Titlebook: Mechanisms in Carcinogenesis and Cancer Prevention; Harri U. Vainio,Eino K. Hietanen Book 2003 Springer-Verlag Berlin Heidelberg 2003 angi

DIGN

書目名稱Mechanisms in Carcinogenesis and Cancer Prevention影響因子(影響力)




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention影響因子(影響力)學(xué)科排名




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention網(wǎng)絡(luò)公開度




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention被引頻次




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention被引頻次學(xué)科排名




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention年度引用




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention年度引用學(xué)科排名




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention讀者反饋




書目名稱Mechanisms in Carcinogenesis and Cancer Prevention讀者反饋學(xué)科排名

legitimate

Genetic and Environmental Factors in Carcinogenesis,even when cultured or when injected in immunologically tolerant experimental animals (. and . 2000; . and . 1998). Yet, the views about the environmental (somatic) and inherited origin of the genetic alterations in human cancer have been debated and any reasonable agreement can be reached only when

教育學(xué)

淺灘

Signalling Pathways as Targets in Cancer Prevention,cell growth, or undergo apoptosis. Transformed cells either fail to respond or receive inappropriate signals which favor proliferation and avoidance of apoptosis. Thus, it is no coincidence that many oncogenes and tumor suppressor genes are components of signalling pathways. Despite the great variet

植物學(xué)

蝕刻

創(chuàng)新

Deficient DNA Mismatch Repair in Carcinogenesis,isincorporation during DNA synthesis. The genes coding for MMR proteins are highly conserved throughout evolution. The human proteins that correspond to the bacterial MutS proteins and participate in MMR include MSH2, MSH3, and MSH6, whereas the human MutL proteins include MLH1, PMS1, PMS2, and MLH3

Adj異類的

Epigenetic Changes, Altered DNA Methylation and Cancer,specialized chromatin structures are capable of stably modulating gene expression over many cell generations. Thus, an epigenetic mutation can have the same effect like a classical, genetic mutation, i.e., loss- or gain-of-function of any given gene. Sensitive methods for the detection of epigenetic

Buttress

Stress-Fracture