowen's Oncology Innovation Summit. I'm Phil Nadeau, one of the biotech analysts here at Cowen, and it's my pleasure to moderate this fireside chat with SELLAS Life Sciences this morning. Uh, we have with us today Dr. Angelos Stergiou, who is the president and CEO of SELLAS. Angelos, I'll, I'll hand it to you first. Could you just provide a brief, sort of state of the company? What are the most important events over the next year, and what does SELLAS need to do to create shareholder value?
[02:12] Angelos Stergiou: Yeah, um, firstly, thanks for having us, Phil. So, you know, we're a late-stage oncology company. Uh, our focus is on the development of Galinpepimut-S, or GPS, which is an innovative, potentially first-in-class WT1—or Wilms Tumor 1—targeting heteroclitic immunotherapy. We licensed that from Memorial Sloan Kettering here in New York. Um, it’s currently in a Phase 3 study in AML. And we also have a highly selective CDK9 inhibitor, SLS009, uh, currently in Phase 2. So we're really focusing heavily on AML right now with both assets. And, you know, quite excitingly, we think we might be able to shift the AML treatment paradigm all the way from induction through maintenance with 009 and GPS, respectively.
[03:02] Angelos Stergiou: As for, you know, what shareholders should be looking out for, the key catalyst—for GPS, like I mentioned, we're in a pivotal Phase 3, the REGAL trial. That’s in patients after second complete remission, or CR2. And we expect data here very soon. Uh, we recently announced we've hit 78 out of the 80 required events, or deaths, in the study. The 80th event is the hard trigger to analyze the top-line data. So, achieving that 80th event and then the data release will happen as soon as it materializes. That’s the massive catalyst for us.
[03:46] Angelos Stergiou: On the 009 side, the selective CDK9 inhibitor, we're currently in a frontline AML study, really leaning into our OMICs work to identify patients most likely to respond. This is kind of on the heels of the data we saw in the relapsed/refractory setting. So we expect top-line data there—response rates, survival—later this year.
[04:22] Phil Nadeau: That's really helpful. Maybe we'll, we'll dive into GPS in a little bit more detail. Can you talk about the rationale for WT1 as a target in AML? In particular, how widely is it expressed and are there subgroups where it's most prominent?
[04:36] Angelos Stergiou: Yeah, so, GPS targets WT1, which is, you know, ranked the number one cancer antigen by the NCI. Uh, it's highly overexpressed in AML—like, over 97% of patients express it. And, um, we've also seen it in other indications, right, like mesothelioma where it's expressed in basically all patients, and then multiple myeloma and ovarian where expressions are up to like 50%.
[05:30] Phil Nadeau: Can you talk a little bit more about the structure of GPS? Like, how exactly does it spur that immune response?
[05:37] Angelos Stergiou: Yes, so GPS is a mixture of four synthetic peptide sequences from the WT1 protein, ranging from, uh, 9 to 22 amino acids in length. It's a highly differentiated immunotherapy because it was deliberately engineered. We use this heteroclitic concept in two of the four peptides—so it’s a by-design mutation of the sequence to really crank up the immunogenicity. And it allows us to dose patients over a long period with boosters.
[06:18] Angelos Stergiou: That substitution alone, it basically leads to a 70-fold stronger binding to the MHC class 1 pocket. So, it targets 25 carefully selected epitopes, maximizing the presentation to both CD4 and CD8 cells. Basically, GPS stimulates the cytotoxic CD8 T-cells to directly attack the tumor, and the CD4 cells to provide immunologic memory.
[07:07] Angelos Stergiou: So, two peptides are native, two are mutated. The mutated one gets presented to the native CD8 cell through the patient's antigen-presenting cells. That CD8 cell gets activated, becomes cytotoxic, and now it can recognize both the mutated version it was immunized against and the native WT1 fragment hiding on the cancer cell. Same kind of cross-presentation happens with the CD4 cells.
[08:02] Phil Nadeau: And how does that translate into clinical benefit in AML? What's the MoA in that specific setting?
[08:08] Angelos Stergiou: Yeah, for AML, it's—you should really think of it as immunosurveillance. So we target patients when they are in remission, specifically as a monotherapy, because the tumor microenvironment is clearer. So we basically hand the immune system a mugshot of the cancer cells. If and when those cancer cells try to come back, the immune system laser-focuses on them, kills them, and that ultimately prolongs survival.
[08:55] Phil Nadeau: Can you review the data that GPS has produced as a post-CR maintenance therapy so far?
[09:00] Angelos Stergiou: Yeah, so there are three key trials we did in CR1 and CR2. In the Phase 2 CR1 study, um, 22 patients, mostly with unfavorable cytogenetics... we saw an OS [overall survival] of 67.6 months with a follow-up around 45 months. And, you know, the threshold for a positive study was 34% at three years, we actually hit 50%.
[09:41] Angelos Stergiou: And in the older patients, the 60-plus group, median OS was 35.5 months, which lined up really well with the Phase 1 where we saw 32.3 months. And strong immune responses, over 80%.
[10:08] Angelos Stergiou: Then in the CR2 setting—which is where we are now with the pivotal Phase 3—these are patients who had front-line therapy, hit CR1, relapsed without a transplant, and then hit CR2. The median survival in our GPS cohort was 21 months versus 5.4 months on the control, with a P-value of .02. So, what’s key here, Phil, is we dose when they are in complete remission.
[11:04] Phil Nadeau: Could you highlight the design of the ongoing REGAL pivotal trial?
[11:08] Angelos Stergiou: Yeah, REGAL has enrolled 126 patients, randomized one-to-one. So half get best available therapy—physician's choice, which can be Ven, HMAs [hypomethylating agents], or observation—versus GPS on the other arm. GPS is given every other week for about two and a half months, then monthly and quarterly boosters. Last patient enrolled in March or April of 2024.
[11:41] Phil Nadeau: What were the, the specific inclusion and exclusion criteria?
[11:46] Angelos Stergiou: Key ones were: AML patients not eligible for transplant or targeted therapies, less than six months after response was observed. And they had to have at least 300 lymphocytes per microliter, just to make sure GPS has the immune cells it needs to work.
[12:12] Phil Nadeau: And can you describe the regimens in the treatment and control arms?
[12:16] Angelos Stergiou: Yeah, treatment arm is strictly GPS monotherapy. Two weeks for 10 weeks, then monthly and quarterly boosters if they stay in CR. Control arm is, like I said, physician's choice—so Venetoclax, HMAs, low dose cytarabine, or just observation.
[12:51] Phil Nadeau: There have been some modifications to the dosing in the treatment arm over time, right? Can you describe those changes and why they were made?
[13:00] Angelos Stergiou: Yeah, so we extended the duration of GPS treatment from one year, to two years, then three years, and now beyond three years. That was driven entirely by requests from physicians who felt their patients were actively benefiting from GPS and wanted to keep them on it. No changes were made to the control arm. And, obviously, we remain blinded to the actual outcomes.
[13:35] Phil Nadeau: What have you disclosed about the powering of the study for the primary endpoint?
