A genomic screen identifies TYRO3 as a MITF regulator in melanoma

Zhu, Shoutian; Wurdak, Heiko; Wang, Yan; Galkin, Anna; Tao, Hai‐Yan; Li, Jie; Lyssiotis, Costas A.; Yan, Feng; Tu, Buu P.; Miraglia, Loren; Walker, John R.; Sun, Fanxiang; Orth, Anthony P.; Schultz, Peter G.; Wu, Xu

doi:10.1073/pnas.0909292106

Cited by 88 publications

(104 citation statements)

References 57 publications

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“…In many settings, however, a definitive demonstration that overexpression is causal for particular features of cancer development or progression has not been made. Elevated expression of TAM signaling components has been reported for leukemias (Graham et al 1994(Graham et al , 2006Hong et al 2008), gliomas (Hutterer et al 2008;Keating et al 2010), colorectal carcinomas (Craven et al 1995), breast cancers (Berclaz et al 2001;Gjerdrum et al 2010), gastrointestinal stromal tumors (Mahadevan et al 2007), hepatocellular carcinoma (He et al 2010), melanoma (Quong et al 1994;Koorstra et al 2009;Zhu et al 2009), pancreatic adenocarcinoma (Song et al 2010), and prostate cancer (Wu et al 2004;Sainaghi et al 2005), among several others.…”

Section: Tam Receptors and Cancermentioning

confidence: 99%

Biology of the TAM Receptors

Lemke

2013

Cold Spring Harbor Perspectives in Biology

491

578

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Section: Tam Receptors and Cancermentioning

confidence: 99%

Biology of the TAM Receptors

Lemke

2013

Cold Spring Harbor Perspectives in Biology

491

578

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“…The role of other TAM receptors in melanoma has been described, suggesting that MERTK may also have a significant role in melanoma development and progression. TYRO3 was identified as an overexpressed receptor in melanoma, a regulator of MITF, and a contributor to the proliferative, antiapoptotic, chemoresistant, and tumorigenic phenotypes of melanoma cells (17). In another study, AXL was commonly expressed in NRAS-mutant melanomas lacking MITF expression and contributed to a migratory and invasive phenotype (18).…”

Section: Introductionmentioning

confidence: 99%

MERTK receptor tyrosine kinase is a therapeutic target in melanoma

Schlegel¹,

Sambade²,

Sather³

et al. 2013

J. Clin. Invest.

131

132

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Metastatic melanoma is one of the most aggressive forms of cutaneous cancers. Although recent therapeutic advances have prolonged patient survival, the prognosis remains dismal. C-MER proto-oncogene tyrosine kinase (MERTK) is a receptor tyrosine kinase with oncogenic properties that is often overexpressed or activated in various malignancies. Using both protein immunohistochemistry and microarray analyses, we demonstrate that MERTK expression correlates with disease progression. MERTK expression was highest in metastatic melanomas, followed by primary melanomas, while the lowest expression was observed in nevi. IntroductionAlthough early cutaneous melanoma is usually curable with surgery, distant metastatic melanoma is an aggressive cancer with a median overall survival time of less than 1 year. In 2012, over 75,000 new melanoma diagnoses were expected and over 9,000 deaths were projected (1). Advances in the understanding of distinct melanoma subtypes as well as melanoma immunobiology have resulted in 2 FDA-approved therapies for metastatic melanoma in 2011: vemurafenib, an inhibitor of mutant BRAF -an oncogene present in approximately 50% of melanomas -and ipilimumab, a monoclonal antibody that targets CTLA-4 (2-4). Despite these rather impressive developments, the overall clinical benefit is limited to either small subgroups of patients who

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“…57) and TYRO3 expression was shown to be upregulated in melanoma cell lines and tissues. 56 Ectopic expression of TYRO3 led to partial abrogation of senescence caused by BRAF V600E as was evidenced by the decrease in the proportion of SA-β-Galpositive cells. It should be noted that in another paper, MITF, one of the major downstream targets of TYRO3 in melanocytes, was shown to cooperate with BRAF V600E in transformation of NHM expressing constitutively active CDK4, dominant negative p53 and telomerase.…”

mentioning

confidence: 99%