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Posted On: 05/21/2025 5:53:54 PM
Post# of 154581
misiu143, you pointed out that a ChatGPT response about how LL turns cold tumors hot did not mention increasing PD-L1.
I told Chat that when it responded to a question about how Leronlimab turns cold tumors hot, it did not note that Leronlimab increased PD-L1 and I gave it a link to the CureToday article that discussed the Munich mTNBC poster. It responded:
I then repeated the question “How does Leronlimab turn cold tumors hot for checkpoint inhibitors to work?” It responded with a lengthy writeup which I won’t include, but it listed 4 items with details for each:
1. CCR5 blockade reprograms the tumor microenvironment
2. Promotes T Cell Infiltration (TILs)
3. Increases PD-L1 expression
4. Enhances responsiveness to immune checkpoint inhibitors (ICIs)
I suspect that most everyone has seen the CureToday article about the poster, but here is the link I gave to Chat:
https://www.curetoday.com/view/leronlimab-lin...wGcvlRSXrw
AIs like Chat are learning all the time. If you ask this question next week, you will probably get even more details. (As many have pointed out, however, AIs can make mistakes.)
I told Chat that when it responded to a question about how Leronlimab turns cold tumors hot, it did not note that Leronlimab increased PD-L1 and I gave it a link to the CureToday article that discussed the Munich mTNBC poster. It responded:
Quote:
You're absolutely right—recent findings have highlighted that leronlimab not only modulates the tumor microenvironment by blocking CCR5 and promoting T cell infiltration but also increases PD-L1 expression on circulating tumor cells (CTCs) in patients with metastatic triple-negative breast cancer (mTNBC).
A study reported that 15 out of 17 patients (88%) who received weekly doses of 525 mg or more of leronlimab exhibited a significant rise in PD-L1 levels on their CTCs within 30 to 90 days of treatment. This upregulation of PD-L1 is significant because it may transform "cold" tumors—those that do not provoke a strong immune response—into "hot" tumors, which are more likely to respond to immune checkpoint inhibitors (ICIs). In fact, all five patients in the study who showed a marked increase in PD-L1 expression and subsequently received ICI therapy were still alive at the time of reporting, with four showing no evidence of disease and one maintaining stable disease.
This suggests that Leronlimab's ability to increase PD-L1 expression could enhance the effectiveness of ICIs in treating mTNBC, offering a potential new therapeutic avenue for patients with tumors that were previously unresponsive to such treatments.
I then repeated the question “How does Leronlimab turn cold tumors hot for checkpoint inhibitors to work?” It responded with a lengthy writeup which I won’t include, but it listed 4 items with details for each:
1. CCR5 blockade reprograms the tumor microenvironment
2. Promotes T Cell Infiltration (TILs)
3. Increases PD-L1 expression
4. Enhances responsiveness to immune checkpoint inhibitors (ICIs)
I suspect that most everyone has seen the CureToday article about the poster, but here is the link I gave to Chat:
https://www.curetoday.com/view/leronlimab-lin...wGcvlRSXrw
AIs like Chat are learning all the time. If you ask this question next week, you will probably get even more details. (As many have pointed out, however, AIs can make mistakes.)
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