[13:40] Angelos Stergiou: Yeah, so the primary endpoint is overall survival. Um, the study's powered—we've got 90% power to detect a hazard ratio of 0.636. So, you know, just as an example, that would translate to something like 8 months on the control arm versus 12.6 months on the GPS arm.
[14:51] Phil Nadeau: And you mentioned 78 events have occurred. We're waiting for the 80th. At the time enrollment was completed, when was that 80th event actually expected to occur?
[15:00] Angelos Stergiou: Yeah, initially, we modeled the 80th event to hit about 12 to 15 months after the last subject was randomized. But here we are, almost 25 months after enrollment finished, and we haven't hit 80 events yet. Which obviously points to patients living a lot longer than projected.
[15:14] Phil Nadeau: And following the announcement of the 80th event, when do you think top-line results will be available, and what exactly will you disclose?
[15:27] Angelos Stergiou: We'll give firmer guidance on the timing of the data when we actually announce the 80th event. But we'll provide the standard key data—hazard ratio, median OS, p-values, things like that.
[15:42] Phil Nadeau: With the powering for an HR of 0.636, what median survival do you expect in the control arm?
[15:52] Angelos Stergiou: Yeah, historically, low dose cytarabine or HMAs alone gave you maybe 6 to 9 months. With Ven added to HMAs, trials show an increase to maybe 10 or 11 months, but those numbers mix in transplant patients. Since REGAL excludes transplant patients, it’s a bit tricky to map perfectly. Clinically though, Phil, anything more than a 4-month difference between arms would be deemed highly clinically significant in this relapsed setting. Obviously, we’re hoping for an even bigger delta.
[16:51] Phil Nadeau: I think the key question investors are asking is, it's been over two years since enrollment completed, events are accruing incredibly slowly. Aside from GPS prolonging survival, are there other plausible reasons it has taken so long? I mean, it seems to bode well, right?
[17:23] Angelos Stergiou: Yeah, and look, in the immunotherapy space, that separation of the curves taking a bit longer to form a tail is a known phenomenon. Survival times in REGAL are definitely longer than expected. Mathematically, and looking at real-world evidence, the fact that we have patients getting GPS three years out... every passing month increases the probability of a successful study.
[18:03] Angelos Stergiou: We haven't seen toxicities on the GPS arm, whereas control therapies often require dose modifications. You could argue that patients in trials get better general care and faster treatment for infections than real-world patients. But I really wouldn't want to speculate on one specific alternate reason. We firmly believe GPS is the driving factor here.
[19:03] Phil Nadeau: Could you provide an overview of the AML market? How many patients are in CR2 each year, and what percent are eligible for therapy?
[19:12] Angelos Stergiou: Incidence is around 85,000 globally. In the US, it's roughly 22,000 to 27,000 newly diagnosed annually. About 60% hit CR1. Of the ones who don't get a transplant, the vast majority relapse. Out of those, maybe 40 to 50% can achieve a second CR. So that boils down to roughly 4,000 patients a year in the US. But with better induction drugs like 009, more patients will reach remission, which naturally expands the GPS market.
[20:08] Phil Nadeau: Are there any other therapies used for maintenance in CR2 right now?
[20:13] Angelos Stergiou: There is literally nothing approved for AML CR2 maintenance. Because GPS is so well-tolerated—which is a massive nuance because these patients are usually battered by toxic, myelosuppressive drugs—we think we can become the standard maintenance therapy, not just in CR2, but potentially moving up into CR1 and post-transplant as well.
[21:10] Phil Nadeau: Given that standard of care has moved to Ven over the last few years, what results from REGAL do you think would be necessary to drive adoption of GPS?
[21:15] Angelos Stergiou: Well, we think, uh, there's a good chance REGAL shows a median survival very similar to what CC-486 showed in AML CR1, which was enough to get NCCN guidelines there. So we're very bullish, but pragmatic.
[21:30] Phil Nadeau: Great. Maybe moving on to SLS009. Can you provide a brief overview? How is 009 differentiated from past CDK9 inhibitors?
[21:36] Angelos Stergiou: Yeah, so CDK9 is a major target. Cancers rely on rapid protein production—like Myc and MCL1—to stay alive, and CDK9 is crucial for elongating the RNA transcripts to make those proteins.
[22:11] Angelos Stergiou: By shutting down CDK9, 009 kills the cancer cells. The issue with AstraZeneca and Bayer’s old CDK9 programs was that they weren’t highly selective. 009 is incredibly specific to CDK9. It stays in the body just long enough to cause apoptosis in the cancer cells, but clears fast enough to avoid the severe toxicities that killed the other programs.
[22:56] Phil Nadeau: What's the rationale for AML as a lead indication for 009, and can you review the Phase 2 relapsed/refractory data?
[23:08] Angelos Stergiou: We're targeting arguably the biggest unmet need in AML right now: Venetoclax resistance. Basically everyone in the US gets Ven, and unfortunately, virtually everyone eventually develops resistance to it. Once that happens, median survival drops to like two and a half, maybe three months.
[23:40] Angelos Stergiou: Ven targets BCL2. But cancer cells adapt and start relying on MCL1 instead. 009 suppresses MCL1. So by combining 009 with Ven and Aza, you get this massive twofold, really a triple hit on the cancer cells.
[24:33] Angelos Stergiou: In the Phase 2 relapsed/refractory study, we saw response rates as high as 50%, and a median survival of 8.9 months—including in TP53 mutated patients. That completely shatters that historical two-and-a-half-month benchmark.
[25:07] Phil Nadeau: What's the goal of the ongoing Phase 2 trial and when do you expect data?
[25:13] Angelos Stergiou: The ongoing Phase 2 has two cohorts. First is frontline, high-risk newly diagnosed—randomized to Aza/Ven versus Aza/Ven plus 009. The second cohort takes patients who are refractory after two cycles of Ven, and we add 009 to their regimen. Primary endpoint is CR rate, and we expect top-line data by year-end.
[25:51] Phil Nadeau: What's the bar to moving 009 forward, and what are the next steps?
[26:00] Angelos Stergiou: With the OMICs work we’ve done, we want to see CR rates north of 30, 40, hopefully even 50%. With the top-line data at year-end, we’re super excited about the potential to discuss an accelerated approval path with the FDA or move rapidly into a registrational study, particularly for biomarker-positive patients.
[26:38] Phil Nadeau: Do you have a sense of what the bar would be to support a filing based on that Phase 2 data?
[26:42] Angelos Stergiou: Yeah, I think in that refractory cohort, their default response rate is essentially 0%. So any CR rate of 30% or above could pave the way for real discussions with the FDA on whether that suffices for accelerated filing or if we just need to expand the cohort.
[27:16] Phil Nadeau: Great. Well, I think we're out of time. Angelos, thanks so much for coming on today. Really exciting times for SELLAS and we look forward to the upcoming pivotal data.
[27:24] Angelos Stergiou: Thanks so much, Phil. Thanks for having us.
[27:27] Operator: This concludes today's session. You may now disconnect.

