| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Advances in Brief |
Ludwig Institute for Cancer Research [G. P. R., M. N., H-J. S. H., W. K. C.], Department of Medicine [H-J. S. H., W. K. C.], Center for Molecular Genetics [W. K. C.], and Cancer Center [W. K. C.], University of California at San Diego, La Jolla, California 92093-0660, and Department of Dermatology and Allergology, Hannover Medical University, D-30449, Hannover, Germany [R. A. H.]
Alteration of chromosome 10 is common in human melanomas and usually entails the loss of an entire chromosome homologue. Although the reasons for monosomy in cancer has remained obscure, one possibility is that multiple tumor suppressor genes residing on this chromosome must be lost in unison during tumor progression, and this is easier to accomplish by chromosome segregation rather than by multiple mutational and/or deletion events. The localization and identification of these genes has been hampered by the monosomy itself, which has resulted in a paucity of small defining deletions in tumors. Here, we have addressed the issue of monosomy in tumor development by using functional complementation mapping to localize and demonstrate the existence of different melanoma suppressor genes on chromosome 10 and assigned each locus a distinct tumorigenic phenotype. We report that a locus on 10q distal to 10q23.1, likely involving the PTEN tumor suppressor, causes a severe reduction in the kinetics of melanoma tumor formation in animals. In contrast, a previously unrecognized region at 10p15.3 has a distinct, but lesser, effect on in vivo melanoma growth. Thus, the loss of both of these regions, which is accomplished by tumor-associated monosomy, provides a significant growth advantage over the individual loss of either region, thereby explaining the monosomy observed in sporadic melanomas.
This article has been cited by other articles:
|
|
 |
|
  A. Mirmohammadsadegh, A. Marini, S. Nambiar, M. Hassan, A. Tannapfel, T. Ruzicka, and U. R. Hengge Epigenetic Silencing of the PTEN Gene in Melanoma. Cancer Res., July 1, 2006; 66(13): 6546 - 6552. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z.-J. Liu, M. Xiao, K. Balint, K. S.M. Smalley, P. Brafford, R. Qiu, C. C. Pinnix, X. Li, and M. Herlyn Notch1 Signaling Promotes Primary Melanoma Progression by Activating Mitogen-Activated Protein Kinase/Phosphatidylinositol 3-Kinase-Akt Pathways and Up-regulating N-Cadherin Expression. Cancer Res., April 15, 2006; 66(8): 4182 - 4190. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Stahl, A. Sharma, M. Cheung, M. Zimmerman, J. Q. Cheng, M. W. Bosenberg, M. Kester, L. Sandirasegarane, and G. P. Robertson Deregulated Akt3 Activity Promotes Development of Malignant Melanoma Cancer Res., October 1, 2004; 64(19): 7002 - 7010. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Mihaila, J. A. Gutierrez, M. L. Rosenblum, I. F. Newsham, O. Bogler, and S. A. Rempel Meningiomas: Analysis of Loss of Heterozygosity on Chromosome 10 in Tumor Progression and the Delineation of Four Regions of Chromosomal Deletion in Common with Other Cancers Clin. Cancer Res., October 1, 2003; 9(12): 4435 - 4442. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Stahl, M. Cheung, A. Sharma, N. R. Trivedi, S. Shanmugam, and G. P. Robertson Loss of PTEN Promotes Tumor Development in Malignant Melanoma Cancer Res., June 1, 2003; 63(11): 2881 - 2890. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. U. Koelsch, A. Kindler-Rohrborn, S. Held, S. Zabel, and M. F. Rajewsky Loss of heterozygosity in malignant rat schwannomas chemically induced in hybrids of inbred rat strains with differential tumor susceptibility Carcinogenesis, June 1, 2002; 23(6): 1033 - 1037. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Mora, N.-K. V. Cheung, S. Oplanich, L. Chen, and W. L. Gerald Novel Regions of Allelic Imbalance Identified by Genome-wide Analysis of Neuroblastoma Cancer Res., March 1, 2002; 62(6): 1761 - 1767. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. G. M. Scholes, T. Liloglou, P. Maloney, S. Hagan, J. Nunn, P. Hiscott, B. E. Damato, I. Grierson, and J. K. Field Loss of Heterozygosity on Chromosomes 3, 9, 13, and 17, Including the Retinoblastoma Locus, in Uveal Melanoma Invest. Ophthalmol. Vis. Sci., October 1, 2001; 42(11): 2472 - 2477. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Itoyama, R. S. K. Chaganti, Y. Yamada, K. Tsukasaki, S. Atogami, H. Nakamura, M. Tomonaga, K. Ohshima, M. Kikuchi, and N. Sadamori Cytogenetic analysis and clinical significance in adult T-cell leukemia/lymphoma: a study of 50 cases from the human T-cell leukemia virus type-1 endemic area, Nagasaki Blood, June 1, 2001; 97(11): 3612 - 3620. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Gimm, H. Chi, P. L. M. Dahia, A. Perren, R. Hinze, P. Komminoth, H. Dralle, P. R. Reynolds, and C. Eng Somatic Mutation and Germline Variants of MINPP1, a Phosphatase Gene Located in Proximity to PTEN on 10q23.3, in Follicular Thyroid Carcinomas J. Clin. Endocrinol. Metab., April 1, 2001; 86(4): 1801 - 1805. [Abstract] [Full Text]
|
|
|
|
|
|
F. Tschentscher, G. Prescher, D. E. Horsman, V. A. White, H. Rieder, G. Anastassiou, H. Schilling, N. Bornfeld, K. U. Bartz-Schmidt, B. Horsthemke, et al. Partial Deletions of the Long and Short Arm of Chromosome 3 Point to Two Tumor Suppressor Genes in Uveal Melanoma Cancer Res., April 1, 2001; 61(8): 3439 - 3442. [Abstract] [Full Text]
|
|
|
|
 |
|
 M. S. Rogers and E. E. Strehler The Tumor-sensitive Calmodulin-like Protein Is a Specific Light Chain of Human Unconventional Myosin X J. Biol. Chem., April 6, 2001; 276(15): 12182 - 12189. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Cell Growth & Differentiation |
