The Role for ink4a in Melanoma Pathogenesis

作者: Jason Pomerantz , Nicole Schreiber-Agus , Nanette Liegeois , Alice Tam , Kenneth P. Olive

DOI: 10.1007/978-1-4899-1352-4_1

关键词:

摘要: Malignant melanoma is a disease with high metastatic potential and poor clinical response to current therapeutic measures1. It represents significant health crisis given its rate of increase in incidence; by year 2000, one 76 Americans will develop melanoma2. Although the molecular pathogenesis this poorly understood, predisposition appears have strong genetic component. Tumor surveys kindred analyses uncovered several chromosomal “hot spots” including frequent loss 6q 10q, non-random karyotypic alterations chromosome 1, 9p21-associated deletion/mutation1. The latter be most compelling etiological link that cytogenetic, linkage documented incidence 9p21 germline somatic mutations both familial sporadic melanomas3–6.

参考文章(62)
Hiroshi Nagura, Tetsuro Nishihira, Hironobu Sasano, Yuji Goukon, In situ hybridization and immunohistochemistry of p53 tumor suppressor gene in human esophageal carcinoma. American Journal of Pathology. ,vol. 141, pp. 545- 550 ,(1992)
R. A. Kratzke, F. J. Kaye, Young Whan Kim, A. Coxon, G. A. Otterson, Absence of p16INK4 protein is restricted to the subset of lung cancer lines that retains wildtype RB. Oncogene. ,vol. 9, pp. 3375- 3378 ,(1994)
A Hangaishi, S Ogawa, N Imamura, S Miyawaki, Y Miura, N Uike, C Shimazaki, N Emi, K Takeyama, S Hirosawa, N Kamada, Y Kobayashi, Y Takemoto, T Kitani, K Toyama, S Ohtake, Y Yazaki, R Ueda, H Hirai, Inactivation of multiple tumor-suppressor genes involved in negative regulation of the cell cycle, MTS1/p16INK4A/CDKN2, MTS2/p15INK4B, p53, and Rb genes in primary lymphoid malignancies Blood. ,vol. 87, pp. 4949- 4958 ,(1996) , 10.1182/BLOOD.V87.12.4949.BLOODJOURNAL87124949
Hiromitsu Hiroumi, Hirotoshi Dosaka-Akita, Takayuki Mishina, Ichiro Kinoshita, Fumihiro Hommura, Yoshikazu Kawakami, Kenji Akie, Motoi Nishi, Altered p16INK4 and Retinoblastoma Protein Status in Non-Small Cell Lung Cancer: Potential Synergistic Effect with Altered p53 Protein on Proliferative Activity Cancer Research. ,vol. 56, pp. 5557- 5562 ,(1996)
Jin Jen, J Wade Harper, Sandra H Bigner, Darell D Bigner, Nickolas Papadopoulos, Sanford Markowitz, James KV Willson, Kenneth W Kinzler, Bert Vogelstein, None, Deletion of p16 and p15 Genes in Brain Tumors Cancer Research. ,vol. 54, pp. 6353- 6358 ,(1994)
C Cordon-Cardo, Mutations of cell cycle regulators. Biological and clinical implications for human neoplasia. American Journal of Pathology. ,vol. 147, pp. 545- 560 ,(1995)
C. J. Sherr, R. A. Ashmun, G. J. Hannon, D. Beach, D. E. Quelle, M. Serrano, C. Walker, K. H. Richter, D. Trono, P. A. Rehberger, Cloning and characterization of murine p16(INK4a) and p15(INK4b) genes ,(1995)