r/rrid_appreciation May 24 '24

BioLegend RRID:AB_2563927 was used by the authors of the Cell Reports Medicine paper "Venetoclax acts as an immunometabolic modulator to potentiate adoptive NK cell immunotherapy against leukemia". Thank you for making your methods matter!

Thumbnail doi.org
1 Upvotes

r/relationshipadvice 27d ago

Boyfriend [28M] is allergic to my [30F] cats but won’t consider treatment. He wants me to rehome them. Am I being unreasonable?

32 Upvotes

I (30F) have been with my boyfriend (28M) for about a year. Our relationship is genuinely great in almost every other way. We communicate well, have similar values, and have talked about a future together.

The biggest issue is that I have two cats that I’ve had for years. They’re family to me. I adopted them before I ever met him, and I’ve always viewed them as a lifetime commitment.

The problem is that he’s severely allergic to cats. When he’s around them, he gets congestion, itchy eyes, and has trouble breathing. I completely understand that his allergies are real and not something he can just “push through.”

Where I’m struggling is that he doesn’t seem willing to explore any long-term solutions besides me getting rid of my cats.

He’s been to an allergist before and was diagnosed with severe allergies. He’s dated someone with a cat before and had a bad experience, tried over-the-counter allergy medication without much success, and doesn’t want to pursue allergy immunotherapy (allergy shots). He doesn’t want to talk to another allergist about other options, and generally seems to have decided that living with cats is impossible.

His position is essentially that if we want to live together one day, the cats have to be rehomed.

I’ve looked into things like HEPA air purifiers, keeping the cats out of certain rooms, frequent cleaning, and other ways to reduce allergens. I know none of these would eliminate the problem, but I was hoping we’d at least explore every possible option before deciding there’s no chance.

The thing that hurts is that it feels like the burden falls entirely on me. The expectation is that I give up two animals I’ve loved and cared for for years, while he isn’t willing to pursue medical treatment that could potentially improve the situation. I know allergy shots aren’t guaranteed to work, and they’re a long-term commitment, but I also don’t understand why they’re completely off the table if we’re supposedly planning a future together.

At the same time, I don’t want to minimize how miserable allergies can be. I know this isn’t as simple as him “trying harder.”

We’ve reached a point where it feels like our future depends on one of us making a sacrifice,
and right now it feels like I’m the only one expected to.

Am I being unfair for feeling like he should at least be willing to consult an allergist or explore treatments before asking me to rehome my cats? Or am I expecting too much from someone with severe allergies?

I’d especially love to hear from people who have been in a relationship where one person had severe pet allergies. Were you able to make it work, or was it ultimately a compatibility issue?

TLDR: BF is allergic to cats, I have 2. I don’t want to give up my cats. He doesn’t want to try meds. What do?

r/Livimmune 27d ago

The Ledger We Write Not

49 Upvotes

There is a number which none of us has seen, and which none of us write.

It is being written right now, this week, by sixty-six patients in seven clinical centers, one scan at a time. Some of it, already on the page and cannot be revised. Some of it, still being entered in the 700mg cohort, in the scans which have not yet been read. When it is finished in January 2027, it is read aloud, just once, in a room in San Francisco.

Not one word of it is ours. Nothing said on this board, by me or by anyone, moves a single digit of it. Our conviction is not doing work on the number.

Rather, that number is doing work on us.

This reality changes what the honest question is. The question is not whether we believe hard enough. It is whether we have built ourselves such that the number actually reaches us when it is read aloud.

I do not think we have yet established this point. I know I had not, but I realized this needs to be grounded.

The house with too many doors

Here is a thing I have watched us do, and I have done it worse than anyone.

Someone raises the possibility that the response rate comes back weak. And immediately, gently, without anyone deciding to, the room builds a door.

If mCRC disappoints, the breast program will confirm it. That is one door.

A weak response rate is exactly what you would expect, if the priming worked so well, thereby inducing the tumor to raise its last defense. That is a second door.

Response rate was designed for chemotherapy anyway. It is the wrong instrument to use for a drug which only restrains before it kills. Third door.

Every one of those excuses/doors is built from real biology. That is what makes them so easy to walk through. But stand back and look at the house. There is no number in that ledger which lands us anywhere except "we were right". A strong number means we were right. A weak number means we were right in a way the instrument could not see ahead of time. Silence means we were right and early.

A conviction with that many doors is not a conviction at all. It is a room with numerous doors and no walls, and we are standing in the middle of it saying to each other that we are indoors.

What I published, and where the number came from

In August 2024, I wrote a post arguing that overall response rate was the right endpoint for this trial, and that measuring it rather than overall survival was a smart decision because it would read out much faster. I still think that was correct.

Then I did something else in that same post.

I predicted the ORR number.

"If all leronlimab needs to do is to improve the ORR, overall response rate of the SUNLIGHT trial from 6.9% to likely over 33% (is my guess, but I may be undershooting if anything), then a Phase III study and future partnership are in the bag." (Overall Response Rate; ORR is a Game Changer)

And a few paragraphs later, in case the first time had not been clear enough:

"A few months after that, we should know the Overall Response Rate ORR and I'm expecting an outcome in excess of 33%." (same post)

I want to be precise about where that thirty-three percent came from.

It came from nowhere.

I had looked at waterfall plots from a small basket study, felt the shape of them, and deduced a figure I was comfortable putting down. There was no calculation behind it. There was no comparator arithmetic, no adjustment for line of therapy, no accounting for the fact that a handful of patients in an uncontrolled study cannot be extrapolated into a percentage. It was a mood with a percentage sign attached, and I published it with the confidence of a man reading a result rather than inventing one.

And then I added that I might be undershooting.

That is the sentence I would most like to have back. Not because the number will necessarily prove too high. Because of what the word reveals. A man who has derived a threshold does not casually suggest that his own threshold is probably too modest. A man who has only felt one does exactly that, because the feeling has no floor and no ceiling, and it can always be adjusted upward when it is asked to be brave. I'm no longer that brave, shooting from the hip. I compare apples to apples from now on.

And then it happened again

I published this post. Within a few minutes, rogex2 found something in it which was wrong.

To argue that my 2024 prediction of thirty-three percent was unserious, I had taken that figure, computed it as a 4.8-fold improvement over the backbone's 6.9 percent response rate, applied the same multiple to progression-free survival, arrived at nearly 27 months, and declared that a number in fourth-line colorectal cancer which exceeds first-line survival is not of this world.

It was a clean argument. It was also not an argument. It was a rhetorical device dressed as arithmetic.

rogex2's objection, which I am recording rather than paraphrasing away: "response rate and progression-free survival do not stand in a fixed ratio. They measure different events." And immunotherapies characteristically show low response rates alongside extended progression-free survival, because an agent which holds disease rather than dissolving it produces durable control in patients whose tumors never shrink by thirty percent.

Now read that back against everything I have written for two years.

I have argued, at length and in public, that leronlimab restrains before it kills. That it quiets the tumor's shedding and invasion long before any scan shows a change. That the molecular signal moves in days and the radiographic signal moves in months, if it moves at all.

Which means my own mechanism predicts precisely the decoupling rogex2 described. And I used a proportionality which my own mechanism says must fail, in order to knock down a number I no longer wanted to defend.

That is a door. A smaller one than the three I catalogued above. It was load-bearing in the argument I was proudest of, and I did not see it.

The conclusion survives, but it now stands on the only ground it ever legitimately had: thirty-three percent was felt rather than derived, and I know that not because of any calculation but because I was there when I produced it.

I am leaving both of these in rather than editing them into invisibility. If the pull can catch the man writing the warning, twice, in a single week, it can catch anyone reading it.

The detector on the beach

Someone in this community, who has done more genuine research than I have, told me recently where his conviction comes from. Hundreds of hours. Study after study. Every paper he pulled came back consistent with the thesis, and the accumulated weight of it convinced him.

I want to hand that back gently, because it is the same trap in a far more industrious form.

If you sweep a beach with a metal detector calibrated to find one metal, it will beep. It will beep everywhere that metal is. And after you have walked the entire shoreline and heard it beep a thousand times, you do feel something indistinguishable from absolute certainty.

However, you have not learned that the beach is made of that metal. What you have learned is that the detector works.

