Misiu, Aceparker--
I am a little confused about this... My understanding was that if your primary tumor expressed CCR5 then leronlimab would be appropriate to use. And whether or not your tumor expressed CCR5 was based on organ and/or indication--which (from memory) included colon, TNBC, glio, and prostate cancers. Aceparker's experience of being rejected for the basket trial confirms this, at least from what was known back then.
Those are huge indications of course, and huge numbers of people could be saved, or lives extended, if leronlimab worked like that. And if your tumor didn't express CCR5 you were shit out of luck, as we say. But Misiu if what you are saying is true--and from your last paragraph it sounds like you are following this very closely--than any tumor that goes rogue is going to be susceptible to leronlimab. And our little molecule becomes a pan-cancer metastasis-killer. Wow! This is staggering...
This makes sense to me from the little bit of reading I've done on the tumor microenvironment--cancer hijacks the immune system via CCR5 and uses it to hide itself in the body and spread. But your references to Drs Pestell and Patterson are new to me. Are these public sources we can look into? Perhaps this was mentioned on the board at some point in time. Anyway, a reference would be appreciated. And of course, comments or qualifications that anyone else may have on this would be welcome.
I have a question right off the bat--anyone know if leronlimab would work on common cancer mutations like KRAS or EFRG?
Getting back to metastatic cancer, I'm wondering if perhaps this is what Dr Lalezari was directly referring to when he said "leronlimab could play a significant role as a paradigm-shifting therapeutic in oncology" in the latest shareholder letter. I guess controlling metastatic cancer would be paradigm-shifting! Are we talking cures here? (At least for those who respond...) That's what the long-term survival news of those mTNBC patients implies, anyway...
Okay--maybe I am getting way ahead of what we know. But even though Lalezari is typically and deliberately low-key, you can tell he's excited. "We are eager to provide updates in the coming months"... and I'm downright eager to hear them.
*. * * *
Aceparker--glad you are still with us. Must be going on several years now. As a cancer survivor myself, I'm curious what kind of treatment you received even though you didn't receive leronlimab. Did you know enough about the drug to be disappointed when you didn't qualify for it, or was it just another possibility in the grand scheme of oncology therapeutics? Hope you are doing well now and your prognosis is good. Thanks for sharing.
And Misiu, thanks again. Those three little words--"it is ok." Lovely and poetic! But references or links to any comments from the Drs P would be welcome.
--Sherlock--
I am a little confused about this... My understanding was that if your primary tumor expressed CCR5 then leronlimab would be appropriate to use. And whether or not your tumor expressed CCR5 was based on organ and/or indication--which (from memory) included colon, TNBC, glio, and prostate cancers. Aceparker's experience of being rejected for the basket trial confirms this, at least from what was known back then.
Those are huge indications of course, and huge numbers of people could be saved, or lives extended, if leronlimab worked like that. And if your tumor didn't express CCR5 you were shit out of luck, as we say. But Misiu if what you are saying is true--and from your last paragraph it sounds like you are following this very closely--than any tumor that goes rogue is going to be susceptible to leronlimab. And our little molecule becomes a pan-cancer metastasis-killer. Wow! This is staggering...
This makes sense to me from the little bit of reading I've done on the tumor microenvironment--cancer hijacks the immune system via CCR5 and uses it to hide itself in the body and spread. But your references to Drs Pestell and Patterson are new to me. Are these public sources we can look into? Perhaps this was mentioned on the board at some point in time. Anyway, a reference would be appreciated. And of course, comments or qualifications that anyone else may have on this would be welcome.
I have a question right off the bat--anyone know if leronlimab would work on common cancer mutations like KRAS or EFRG?
Getting back to metastatic cancer, I'm wondering if perhaps this is what Dr Lalezari was directly referring to when he said "leronlimab could play a significant role as a paradigm-shifting therapeutic in oncology" in the latest shareholder letter. I guess controlling metastatic cancer would be paradigm-shifting! Are we talking cures here? (At least for those who respond...) That's what the long-term survival news of those mTNBC patients implies, anyway...
Okay--maybe I am getting way ahead of what we know. But even though Lalezari is typically and deliberately low-key, you can tell he's excited. "We are eager to provide updates in the coming months"... and I'm downright eager to hear them.
*. * * *
Aceparker--glad you are still with us. Must be going on several years now. As a cancer survivor myself, I'm curious what kind of treatment you received even though you didn't receive leronlimab. Did you know enough about the drug to be disappointed when you didn't qualify for it, or was it just another possibility in the grand scheme of oncology therapeutics? Hope you are doing well now and your prognosis is good. Thanks for sharing.
And Misiu, thanks again. Those three little words--"it is ok." Lovely and poetic! But references or links to any comments from the Drs P would be welcome.
--Sherlock--
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