Titlebook: Neoplastic Transformation in Human Cell Culture; Mechanisms of Carcin Johng S. Rhim,Anatoly Dritschilo Book 1991 Springer Science+Business

Conflict

爭(zhēng)吵加

Deficient DNA Repair, an Early Step in Neoplastic Transformation of Human Cells in Cultureenes. Continued cell proliferation alone leads to hyperplasia and benign growths. Deficient repair of DNA damage provides the genomic instability that can result in production of new genetic variants characterizing malignant neoplasia.

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Infelicity

Use of Immortalized Human Keratinocytes for the Study of Squamous Differentiation and Mutagenesislomavirus type 16 DNA (HPV16) (3), respectively. Malignant conversion was achieved by transfection with an activated . oncogene (2,4). RHEK-1 and HPK-1A are immortal but nontumorigenic, whereas RHEK-1/ras and HPKlA/ras produce aggressively growing tumors in nude mice (Table 1).

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散步

https://doi.org/10.1007/978-1-4612-0411-4Activation; DNA; aging; cancer; cancer research; carcinogenesis; carcinoma; cell; cell culture; mutation; onco

Vulnerable

p53, a Direct Target of Mutational Activation by Chemical Carcinogens?of tumor suppressor genes as negative regulators of cell growth is believed to lead to tumor development. Loss of function of these genes may occur in the germ line, their absence predisposing the individual to cancer. More frequently, progressive loss of function in tumor suppressor genes occurs through an accumulation of somatic mutations.

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