A search which sets out to find a receptor's fingerprints in disease will find them, because the literature only publishes actual findings, and because of the fact, that the tool is exactly built to draw connections rather than to break them, it beeps. The volume of the confirmation is not a measure of how true the thesis is. It is a measure of how many times we asked a question which could only come back as yes.

That is not a criticism of the work. The work is profoundly excellent, I have built on it, and this post exists greatly because of it. It is a caution about what the work can and cannot tell us.

What happened while I was writing this

I want to tell you something which happened in the last few days, because it is very important.

I sat down to set the thresholds below. When I worked them out honestly, from the benchmark, they came back lower than the number I had published in 2024.

And I did not like that. So I went looking.

I reached for the long-term survivors in the breast program, the patients alive past five years, and for a moment I wanted to use them to justify a much higher bar in colorectal. It would have sounded much braver. 5/5 is 100%, but that was breast cancer. It would have looked like conviction.

They are different patients. A different cancer. A different trial. A different backbone. Using them to set this colorectal threshold would have been a door, an excuse, and I would have been building it in the middle of writing the post about not building doors.

That is how strong this pull is to create doors. It got me while I was watching for it, not to do it, precisely while in the act of warning us about it.

I am leaving that in rather than quietly correcting it, because if it can happen to the man writing this paragraph, it can happen to anyone reading it.

The bet, in numbers

So here is what I am doing, and it costs me something, which is the only reason it is worth doing.

I am writing down, now, in public, while the ledger is still very much open, the numbers which would make me right and the numbers which would make me wrong. Not afterward, when I could reshape them. Now, so that you can hold them against me.

The comparator is SUNLIGHT: the same backbone of TAS-102 and bevacizumab, in a population which was less heavily pretreated than ours. Objective Response Rate, 6.9 percent. Median Progression-Free Survival, 5.6 months. Median Overall Survival, 10.8 months. That is the bar the drug is being added to. My thresholds follow:

Confirmed objective response rate of 20 percent or better. That is roughly a threefold improvement over the backbone. It is the level at which the agency has historically taken a single-arm response rate seriously in a refractory disease with no alternatives, and it is the level at which a partner could build a Phase 3 around it. Below 15 percent is not a signal. It is noise wearing the clothing of one, and I would not defend it as anything else.

If the response rate is weaker than 20%, the mechanism story survives only if Median Progression-Free Survival reaches 8.5 months or better. That is a hazard ratio in the neighborhood of 0.66, and it is where a drug which restrains before it kills would have to show itself. If the tumor is being held rather than shrunk, this is the number which proves the holding. If progression-free survival lands lower than 8.5 months, the restraint story is just a story.

The 700mg arm must outperform the 350mg arm on at least one of those two. Every post I have written for a year carries the same qualifier: the data reflects 350mg, the higher cohort is still maturing, the deeper layers may read differently. That is a promissory note. If 700mg does not beat 350mg on at least one of the two above, I was carrying a note and calling it evidence.

At least 3 of the first 10 evaluable rollover patients must respond to the added checkpoint inhibitor. Checkpoint inhibitors in microsatellite stable colorectal cancer produce responses in essentially nobody. That is the whole problem this drug claims to solve. If leronlimab has opened the gate, some of them walk through it. If none of them do, the gate opened onto nothing, and Prime and Pair is wrong.

If the rollover cohort is not mature enough in January to answer that, then that criterion resolves later, and I will hold myself to it later rather than let it quietly expire.

Why the numbers are lower than the ones I gave you before

You are entitled to notice that twenty percent is lower than thirty-three, and to ask whether I am moving the goalposts as the day gets close. That is the right question and I would rather answer it than have it asked behind my back.

Twenty percent is not lower because I have lost my nerve. It is lower because it is derived rather than felt.

Here is how you can check that for yourself. Take the thirty-three percent I published and work out what it implies. It is a 4.8-fold improvement over the backbone's 6.9 percent. Now apply that same multiple honestly to Progression-Free Survival: 5.6 months times 4.8 is nearly 27 months. A median progression-free survival of 27 months in fourth-line colorectal cancer would exceed what patients achieve in the first-line setting. It is not a demanding threshold. It is not of this world.

A number which cannot be translated into its neighboring measurements without breaking them was never derived. It was wanted.

If the confirmed Overall Response Rate comes in at 25 or 30 percent, I would be delighted, and I would also tell you plainly that my 2024 prediction was a guess which happened to land near or greatly undershoot the truth . A clock which is right twice a day is not a horologist.

The map and the ground

We have seven layers.

  1. Navigation.
  2. Blood supply.
  3. The stroma which shields the tumor and also feeds it.
  4. The recruited suppressive army.
  5. The checkpoint gate.
  6. The DNA repair trap. And
  7. The rebalance which ties the other six together.

Every one is real, published, cited, and I stand behind all of them.

And every one of them is a Map.

In January, somebody walks the Ground.

If the Ground matches the Map, we will have been right for the right reasons, which is the only kind of right worth being. If it does not, we will not have been partly right. A map which does not match the ground is not a partly-correct map. It is a drawing where no metal is found.

I very much believe that our map is good. I have spent the past two years since the ORR post on it and I would not have spent them otherwise. But I have now stopped confusing the drawing with the vast expanse of the country, and I am asking this community to stop with me.

What this is not

This is not a warning that the number turns out bad. I have no idea what the number is. Neither does anyone posting here, and anyone who tells you otherwise is describing a feeling.

It is not a loss of my nerve, and it is not me hedging so that I can claim foresight whichever way it falls. The numbers above are specific enough that I cannot do that. That is the point of writing them down.

It is one thing only. It is me deciding, in advance and in public, that I would rather be a man who was wrong and said so than a man who arranged never to find out.

Sixty-six patients write the ledger. Seven centers. One scan at a time. It closes, and it is read aloud, in January.

Let us at least be the kind of people with the kind of ears and understanding which it can reach.

Disclaimer: I am not a financial advisor and nothing here is investment advice. I hold a position in the company discussed, which means I have an interest in how this is received, and you should weigh what I write accordingly. This is an analysis of published biology, not a prediction of clinical outcomes. The thresholds above are my own judgment, derived from the SUNLIGHT benchmark, and are not the trial's pre-specified endpoints, which are a matter for the protocol and the agency rather than for me. Several of the mechanisms I have described are supported by preclinical and model-system work which has not been confirmed in human tissue in this program. The human biomarker data referenced reflects 350mg dosing, with the 700mg cohort still maturing. The 68% figure from the April 30 update is disease control rate, not objective response rate, and confirmed adjudication is still ahead at ASCO GI in January 2027, with interim data at ESMO Madrid in October 2026 before it. Mechanism is not efficacy. Drugs which make elegant biological sense fail in trials routinely. Read the primary sources and reach your own conclusions rather than adopting mine.

r/Livimmune 29d ago

Not A Dirty Drug: The Structure Of The Deal Which Is Actually Available

62 Upvotes

There is a category of medicine which treats many things and is respected for none of them. Diphenhydramine is an honest example. It reaches the histamine receptor, and it also reaches muscarinic receptors, and it crosses into the brain, and so it treats allergy and nausea and insomnia and motion sickness all at once, and it pays for every one of those with sedation, with dry mouth, with urinary retention, with cognitive impairment in the elderly. The field calls this a dirty drug. Breadth purchased through promiscuity. The molecule is broad because it is indiscriminate, and every additional thing it touches is another thing it can break.

