Oncogenes in melanoma

Polsky, David; Cordon‐Cardo, Carlos

doi:10.1038/sj.onc.1206449

Cited by 109 publications

(82 citation statements)

References 41 publications

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“…These proteins are induced at the beginning of the G1 phase and associate with serine/threonine cyclindependent kinases to form activated holoenzymes. Cyclin D1 expression is increased in several human cancers (colorectal and mammary adenocarcinomas, mantle cell lymphomas, oral squamous cell carcinomas and pancreatic tumors) (Wang et al, 1994;Guo et al, 2003;Hui et al, 2003;Miyamoto et al, 2003), as well as in several cancer cell lines (hematopoeitic lineage) (Matsumura et al, 1999) (reviewed in (Johnson andWalker, 1999;Diehl, 2002;Graff and Zimmer, 2003;Park and Lee, 2003;Polsky and Cordon-Cardo, 2003;Stacey 2003). Interestingly, both cyclin D1 and polyamines are required for entry into S phase and their increased expression has been linked to transformation (reviewed in De Benedetti and Harris, 1999).…”

Section: Cyclin D1mentioning

confidence: 99%

eIF4E – from translation to transformation

et al. 2004

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Section: Cyclin D1mentioning

confidence: 99%

eIF4E – from translation to transformation

et al. 2004

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“…Although a significant percentage of melanomas are defective in Ras or associated signalling pathways, 14,15 reovirus has not previously been tested against this disease. Melanoma is an increasing clinical problem, with incidence rates across the world approximately doubling over the last 10 years.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory tumour cell killing by oncolytic reovirus for the treatment of melanoma

et al. 2008

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Reovirus is a promising unmodified double-stranded RNA (dsRNA) anti-cancer oncolytic virus, which is thought to specifically target cells with activated Ras. Although reovirus has been tested in a wide range of preclinical models and has entered early clinical trials, it has not previously been tested for the treatment of human melanoma. Here, we show that reovirus effectively kills and replicates in both human melanoma cell lines and freshly resected tumour; intratumoural injection also causes regression of melanoma in a xenograft in vivo model. Reovirus-induced melanoma death is blocked by caspase inhibition and is dependent on constituents of the Ras/RalGEF/p38 pathway. Reovirus melanoma killing is more potent than, and distinct from, chemotherapy or radiotherapy-induced cell death; a range of inflammatory cytokines and chemokines are released by infected tumour cells, while IL-10 secretion is abrogated. Furthermore, the inflammatory response generated by reovirus-infected tumour cells causes bystander toxicity against reovirus-resistant tumour cells and activates human myeloid dendritic cells (DC) in vitro. Hence, reovirus is suitable for clinical testing in melanoma, and may provide a useful danger signal to reverse the immunologically suppressive environment characteristic of this tumour.

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“…A mutation in an oncogene can alter the function of its product, and the oncogenic signaling from the mutated protein can result in various neoplastic properties. 14,15) RET proto-oncogene encodes a transmembrane receptor with a tyrosine kinase domain which is expressed in cells derived from neural crest. [16][17][18] Glial cell line-derived neurotrophic factor (GDNF) activates RET, and the GDNF-RET signaling pathway plays an important role in the development of the enteric nervous system and the kidney.…”

mentioning

confidence: 99%

Identification of a mouse cytoskeleton‐associated protein, CKAP2, with microtubule‐stabilizing properties

Jin¹,

Murakumo²,

Ueno³

et al. 2004

Cancer Science

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Microtubule dynamics is an important factor in cell proliferation and one of the main targets of cancer chemotherapy. Since microtubule-associated proteins (MAPs) are known to influence microtubule stability, study of MAPs may contribute both to knowledge of cancer cell biology and to the production of new anti-cancer drugs. In this study, we identified a new mouse gene which is a homolog of human cytoskeleton-associated protein, CKAP2 gene, by differential display analysis. The level of expression of mouse CKAP2 (mCKAP2) was significantly higher in NIH3T3 cells expressing RET with a multiple endocrine neoplasia (MEN) 2A or MEN2B mutation than in parental NIH3T3 cells. Immunocytochemical analysis showed that mCKAP2 protein is localized in cytoplasm with a fibrillar appearance, and is co-localized with microtubules throughout the cell cycle. Furthermore, overexpression of mCKAP2 in cells appeared to stabilize microtubules against treatment with nocodazole, a microtubule-depolymerizing agent. In addition, levels of human CKAP2 were increased in some human tumor cell lines examined. These findings suggest that CKAP2 is a new MAP with microtubule-stabilizing properties and may represent a new molecular target for cancer chemotherapy. (Cancer Sci 2004; 95: 815-821) ell proliferation is closely associated with cytoskeleton organizing proteins, which play crucial roles in maintenance of cell structure, as well as mitotic progression. Of the three main filamentous components, microtubules, actin filaments and intermediate filaments, microtubules are known to play roles in intracellular organelle transport, cell division, and maintenance of cell morphogenesis.1-3) Microtubules are composed of α-and β-tubulin proteins, and since their polymerization and depolymerization are essential for cell proliferation, various anti-cancer drugs have been produced to target microtubule dynamics and thereby inhibit mitotic progression. Some of these drugs inhibit microtubule polymerization, while others inhibit microtubule depolymerization. [3][4][5] Microtubule dynamics is regulated by accessory proteins called microtubule-associated proteins (MAPs).6, 7) Many proteins have been identified as MAPs, and can be generally classified into two categories, microtubule-stabilizing proteins and microtubule-destabilizing proteins. The former include tau, MAP2 and MAP4, while the latter include Op18/stathmin and heat shock protein HSP90. [8][9][10][11][12][13] Thus, characterization of the effects of MAPs on microtubule dynamics is necessary for investigation of the mechanisms of tumorigenesis and production of new anti-cancer drugs.Neoplastic transformation of cells is triggered by genetic alterations which cause extraordinary cell growth and proliferation. A mutation in an oncogene can alter the function of its product, and the oncogenic signaling from the mutated protein can result in various neoplastic properties.14, 15) RET proto-oncogene encodes a transmembrane receptor with a tyrosine kinase domain which is expressed in cells derived ...

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Oncogenes in melanoma

Cited by 109 publications

References 41 publications

eIF4E – from translation to transformation

eIF4E – from translation to transformation

Inflammatory tumour cell killing by oncolytic reovirus for the treatment of melanoma

Identification of a mouse cytoskeleton‐associated protein, CKAP2, with microtubule‐stabilizing properties

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