RT by @EMA_News: Join us on 19 October for a Conversations on Cancer panel discussion with the European Medicines Agency @EMA_News on metastatic breast cancer. 9:30am ET/3:30pm Central European time.
Info: https://www.fda.gov/news-events/fda-meetings-conferences-and-workshops/conversations-cancer-living-metastatic-breast-cancer-10192023
🐦🔗: https://nitter.cz/FDAOncology/status/1710035911939912073#m
[2023-10-05 20:55 UTC]
RT by @EMA_News: Join us on 19 October for a Conversations on Cancer panel discussion with the European Medicines Agency @EMA_News on metastatic breast cancer. 9:30am ET/3:30pm Central European time.
Info: https://www.fda.gov/news-events/fda-meetings-conferences-and-workshops/conversations-cancer-living-metastatic-breast-cancer-10192023
🐦🔗: https://nitter.cz/FDAOncology/status/1712119143875375109#m
[2023-10-11 14:53 UTC]
Sometimes companies do the bizarrest things...
Why would you make a 4 pack of #fulvestrant?
New data supporting a deeper #ESR1 variant characterization in #BreastCancer. Y537S is resistant to #SERD #SERM due to stable conformation and activity. L536 shows varying sensitivity, greatest resistance: AZD9833 GDC-0810 RAD1901 #PrecisionMedicine #bcsm
Mutations in the estrogen receptor (ESR1) gene are common in ER-positive breast cancer patients who progress on endocrine therapies. Most mutations localise to just three residues at, or near, the C-terminal helix 12 of the hormone binding domain, at leucine-536, tyrosine-537 and aspartate-538. To investigate these mutations, we have used CRISPR-Cas9 mediated genome engineering to generate a comprehensive set of isogenic mutant breast cancer cell lines. Our results confirm that L536R, Y537C, Y537N, Y537S and D538G mutations confer estrogen-independent growth in breast cancer cells. Growth assays show mutation-specific reductions in sensitivities to drugs representing three classes of clinical anti-estrogens. These differential mutation- and drug-selectivity profiles have implications for treatment choices following clinical emergence of ER mutations. Our results further suggest that mutant expression levels may be determinants of the degree of resistance to some anti-estrogens. Differential gene expression analysis demonstrates up-regulation of estrogen-responsive genes, as expected, but also reveals that enrichment for interferon-regulated gene expression is a common feature of all mutations. Finally, a new gene signature developed from the gene expression profiles in ER mutant cells predicts clinical response in breast cancer patients with ER mutations.
Liz Szabo
EU Medicines Agency
SPC Chemo Bot
SusanBee 
TumorBoardTuesday
Yan Leyfman, MD
Leslieks
Lorenzo Gerratana