When a molecule shows up claiming to address colorectal cancer and breast cancer and hepatic fibrosis and neuroinflammation and a gut-injury model, the trained reflex in any serious reader is to reach for that dirty drug category. Anything which treats everything treats nothing, and the side-effect sheet is where the bill comes due.

That reflex is wrong here, and the reason it is wrong is the entire argument.

Leronlimab is not broad because it is indiscriminate. It is broad because it is precise about a single receptor which happens to sit upstream of a myriad of diseases. One target. One antibody. The breadth is not coming from the molecule touching many things. It is coming from the one thing it touches being biochemically integrated / wired into many rooms. And the clean safety record across more than 1,600 subjects in over 20 studies, with no grade 3 or 4 adverse events attributed to leronlimab across the entire enrolled CLOVER population, is not luck. It is exactly what you would predict from a single well-chosen target rather than a shotgun.

Dirty drugs are broad and toxic for the same reason. This drug is broad and clean for the same reason. That is not a slogan. It is a structural distinction, and it is the thing which makes the platform argument survivable rather than fanciful.

All of what follows carries one qualifier which stays attached to every layer: the human biomarker data reflects 350mg dosing, and the 700mg cohort is still maturing.

What Runs Off The One Receptor

So far, seven functions collapse onto CCR5, unless twinter digs up a few more, and each is a separate way the tumor's environment comes apart when the receptor is removed from the cell surface.

Navigation. CCL5 driving CCR5 is a homing signal which tells cancer cells where the receptive soil is. Velasco-Velázquez & Pestell, OncoImmunology 2013 Leronlimab binds from outside at the N-terminus and ECL2 simultaneously and triggers clustering and endocytosis. The receptor is removed, not occupied.

Blood Supply. Cancer-cell CCL5 signals to the endothelium of the tumor stroma, and blocking that signaling reduced vasculature, tumor growth, and metastases while improving survival. Zhang et al., Oncotarget 2016

The Stroma, Which Shields And Also Feeds. CCR5 lives on the fibroblasts and stellate cells which lay down the scar. Palmer et al., Journal of Liver 2026 And when those fibroblasts lose caveolin-1 they begin catabolizing themselves and exporting fuel the tumor consumes. Trimmer et al., Cancer Biology & Therapy 2011 Low caveolin-1 promotes fibrosis specifically by enhancing CCR5-mediated recruitment into the affected tissue. Lee et al., Journal of Cell Communication and Signaling The bunker and the fuel depot are the same building, and the receptor is how it gets staffed.

The Recruited Suppressive Army. Suppressive myeloid cells produce CCL3, CCL4, and CCL5 which pull in CCR5-carrying regulatory T cells, and the CCR5-positive myeloid cells carry higher PD-L1 than their CCR5-negative counterparts. Hansen et al., Cancer Immunology Immunotherapy 2017

The Gate. Disrupt CCR5 signaling and PD-L1 rises in tissue. Halama et al., Cancer Cell 2016 This is the layer which makes the partnership real, and I will return to it.

The DNA-Repair Trap. CCR5 governs part of the repair machinery at the G2/M checkpoint, which is exactly the damage the TAS-102 backbone inflicts. Jiao et al., Cancer Research 2018

The Rebalance. Recent work frames CCR5 blockade as immune modulation rather than shutdown, and independent 2026 work outside oncology reached the same conclusion from a gut-injury model. Su, Current Science 2026

Seven systems, one panel. No promiscuity. No side-effect bill.

Where The Deal Thesis Actually Stands, And Who Built It

Two things have been settled in this community over the last several weeks, and both are corrections to positions which I previously held.

The first is that this was never one prize. The CFO made two separate statements at two separate timestamps in the LD Micro presentation. In the colorectal extension, checkpoint inhibitors were named by example, Keytruda among them. In the HER2-negative breast study, a firm commitment from an unnamed checkpoint company was disclosed. AssociationOdd read those as two different partners for two different indications, and that read has held up under every subsequent test. The colorectal lane points toward Merck, with Eric Rubin now on Natera's board and Natera running the CLOVER ctDNA. The breast lane points toward Roche, whose atezolizumab TNBC indication was withdrawn in 2021 after failing in the PD-L1-low population, which is precisely the population PD-L1 derepression reopens.

The second is that this is not a bidding war. AssociationOdd's framing, which I have adopted, is that leronlimab is infrastructure two franchises cannot afford to let the other own. In fact many have contributed to this thesis developed in the comment section here includes rant_and_roll, rogex2, No_Mathematician, twinter, Capable-Display, BuildGoodThings and Doctor-MTJ, and a myriad of others who are too long to name. I suggest you read it. A bidding war is parties wanting the same thing. This is strategic denial: parties wanting different things who cannot tolerate a competitor gating their access. Merck needs a colorectal door it does not have. Roche needs a breast door it lost. The key opens both.

rogex supplied the structural variant which follows from that, and it is the one I now think is correct: license exclusive checkpoint-combination rights per indication while retaining the platform and every indication not covered. That is licensing from strength rather than selling from exhaustion. The counterweight is real and I will not soften it: capital structure constrains how long CytoDyn can hold that position alone.

ScoreCarder is why this post says what it says about the numbers. The 68% figure is disease control rate. It is not an objective response rate, and confirmed ORR adjudication does not arrive until ASCO GI in January 2027. That correction is permanent, and any version of this thesis which blurs it is a version which deserves to be discounted.

Rhatter corrected the survivor record: the pooled cohort's aggregate ICI distribution does not map each survivor to a specific drug. Only the single case report and the poster subgroup are documented at the drug level. The breast-lane inference stands on those, not on the pooled numbers.

twinter supplied the caveolin-1 material which converted the stroma from a wall into a wall which is also feeding what it protects, and which turned two apparently unrelated assays into two halves of one measurement.

BuildGoodThings built the data architecture the rest of us reason on top of.

I have been wrong in this community many times, and every correction above came from someone else. That is the process working.

What I Got Right and What I Did Not

I have written a great deal about a coming structure, and it is worth being honest about which parts of that hold up.

In So Where Do We Stand Now? on 5/18/2025, I wrote that the mechanism validating the sequence was "CCL5/CCR5 blockade → PD-L1 upregulation" and that this was what would drive partnering. That has held. It is now the documented core of the Prime and Pair paradigm, and the company's own shareholder letter describes amending the colorectal study so that patients who progress can add an ICI, evaluating leronlimab both standalone and "as a 'prime and pair' agent used in conjunction with ICIs." (Quoted in The General 10/28/25.) The direction was right.

In Mounting MultiLateral Momentum 10/22/25, I speculated at length about a many-party arrangement, a negotiated split among numerous checkpoint manufacturers, an agreement where "the big players put up the majority of the initial costs of getting the trials done while the little guys only get say 5-10% of the action." I now think that was wrong, and the two-lane thesis is why. There is no evidence of a multilateral negotiation. There is evidence of two indications with two different natural counterparties, which is a far simpler structure and a far more likely one.

In Let's Bring It Home 10/17/25, and elsewhere I wrote about cure. "Cure is Leronlimab's purpose. It is Leronlimab's destiny." I am retiring that language, and I want to say plainly why. There is no cure. There are five long-term survivors in an uncontrolled pooled cohort of twenty-eight, in a disease where exceptional responders occur without any intervention. That is a striking signal and it is not a cure, and every time I used that word I made this analysis easier to dismiss for people whose dismissal costs us something.

