Molecular Mechanisms of Cancer

Molecular Mechanisms of Cancer

Language: English

Pages: 645

ISBN: 1402060157

Format: PDF / Kindle (mobi) / ePub

This book describes molecular processes whose deregulation is important in the formation of tumors. The material is developed from basic cell signaling pathways to their roles in the clinical manifestation of specific cancers. Topics covered include molecular events intrinsic to tumor cells (leading to growth deregulation, extended lifespan, and the ability to invade surrounding tissue), protective mechanisms that prevent transformation (including DNA repair and epigenetic regulation), tumor-host interactions (with the endocrine system, the immune system, and blood vessel formation), and the underlying molecular defects of individual cancers.

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(Figure 3.3.12.B). The activity of the ABL protein is negatively regulated by its SH3 domain, the loss of which turns it into an oncoprotein. Oncogenic forms of ABL can autophosphorylate on tyrosine 412. The COOHterminal domain contains three distinct nuclear localization sequences, one nuclear export sequence, three HMG-like boxes that bind cooperatively to A/T-rich DNA, a G-Actin binding domain, and an F-Actin binding domain. P73 is a target of regulation by c-ABL in DNA damage responses.

deletion affecting one allele, loss of heterozygosity at loci along the entire chromosome 11 indicated an earlier chromosomal nondisjunction and reduplication. The product of this mutation of the wt1 gene behaves as a dominant negative, suppressing the function of the wild-type protein by a trans-dominant mechanism. The mutant wt1 gene cooperates with the adenoviral E1A gene in transforming kidney cells. The wild-type WT1 gene product in all of its alternatively spliced forms neither suppresses

4-(Methylnitroamino)-1(3-pyridyl)-1-butanone Cancer Lung and pancreas cancer Lung carcinoma Bladder and skin cancer Mammary carcinoma Bladder carcinoma Bladder carcinoma Bladder, kidney, and liver cancer Liver tumors Hepatocellular carcinoma Skin cancer, lung cancer Lung cancer Sarcomas, testicular cancer Lung cancer Liver cancer Liver cancer, esophagus cancer Intestinal cancer, squamous skin cancer Liver cancer Liver cancer Bladder cancer, skin cancer Leukemia, kidney cancer, uterine cancer

esophageal squamous carcinoma, amplification of 11q21–q23 frequently occurs. This leads to overexpression of the antiapoptotic gene ciap1 [Imoto et al. 2001]. ● The deletion of one allele of a tumor suppressor gene (loss of heterozygosity) [Cavenee et al. 1983] leads to symptoms if the remaining allele is mutated. Losses of heterozygosity, i.e., losses of a maternal or paternal allele in a tumor, are widespread and are often accompanied by a gain of the opposite allele. On average, cancers of

after asparagine residues. The Caspases -3, -7, and -9 recognize the tetrapeptide sequences DEXD, which is present in Poly(ADP-ribose)Polymerase. The motif WEHD is cleaved by Caspases -1, -4, and -5. Caspase-6 is the only Caspase known to cleave Lamin A with the recognition sequence VEID. This cleavage contributes to chromatin condensation and nuclear shrinkage. Caspase-1 [Yuan et al. 1993] cleaves the cytokine pro-IL-1β. In general, the most significant differences in Caspase specificities are

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