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By Andrew Yen, Tracy French, Karen Russell, Susi Varvayanis, Mary Forbes (auth.), Maryce M. Jacobs (eds.)

The American Institute for melanoma study (AICR) backed its 3rd annual confer­ ence on meals and melanoma. The subject matter used to be "Diet and melanoma: Markers, Prevention, and remedy. " The convention was once held October 29-30, 1992 on the Ritz Carlton inn in McLean, Virginia. This court cases comprises chapters from the platform displays and abstracts from the poster displays. a number of chapters handle each one of 4 consultation issues: Retinoids as Differentiation brokers in melanoma remedy, organic Markers of melanoma possibility, Chemoprevention of melanoma by means of Non-Nutrients in meals, and dietary difficulties and help within the therapy of melanoma. the 1st 3 chapters talk about intimately assorted mechanisms wherein retinoids impression differentiation and supply facts to aid their use in melanoma remedy. In vivo and in vitro stories exhibit the consequences of retinoic acid (RA) on tumorigenicity and cellu­ lar/molecular occasions. A synopsis of knowledge exhibiting the involvement of the retinoblastoma (RB) gene in HL-60 mobilephone differentiation triggered by way of RA and 1,2S-dihydroxy nutrition D3 (VD) is gifted. In SCID (severe mixed immunodeficiency) mice injected with HL-60 three human leukemia cells and gavaged day-by-day with RA, the variety of tumor websites and variety of mice with tumors are decreased. All trans-RA induces myeloid differentiation in HL-60 cells. equally, VD3 induces HL-60 monocytic differentiation. In either situations an early down legislation of retinoblastoma (RB) gene expression precedes the differentiation.

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A. Yen, S. E. -K. Fung, A. T' Ang, R. 57:21O-221 (1992). 25. W. A. -M. -H. Lee, E. M. Livingston, SV40 large T antigen binds preferentially to an underphosphorylated member of the retinoblastoma susceptibility gene product family, Cell 56:57-65 (1989). 26. w. Ludlow, J. M. M. A. DeCaprio, The retinoblastoma susceptibility gene product undergoes cell cycle-dependent dephosphorylation and binding to and release from SV40 large T, Cell 60:387-396 (1990). 27. L. Szekely, E. -Q. Jiang, M. G. Wiman, G.

Yen, S. Chandler, S. Sturzenegger-Varvayanis, Regulated expression of the RB "tumor suppressor gene" in normal lymphocyte mitogenesis: Elevated expression in transformed leukocytes and role as a "status quo" gene, Experimental Cell Research 192:289-297 (1991). 22. W. Zhang, W. Hittelman, N. Van, M. Andreeff, A. Deisseroth, The phosphorylation of retinoblastoma gene product in human myeloid leukemia cells during the cell cycle, Biochem Biophys Res Comm 184:212-216 (1992). 23. A. Yen, S. Chandler, Inducers of leukemic cell differentiation cause down-regulation of RB gene expression, Proc Soc Exper Bio Med 199:291-297 (1992).

In addition to retinoids modulating growth of HKc/HPVI6 by directly controlling the expression of HPVl6 genes through the URR, more indirect mechanisms may also exist. We have recently found that RA induces the secretion of latent transfonning growth factor-beta (TGF-S) in nonnal HKc and HKc/HPVI6,69 and Glick et al. 70 reported that RA induced the secretion of TGF-S in mouse keratinocytes. 75 Therefore, an autocrine loop may exist whereby retinoids induce the secretion of TGF-S, which in tum inhibits growth, in part through an inhibition of E6 and E7 expression in HKc/HPVI6.

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