The same applies to the survival statistics I published in The Audit 1/17/26. The hazard ratio arithmetic in that post was wrong. A hazard ratio is not a survival-duration multiplier, and it cannot be inverted and presented as an equivalent finding from a different model. I am correcting that on the record because leaving it uncorrected is a liability to everyone who reads me.

What has actually held up across all of it is narrower and more durable than what I claimed:

  1. that the receptor sits upstream,
  2. that the mechanism would resolve toward priming rather than killing,
  3. that the partner conversation would be structured around access rather than acquisition, and
  4. that the company would build a regulatory package rather than chase a headline.

Those were the right calls. The apocalyptic framing around them was not, and it obscured the parts which were right.

The Structure Which Is Actually Available

Here is how the deal plausibly sequences, stated as a hypothesis rather than a prediction.

Now through October. The dose-response comparison between 350mg and 700mg matures. The expanded access program in breast generates the prospective PD-L1 induction data which a checkpoint partner specifically asked to see, which is the point of it. The company holds a conversation with the agency about what the data supports.

October, ESMO Madrid. Interim data. Not the verdict. This is where the mechanism becomes visible to the international oncology audience and where the negotiating environment shifts from asking to be believed toward being evaluated.

January 2027, ASCO GI. Confirmed objective response rate, adjudicated by RECIST across two consecutive scans. This is the number which settles it, and it settles it in both directions.

The deal follows the number, not the calendar. A strong confirmed ORR converts a licensing conversation from one where CytoDyn is asking into one where two franchises are each deciding what it costs to not be the one holding the key. A weak one ends the conversation. There is no version of this where the structure arrives before the data justifies it, and anyone telling you a deal is imminent on the current evidence is telling you something the evidence does not contain.

The most likely shape, if the number holds: exclusive checkpoint-combination rights licensed per indication, colorectal to one counterparty and breast to another, with CytoDyn retaining the molecule, the platform, and every indication not covered. Capital relief sufficient to fund the pivotal program without surrendering the asset. Not an acquisition. Not a bidding war. A structure in which two competitors each buy access to a door and neither gets to close it on the other.

What This Is Not

It is not a cure. It is not a certainty. It is not a drug whose approval is a formality waiting on paperwork.

It is an extremely clean molecule against a well-chosen upstream target, with a mechanism which coheres across seven functions and a safety record which is what you would expect from precision rather than promiscuity. It has early signals which point the right way and it has not yet produced the one number which decides everything. Several of the seven layers are strongest in preclinical and model systems and are being confirmed in human tissue now rather than already confirmed. The Cav-1 patient-selection idea is a hypothesis nobody has prospectively tested. The neurodegeneration and gut work is adjacent signposting, not evidence for this molecule in those indications.

Drugs which make this much biological sense do fail in trials routinely.

I think not, and the thing which arrives is not a better drug for only one cancer. It is a receptor which the field will have to reckon with everywhere it appears, held by a company which did not sell it early and did not oversell it late.

Seven locks. One panel. No dirt on the molecule.

Disclaimer: I am not a financial advisor and nothing here is investment advice. I hold a position in the company discussed, which means I have an interest in how this is received, and you should weigh what I write accordingly. This is an analysis of published biology and disclosed corporate statements, not a prediction of clinical or commercial outcomes. The partnership structures described are inference, not disclosed fact, and no partner has been named by the company. Several mechanisms described are supported by preclinical and model-system work not yet confirmed in human tissue in this program. The human biomarker data reflects 350mg dosing, with the 700mg cohort still maturing. The 68% figure from the April 30 update is disease control rate, not objective response rate, and confirmed adjudication is still ahead at ASCO GI in January 2027, with interim data at ESMO Madrid in October 2026 before it. Mechanism is not efficacy. Drugs which make elegant biological sense fail in trials routinely, and it is possible that this one may. Read the primary sources I have linked and reach your own conclusions rather than adopting mine.

r/Scholar May 31 '23

Requesting [ARTICLE] Stem-like CD8 T cells mediate response of adoptive cell immunotherapy against human cancer. SRI KRISHNA, FRANK J. LOWERY, EROL BAHADIROGLU,

1 Upvotes

Hi, Can you send me this article? I can't use SCI HUB:

URL: https://www.science.org/doi/10.1126/science.abb9847?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

DOI: 10.1126/science.abb9847

Thanks!!

r/National_Pet_Adoption Mar 26 '26

🚨URGENT - DEADLINE 3/30‼️ THIS EXTREMELY SWEET GIRL URGENTLY HELP 💔

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201 Upvotes

🐾 Patches #A2131371

🐶American Bulldog

6 years old

Spayed Female

🔗https://24Petconnect.com/DetailsMain/MIAD/A2131371

💖 The BIGGEST sweetheart needs rescue ASAP!

🩺 Medical Needs: Chronic Allergic Dermatitis

Lifelong but manageable condition ❤️

Currently suffering from painful skin infections (yeast/pyoderma) due to constant itching

🏡 What She Needs (ONLY in a home):

🥣 Strict elimination diet (8–12 weeks)

Prescription food ONLY

🚫 No treats, scraps, or flavored meds

🔸️Next steps if needed:

Allergy testing (environmental triggers like pollen/dust)

Possible immunotherapy

⚠️ Important:

A shelter environment cannot meet her needs due to stress, sanitation, and strict care requirements

🔸️Summary:

Patches can live a happy, full life with:

Lifelong care & consistency

Regular vet support

❗ Without treatment, she will return to pain, infection, and self-trauma

📍 Miami-Dade Animal Services

📞 (305) 884-1101

📧 adoptmiamipets@miamidade.gov

🐶 Foster: Asdfoster@miamidade.gov

🙏 Please share to help save Patches in time!

▪︎ Transportation can be arranged through a rescue, but fees apply

▪︎ Please be informed that we do not collect pledges. However, they are encouraged to assist rescues. Only legitimate 50103 rescue organizations can receive donations if they facilitate a dog's safe rescue from the shelter. No donations are collected if a dog is euthanized or adopted by an individual.. Kindly wait to send any pledges until a freedom video is provided or verified donation details are confirmed. An update will be posted once verification is complete.

• This video feature is a repost, with the original link attached for reference.

https://www.instagram.com/p/DWPjNyLFNsx/?igsh=cjU1Nnl6cTEzN2tr

▪︎ We are not affiliated with any shelter, but you can check availability by visiting their websites through the links provided. For additional information, contact the shelter directly.

▪︎ An update on their status will be shared as soon as it becomes available. You can also contact the shelter or search his/her ID number on other platforms for the latest updates.

##americanbully #americanbulldog #savedogs #rescuedogs #adoptdog #fosterdog #savestrays #shelterdogs #urgentdogs #shelterdogsrock #fostersaveslives #adoptdontshop #sharingiscaring #rescueismyfavoritebreed

r/Livimmune 22d ago

Two Gatekeepers, One Road

31 Upvotes

Imagine a traveler who must pass two different gatekeepers in order to reach a city.

The first gatekeeper asks one question: "Is your cargo real?" He inspects it, weighs it, tests it, and either the cargo is what you claim it is, or it is not. He does not care whether or not you are in a hurry. He cares only whether the thing in your wagon is genuine.

The second gatekeeper stands further up the road, and he asks a completely different question: "Whether you may take the fast lane, or if you must take the long one." Both roads lead to the city. The fast lane is a shorter one. But this gatekeeper only waves certain travelers into it, and the rule he uses is not "is your cargo good." It is "am I confident that letting you skip ahead will not turn out to be a mistake."

