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Relapsed/metastatic skin squamous cell carcinoma (cSCC) is mostly chemotherapy or radiotherapy, but the clinical efficacy of cSCC is still poor.
in clinical trials in patients with late-stage and metastasis cSCC, it was observed that such cSCC patients had limited responses to EGFR targeted therapy (up to 45% of cases).
study aims to analyze the potential molecular characteristics of the response of cSCC patients to EGFR inhibitors and the molecular mechanisms of resistance to EGFR-targeted treatment in cSCC patients.
researchers collected tumor tissue from patients with cSCC and established progeny cell and xeno-transplant tumor models (cSCC-PDX), successfully simulating the pathological and molecular characteristics of tumor tissue in patients.
also tested the response of progenitic cells and heterogeneity transplant tumor models to Gefitinib's treatment.
EGFR signal activation promotes the proliferation of cortogenic cells compared to interstational sample cSCC, the EGFR signal of cSCC, which retains the characteristics of the corted cell, is significantly activated, and EGFR signal activation promotes the proliferation of tumor cells.
Giffeitinib inhibits the growth of PIC3CA mutation cSCC without EGFR and RAS gene mutations, Gifinistinib therapy can significantly block the growth of epithirsty cSCC-PDX tumors, while tumors carrying PIK3CA activation mutations (E545K) are resistant to Gifetinib treatment.
a group of tumors that were initially effective in the treatment of gyfeitinib gained resistance after long-term treatment, which was induced by bypassing the signals from EGFR to FGFR, allowing tumor cells to survive and multiply while receiving gyfetinib treatment.
drug inhibition of FGFR signals overcomes resistance to EGFR inhibitors, even in tumors with PIC3CA mutations.
, EGFR targeted therapy may be suitable for treating epithirsis cSCC without PIK3CA activation mutations.
combined FGFR targeted therapy or can be used to treat cSCC that is inherently or obtainively resistant to EGFR inhibitors.
