Science paper 11-13-2014 旁路抑制 联用原理
本帖最后由 jaydad 于 2014-12-3 23:34 编辑AS Crystal, AT Shaw et al (Harvard medical school)
Patient-derived models of acquired resistance can identify effective drug combinations for cancer
Fig 2 (图2)
9 ALK+ patient cell lines 九位病人抗克药癌细胞株的有效旁路抑制
1) EGFG PI3K SRC
2) EGFR BCL SRC
3) EGFR BCL SRC
4) EGFR SRC IGFR
5) EGFR SRC
6) SRC FGFR
7) BCL MEK Aurora-kinase
8) EGFR
9) none known
总结一下: 6/9 SRC, 5/9 EGFR (这个解释了我当年用特药半年多有稳定效果), 3/9 BCL, 1/9 PI3K, 1/9 MEK, 1/9 IGFR, 1/9 FGFR, 1/9 AURORA-KINASE
SRC 药: dasatinib (Sprycel), sarcatinib, WH-4-025
EGFR: gefitinib, erlotinib
BCL: Navitoclax
PI3K: BEZ235
MEK: AZD6244 (selumetinib)
IGFR: linsitinib (CEP-701), also ap26113, ldk378
FGFR: NVB-BGJ-398 (dovitinib)
11 EGFR+ patient cell lines 十一位病人抗特药癌细胞株的有效旁路抑制
1) PI3K BCL PLK
2) PI3K AKT FGFR
3) FGFR
4) FGFR
5) FGFR
6) IGFR
7) IGFR
8) MET
9) none known
10) none known
11) none known
总结一下: 4/11 FGFR, 2/11 PI3K, 2/11 IGFR, 1/11 BCL, 1/11 PLK, 1/11 AKT, 1/11 MET
MET 药: 克药!!
PLT: BI-2536
AKT: MK-2208
克药对部分EGFR+病人合用有效, 特药对更多ALK+病人合用克药有效!
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