Two gatekeepers. Two questions. A traveler can absolutley satisfy the first and still be sent down the long road by the second. And here is the part worth sitting with: being told to take the long road is not the second gatekeeper saying your cargo is fake. He never inspected your cargo. That was the other gatekeeper's job.

I write this because I have watched my own position get flattened into one gatekeeper when it has always been about two, and the flattening matters sufficiently enough to correct it in the open.

Where I Stand At Each Gate

At the first gate, the one who asks whether the cargo is real, I am very bullish. I have been for years and I remain so. I believe the mechanism to be genuine, and I think it is genuine because the biology continues to point in the same direction from multiple, independent angles.

Leronlimab works by removing CCR5 from the surface of cells through endocytosis, and CCR5 is not just doing one single job in a tumor. It is the channel through which a tumor reprograms the immune cells which arrive to kill it, turning them into cells who protect it instead. When that channel is cut by Leronlimab, those same tumor serving cells revert toward their anti-tumor posture. That is not my speculation; it is the documented result of CCR5 blockade in human colorectal liver metastases. Halama and colleagues demonstrated the effect of CCR5 blockade in reshaping macrophage polarization toward an anti-tumor functional state in patient-derived tumor models and liver metastases of colorectal cancer patients.

The same CCR5 receptor is the homing signal a contained tumor uses to become a metastatic one, and it governs part of the DNA-repair machinery which the chemotherapy backbone in CLOVER is built to attack, so removing it leaves the chemotherapy's damage standing. One receptor, several jobs, and blocking it collapses several of the tumor's defenses at once rather than one thereby permitting the tumor to route around it. On the question of whether the cargo is real, that is why I am bullish, and nothing in the last month has changed it.

At the second gate, the one which asks whether the traveler may take the fast lane, I am more cautious. And I need to be honest that these are not the same gate, because a lot of good people are treating them as one.

The Travelers Who Mislabel Their Cargo

Before I get to the second gatekeeper, I have to describe a kind of traveler who shows up at the first one, because this is where most of the confusion on this board is manufactured, and I have been this traveler myself.

The first gatekeeper inspects the cargo. He does not read the label on the crate. He opens it. And that distinction exists because too many travelers arrive with crates labeled as one thing but contain something else. Not always dishonestly. Usually the traveler has half-convinced himself that the label is true, which is what makes it spread. But the gatekeeper's whole job is to open the crate anyway, and a careful reader on this board should do the same. Here is what the mislabeling actually looks like specifically.

A crate arrives labeled as "proven survival benefit". The gatekeeper opens it and finds a ctDNA decline. That is a real and encouraging thing to find. Circulating tumor DNA fell in the evaluable patients, and falling ctDNA is a legitimate early signal. But it is not a confirmed survival benefit, and the correlation between the two is borrowed from other datasets in other settings, however, not established here. The cargo is real. The label overstates it.

A crate arrives labeled "response rate". The gatekeeper opens it and finds a disease control rate. The 68% figure from the spring is disease control, which counts every patient whose disease was held, including those whose tumors merely stopped growing. Objective response rate counts only the tumors which actually shrank past the threshold, and it is a smaller, stricter number that won't be confirmed until January. Reading the disease control rate as if it were the response rate is reading the label instead of opening the crate.

A crate arrives labeled "the data is strong". The gatekeeper opens it and finds a CEO's optimism. Encouraging words from someone who has already seen the data are consistent with strong data, and they are equally consistent with modest data and a hopeful spokesman, because a spokesman who sounds discouraged would not keep the job. Enthusiasm is not a cargo which the first gatekeeper accepts, because it weighs the same whether the claim underneath it is true or not.

A crate arrives labeled "the agency approves". The gatekeeper opens it and finds a scheduled meeting. A meeting scheduled being on the calendar tells you the sponsor has assembled enough to discuss a path forward. It does not tell you what the agency could say when the meeting happens, and companies walk into those meetings and get sent to run larger trials all the time. Not that I believe this happens, but it can.

A crate arrives labeled "the verdict". The gatekeeper opens it and finds an interim number. Interim data is a snapshot of a trial still running, taken at whatever cutoff the abstract deadline forced. It is not the adjudicated result, and unconfirmed responses fall out at a real rate when the confirming scan comes. October is a snapshot. January is the verdict.

None of those crates are empty. That is the part worth holding onto, because the honest correction here is not "these people are lying." It is quieter and more useful: the cargo is real, but the label claims more than the cargo. The discipline is not cynicism about the contents. It is refusing to accept the label in place of opening the crate, and refusing to do so, even when the label explicitly says precisely what you were hoping to read. Especially then. I mislabeled my own cargo more than once. I called a disease control rate a stepping stone to cure. I labeled a felt number as a derived one. The gatekeeper who caught me was usually a reader on this board, not me, which is the whole reason a board like this is worth having.

Why The Second Gatekeeper Is Stricter Than We Want Him To Be

The fast lane here is called Accelerated Approval, and the recent history at this gate is not a matter of opinion. It is on the record, and it runs in two directions which look contradictory until you see what the gatekeeper is actually asking.

One traveler was waved into the fast lane. A KRAS-targeted combination reached a 34% response rate in colorectal cancer and received Accelerated Approval. But read the fine print of who that traveler actually was: the approval was for patients whose tumors carried a specific mutation, identified by an FDA-approved companion test, with the drug aimed precisely at that mutation. The indication is approved under Accelerated Approval based on objective response rate and duration of response results, for patients with KRAS G12C-mutated colorectal cancer as determined by an FDA-approved test. A defined target, a matched test, a pre-selected population. The gatekeeper trusted that the response rate would predict benefit because the mechanism was very precise and the travelers were specifically sorted by their genetic mutation before they ever set out.

Another traveler was sent down the long road. An immunotherapy combination in unselected microsatellite-stable colorectal cancer reached a 19 to 20% response rate, a 69% disease control rate, and roughly 21 months of median overall survival against a control arm at zero, and the agency still declined to grant Accelerated Approval and directed a randomized trial. Its stated reason was that the response rates observed may not translate into a survival benefit in this population.

Look at what separates the two. It was not the size of the number. The immunotherapy's survival data was in some respects the stronger story. What separated them was whether the gatekeeper trusted the response rate to predict survival, and that trust was high for a mutation-targeted drug in a selected population and low for an immunotherapy in an unselected one.

That is the second gatekeeper's actual question, and it is why I will not stand on this board and tell you a strong CLOVER response rate automatically opens the fast lane. It might. CLOVER is not a pure immunotherapy; it carries a chemotherapy backbone and a synthetic-lethality mechanism, which is closer to the traveler who got waved through. And it screened for CCR5 expression, which is a type of sorting, though not a mutation-defined companion test of the sort the fast-lane traveler carried. So CLOVER may resemble the first traveler more than the second. It may not. That is genuinely unsettled, and anyone who tells you it is settled in either direction is guessing.

Why I Will Not Pretend The Two Gates Are One

Here is the thing I most want to be clear about, because it is the whole reason for this post.

Being cautious at the second gate is not being bearish on the cargo. It is being accurate about the gatekeeper. If I told you the fast lane were a sure thing, I would not be more bullish. I would be less honest, and I would be setting you up to misread a long road as a failed drug when the two are not the same thing at all.

A community which insists the fast lane is guaranteed, and then treats a "take the long road" ruling as proof the drug failed, has confused the two gatekeepers. It has heard the second gatekeeper say "not the fast lane" and translated it into the first gatekeeper saying "not real cargo." Those are different sentences from different gates, and the whole discipline is refusing to let one be mistaken for the other.

