T1796A BRAF mutation is absent in Merkel cell carcinoma

Worda, Miriam; Sreevidya, C.S.; Ananthaswamy, Honnavara N.; Cerroni, Lorenzo; Kerl, Helmut; Wolf, Peter

doi:10.1111/j.1365-2133.2005.06713.x

Cited by 18 publications

(7 citation statements)

References 17 publications

(30 reference statements)

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“…The importance of the Ras/Raf/MEK/ERK signalling pathway for carcinogenesis is reflected by the facts that Ras genes are the most frequently mutated oncogenes detected in human cancer [ 9 , 10 ] and that B-Raf is activated in several malignancies with the highest frequency found in melanoma [ 11 ]. In MCC, however, we and others did not detect any B-Raf or Ras mutations [ 4 , 12 , 13 ].…”

Section: Resultscontrasting

confidence: 66%

RKIP does not contribute to MAP kinase pathway silencing in the Merkel Cell Carcinoma cell line UISO

Houben¹,

Ortmann²,

Becker³

2007

Journal of Carcinogenesis

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BackgroundThe Raf kinase inhibitor protein (RKIP) has been shown to block MAP kinase pathway as well as NFκB signalling. By means of immunohistochemistry, we previously demonstrated that the MAP kinase pathway is virtually inactive in Merkel cell carcinoma (MCC). Similarly to MCC in situ high RKIP expression accompanies absence of ERK phosphorylation in the MCC cell line UISO suggesting that RKIP might be causative for MAP kinase pathway silencing.MethodsApplying an siRNA approach RKIP expression was knocked down in UISO cells and a possible influence on MAP kinase pathway activity was assessed by Western blot analysis using phospho-specific antibodies. Moreover, a possible effect of RKIP knock down in UISO cells on proliferation as well as chemosensitivity to cisplatin were examined applying the MTS assay.ResultsSurprisingly the absence of phosphorylation of the MAP kinases ERK1 and ERK 2 even following growth factor stimulation was not affected by the RKIP knock down indicating that RKIP is not essential for blocking the MAP kinase pathway in the MCC cell line UISO. Moreover, proliferation as well as chemosensitivity towards cisplatin were not altered upon knock down of RKIP.

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Section: Resultscontrasting

confidence: 66%

RKIP does not contribute to MAP kinase pathway silencing in the Merkel Cell Carcinoma cell line UISO

Houben¹,

Ortmann²,

Becker³

2007

Journal of Carcinogenesis

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“…Recently, Swick et al determined that although eight of nine MCC tumors were positive for c-kit by immunohistochemical staining, no activating mutations were present in the four exons commonly found to have mutations in this gene [28]. Similarily, the analysis of MCC samples did not reveal presence of any activating B-Raf mutations [29,30]. Moreover, immunohistochemical studies revealed that despite high proliferation indices and existing expression of ERK, the ERK protein generally occurs in the non-phosphorylated form and is thus inactive [29].…”

Section: Pathogenesismentioning

confidence: 79%

Merkel cell carcinoma

Becker

Schrama

Houben

2008

Cell. Mol. Life Sci.

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Merkel cell carcinoma (MCC) is a highly aggressive neuroendocrine carcinoma of the skin. More than one-third of MCC patients will die from this cancer, making it twice as lethal as malignant melanoma. Despite the fact that MCC is still a very rare tumor, its incidence is rapidly increasing; the American Cancer Society estimates for 2008 almost 1,500 new cases in the USA. These clinical observations are especially disturbing as the pathogenesis of MCC is not yet fully understood; however, a number of recent reports contribute to a better understanding of its pathogenesis. Here we describe findings regarding the role of Wnt, MAPK and Akt signaling as well as possible aberrations in the p14ARF/p53/RB tumor suppressor network in MCC. Most important, and possibly with high impact on future therapeutic approaches is the demonstration that a polyomavirus has frequently integrated in the genome of the MCC cells prior to tumor development.

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“…Cyclin D1 and beta catenin were not significantly overexpressed in MCCs 88 . BRAF (T1796A and V600E) mutations were absent in MCC 89 90. Depending on the antibody clone used, ALK overexpression on IHC ranges from 12.5% to 93.8%.…”

Section: Molecular/immunohistochemical Studies With Possible Therapeumentioning

confidence: 99%

Molecular characteristics and potential therapeutic targets in Merkel cell carcinoma

et al. 2016

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Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin tumour occurring preferentially in elderly and immunosuppressed individuals. Multiple studies have provided insight into the molecular alterations of MCC, leading to the design of several ongoing clinical trials testing chemotherapy, targeted therapy and immunotherapy in patients with recurrent or metastatic disease. The results of some of these studies are available, whereas others are eagerly awaited and will likely shed light on the understanding of MCC biology and potentially improve the clinical outcomes of patients with this rare disease.

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T1796A BRAF mutation is absent in Merkel cell carcinoma

Cited by 18 publications

References 17 publications

RKIP does not contribute to MAP kinase pathway silencing in the Merkel Cell Carcinoma cell line UISO

RKIP does not contribute to MAP kinase pathway silencing in the Merkel Cell Carcinoma cell line UISO

Merkel cell carcinoma

Molecular characteristics and potential therapeutic targets in Merkel cell carcinoma

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