in a study published in cancer cell led by kyle furge, ph.d. and aikseng ooi, ph.d., researchers provide a more complete understanding of the biology of type 2 papillary(乳突的) renal cell carcinoma(肾细胞癌) (prcc2), an aggressive type of kidney cancer with no effective treatment, which lays the foundation for the development of effective treatment strategies.
despite obvious morphological, 2, and clinical differences, 3 prcc2 is thought to share similar pathway deregulation due to genetic 4 with its counterpart, clear cell renal cell carcinoma (ccrcc), a subtype that accounts for 75% of all kidney cancers and that, unlike prcc2, responds favorably to drugs targeting 5(血管的) endothelial(内皮的) growth factor (vegf), a signal protein produced by cells that 6 blood 7 formation.
the study, which included international 8 with researchers from the national cancer centre singapore, génétique oncologique epfe-inserm u753 and faculté de médecine paris-sud, le kremlin-bicêtre and institut de cancérologie gustave roussy, michigan state university, northwestern memorial hospital, cleveland clinic, singapore general hospital, and the wistar institute, identified deregulation of the keap1-nrf2 signaling pathway as a factor that distinguishes prcc2 from ccrcc, but links both hereditary and 9(零星的,分散的) prcc2.
in another study published in cancer research, led by yan ding, ph.d., and 10 tean teh, ph.d. and carried out in collaboration with the national cancer centre singapore, researchers integrated 1 expression profiling and rnai screening data to identify 11 involved in ccrcc development and progression.
in recent years, several 12 targeted therapies such as sunitinib, sorafenib, and pazopanib, which target the receptor tyrosine kinases of vegf have been approved for ccrcc. although these therapies significantly extend overall survival, nearly all patients with advanced ccrcc eventually 13 to the disease.
gene set enrichment analysis indicated that cell-cycle-related genes, in particular plk1, were associated with disease aggressiveness. further, the association of plk1 in both disease 14 and in vitro growth prompted researchers to examine the effects of a small-molecule inhibitor in ccrcc cell lines. their findings highlight plk1 as a 15 potential 16 target for ccrcc.