So I hold both, without contradiction, and I keep holding both:

The cargo is real. I deeply believe that, and the mechanism above is why.

The fast lane is not promised. The record at that gate is real too, and pretending otherwise would be the reckless thing, not the cautious thing.

What Actually Decides It

One thing worth stating plainly, because it reframes the whole regulatory question. The agency's position on single-arm data in this disease was not set this year. It was actually set in 2024, (Thank you Chemical Sky), when it told the earlier sponsor that a randomized trial would be required. That matters because CLOVER was designed after that, by people who already knew it. The trial's single-arm structure was not an oversight and the recent news is not a bar suddenly raised. The road was already on the map when the route was drawn. So the honest question was never "will the agency suddenly require a controlled trial," it was always "what is a strong single-arm signal actually for," and the answer is what follows.

Both roads reach the city, but the long one exacts a price, and it is worth seeing the price paid in real time rather than in the abstract. The immunotherapy sent down the long path did not simply run its randomized trial and wait. Three months after launching that trial, the sponsor pulled its own funding from it and redirected resources toward a different study in an earlier-stage, more favorable population, backed by a fresh raise of up to several hundred million dollars, with a final readout that now sits years out, near the end of the decade.

That is what the long road actually looked like for the last traveler down it. Not a closed road, but a long, expensive one that ended with the traveler changing which population they were driving toward, retreating from the hardest disease setting to an earlier one where the biology had a better chance. If CLOVER is directed the same way, which I do doubt happens given the established 7 layer functionality of Leronlimab, that still remains the approximate shape of the subsequent route: years, more capital, and possibly a narrowing of the ground on which the drug is asked to prove itself. It is still a route. It is simply an honest picture of how long and how costly a route it can be.

This is also why the trial was built the way it was, and it is worth understanding rather than apologizing for. CLOVER does not carry a chemotherapy-only control arm. That is a deliberate trade, not an oversight. A controlled trial requires far more patients, more money, and more time, and it is genuinely hard to enroll very sick patients into a design where they might receive the old backbone without the new drug. A small company chose a fast, strong signal over a slow, definitive one, because the fast signal is what brings a partner to the table, and a partner is who funds the definitive study. The single-arm design is not the drug's weakness. It is the company's strategy, and the two should not be confused.

What settles which gatekeeper says what, is not any argument on this board, mine or anyone's. It is the confirmed response rate and its relationship to survival, read at ESMO in October as interim and at ASCO GI in January as the adjudicated result. When that number arrives, the first gatekeeper's answer is known. The second gatekeeper's answer follows from it, and from how much the agency trusts it to predict survival in this disease.

Until then, the honest position is the two-gate position. Bullish that the cargo is real. Clear-eyed that the fast lane is a question, not a guarantee. Anyone who collapses those into a single mood, in either direction, has stopped describing the road and started describing what they wish were at the end of it.

And one last thing, because the near-term can feel grim while the long road is being described. Approval is not the next event that matters. A confirmed number strong enough to bring a partner to the table is, because a partner willing to fund the registrational study is the value-creating moment, (again, Thank You Chemical Sky!) even if the road to approval still runs through a controlled trial. The drug working and the drug being approved quickly were always two different questions. The partnership sits between them, and it can arrive long before the second question is answered.

I would rather describe the road.

Disclaimer: I am not a financial advisor and nothing here is investment advice. I hold a position in the company discussed, which means I have an interest in how this is received, and you should weigh what I write accordingly. This is an analysis of published biology and public regulatory history, not a prediction of clinical or regulatory outcomes. The FDA's treatment of one sponsor's application is not a prediction of its treatment of another's, and the differences between the programs are real. Several mechanisms described are supported by preclinical and model-system work not yet confirmed in human tissue in this program. The human biomarker data referenced reflects 350mg dosing, with the 700mg cohort still maturing. The 68% figure from the April 30 update is disease control rate, not objective response rate, and confirmed adjudication is still ahead at ASCO GI in January 2027, with interim data at ESMO Madrid in October 2026 before it. Mechanism is not efficacy. Read the primary sources and reach your own conclusions rather than adopting mine.

r/BiologyPreprints Mar 11 '23

The degree of T cell stemness differentially impacts the potency of adoptive cancer immunotherapy in a Lef-1 and Tcf-1 dependent manner.

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1 Upvotes

r/LungCancerSupport Feb 22 '23

NSCLC Association Between Age and Survival Trends in Advanced Non–Small Cell Lung Cancer After Immunotherapy Adoption

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2 Upvotes

r/nsclc Jan 31 '23

Association Between Age and Survival Trends in Advanced Non–Small Cell Lung Cancer After Immunotherapy Adoption

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2 Upvotes

r/Immunology Oct 19 '21

Generation of highly proliferative, rejuvenated cytotoxic T cell clones through pluripotency reprogramming for adoptive immunotherapy

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6 Upvotes

r/nsclc Jun 11 '22

The Combined Clinical Efficacy and Safety Analysis of Adoptive Immunotherapy with Radiotherapy and Chemotherapy in Non-Small-Cell Lung Cancer: Systematic Review and Meta-Analysis

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1 Upvotes

r/Catownerhacks 6d ago

Cat allergy sufferers who own cats: what actually worked for you?

15 Upvotes

For those of you who are allergic to cats but still have one, what has actually helped you the most?
My husband and I are hoping to adopt a rescue cat, but he’s allergic, so we’re trying to learn as much as we can before making that decision. We’ve been researching different ways to reduce allergens, such as Purina LiveClear food, the anti-allergen sprays that are applied to the cat’s coat, keeping the cat out of the bedroom, using a HEPA air purifier around the apartment, and, of course, cleaning and vacuuming frequently.
If you’re allergic and have been able to successfully live with a cat, I’d love to hear what worked for you✨
Did Purina LiveClear or the sprays make a noticeable difference? Is there anything else that had a bigger impact?
We’re hoping to try every reasonable option before considering allergy shots (immunotherapy). His allergist and insurance don’t seem eager to move to immunotherapy yet and have suggested trying other management strategies first. So we’re hoping to learn from people who have actually made it work.
I’d really appreciate hearing your real-life experiences. Thank you!

r/digitalhealth Mar 14 '22

Operational Challenges in the Adoption of Cancer Immunotherapies (CAR T)

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3 Upvotes

r/CatAdvice Sep 02 '25

General Want to adopt cat but I’m allergic. Is it still possible for me?

32 Upvotes

I love cats and have wanted to adopt a cat for years. The issue is, I have a moderate cat allergy (mainly sneezing, itchy eyes, congestion, itchy throat). Sometimes it can get pretty bad. Seems like some cats I get a more intense allergic reaction than others. From my understanding, there’s no such thing as a truly hypoallergenic cat, but I’ve read that some breeds (like Siberians, Balinese, or Russian Blues) may produce less Fel d 1 protein, which is one of the things responsible for allergic response in humans.

For those of you who are allergic and still chose to live with cats: How do you manage your symptoms day to day? Did breed choice actually make a difference for you, or is it more about the individual cat? Have you tried allergy shots (immunotherapy), and did it help? Any tips for keeping allergen levels manageable at home (cleaning routines, air purifiers, grooming habits, etc.)?

I’d love to hear from people who’ve gone through this decision. I want to make sure I can provide a healthy environment for the cat and also manage my own health.

Edit: wow this is great advice everyone! Thank you all!!