Peering into the aftermath

被引:22
作者
Kerbel, Robert S. [1 ,2 ]
Ebos, John M. L. [1 ,2 ]
机构
[1] Sunnybrook Hlth Sci Ctr, Sunnybrook Res Inst, Dept Mol & Cellular Biol, Toronto, ON M4N 3M5, Canada
[2] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada
关键词
ANTIANGIOGENIC THERAPY; CELL MOBILIZATION; SUNITINIB; VEGF; ANGIOGENESIS; METASTASIS; INHIBITION; BIOMARKERS; RESISTANCE; TUMORS;
D O I
10.1038/nm1010-1084
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Much of how the human host responds to a tumor and to anticancer therapy is still not fully fleshed out. The cytokines and other mediators involved in this response may be both allies and enemies in the quest for more effective treatments or even a cancer cure. In 'Bedside to Bench', Robert Kerbel and John Ebos discuss recent human studies in healthy individuals and people with minimal residue or no disease showing release of host-derived cytokines after antiangiogenic therapy. The increase in proangiogenic factors such as VEGF and PIGF and other cytokines involved in metastasis and tumor repopulation in a host may threaten therapeutic success but may also suggest new prognostic markers and other treatment strategies. In 'Bench to Bedside', Michael Karin and Florian Greten peruse how using JAK2 inhibitors to block STAT3 in tumors could halt cancer progression. JAK2 inhibitors, already being tested in clinical trials to treat myeloproliferative diseases, may also prove valid as anticancer drugs.
引用
收藏
页码:1084 / 1085
页数:2
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