Merkel cell carcinoma

Becker, Juergen C.; Schrama, David; Houben, Roland

doi:10.1007/s00018-008-8483-6

Cited by 70 publications

(68 citation statements)

References 55 publications

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“…The large T antigens of polyomaviruses are able to inactivate p53, but the large T antigens of MCPyV usually show truncated mutations requiring a loss of the interacting domain of p53 [2,14,29]. The typical specific hot spots of p53 mutations are located on codon 177, 196, 247, 278, and 294 [12].…”

Section: Discussionmentioning

confidence: 97%

“…They are very aggressive neuroendocrine carcinomas occurring with an incidence of 1,500 new cases in the USA alone in 2008, whereas similar data was published for Europe [2][3][4]. Despite a recent progress in developing several new therapies for carcinomas of different origin, MCCs are still associated with poor prognosis and a poor disease specific survival due to lymph node metastasis and recurrent disease with an overall mortality rate of 33% [2].…”

Section: Introductionmentioning

confidence: 93%

“…Despite a recent progress in developing several new therapies for carcinomas of different origin, MCCs are still associated with poor prognosis and a poor disease specific survival due to lymph node metastasis and recurrent disease with an overall mortality rate of 33% [2]. MCCs occur in elder patients, with a mean age at initial diagnosis of approximately 70 years [2].…”

Section: Introductionmentioning

confidence: 99%

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P53 mutation is a rare event in Merkel cell carcinoma of the head and neck

Lill

Schneider

Item

et al. 2011

Eur Arch Otorhinolaryngol

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The aim of this retrospective analysis was to evaluate the status of p53 and possible mutations in Merkel cell carcinoma (MCC) cell lines and MCC tissue samples. The p53 mutations are common in different cancer origins but rare in MCCs detected so far. MCCs are highly aggressive neuroendocrine tumors with an enhanced potential to metastasize. Until now, less is known about MCC and new approaches to understand this disease are necessary. RNA and DNA were extracted from two MCC cell lines and 27 archival paraffin-embedded patient samples. After reverse transcription, a real-time PCR and a high-resolution melt analysis were carried out. In both MCC cell lines, we could detect a p53 missense mutation at codon 193 (exon 6) with a change in amino acids (His → Leu). This mutation was equal in both cell lines and was investigated in 27 tissue samples in succession to detect possible accounts for the aggressive behavior of MCCs. Unfortunately, no corresponding p53 mutation could be observed in the investigated tissue samples. A new p53 mutation was detected in MCC cell lines. This mutation could not be determined in patients' samples. Therefore, the aggressiveness of MCC seems to be independent of p53 mutations and other mutations might be responsible for developing MCC.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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P53 mutation is a rare event in Merkel cell carcinoma of the head and neck

Lill

Schneider

Item

et al. 2011

Eur Arch Otorhinolaryngol

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“…Although it is rare, its reported incidence is increasing (19). MCC is associated with UV exposure and affects primarily elderly and immune-suppressed patients (5,11,17,26). The susceptibility of MCC to immune surveillance is similar to that of known virus-induced cancers and suggests that MCC has an infectious trigger (9).…”

Section: Merkel Cell Carcinoma (Mcc) Is the Most Aggressive Skin Cancmentioning

confidence: 99%

Merkel Cell Polyomavirus-Infected Merkel Cell Carcinoma Cells Require Expression of Viral T Antigens

Houben

Shuda

Weinkam

et al. 2010

J Virol

400

439

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Merkel cell carcinoma (MCC) is the most aggressive skin cancer. Recently, it was demonstrated that human Merkel cell polyomavirus (MCV) is clonally integrated inMerkel cell carcinoma (MCC) is a highly aggressive neuroendocrine skin cancer. Although it is rare, its reported incidence is increasing (19). MCC is associated with UV exposure and affects primarily elderly and immune-suppressed patients (5,11,17,26). The susceptibility of MCC to immune surveillance is similar to that of known virus-induced cancers and suggests that MCC has an infectious trigger (9). Recently, a new human polyomavirus, termed Merkel cell polyomavirus (MCV), was discovered to be clonally integrated into MCC tumor genomes (14). While MCV integration occurs at distinct sites in MCC tumors from different individuals, primary tumors and corresponding metastases have identical integration sites, consistent with the occurrence of MCV infection and integration prior to clonal expansion and metastasis (14,37). A number of studies have confirmed that MCV is present in 69 to 85% of MCC tumors collected from Europe and the United States (4, 15, 21, 41). Surveys of control non-MCC skin, hematolymphoid, and neuroendocrine tumors are generally negative for MCV, although incidental low-level infection can be detected (4,14,22,33,34,39,42,44).All polyomaviruses encode alternatively spliced large T (LT) and small T (sT) antigen transcripts that share exon 1 of the T-antigen (TA) locus. Additional multiply spliced TA transcripts have been described for different polyomaviruses, including the 17kT and 57kT antigens in simian virus 40 (SV40) and MCV, respectively (40,46). Research on viral proteins encoded by the TA locus has been central to uncovering cell signaling networks important in cancer biology (10, 38). The targeting of cellular proteins, such as retinoblastoma protein (Rb), p53, and protein phosphatase 2A (PP2A), by TAs contributes to polyomavirusinduced cell transformation (for reviews, see references 1 and 2). MCV TAs that are expressed in MCC tumors lack a putative p53 binding domain because of tumor-associated T-antigen deletion mutations (37,40). Other conserved tumor suppressor-targeting motifs, including the Rb binding domain (LXCXE motif), the J domain (HPDK) in LT/57kT, and a putative PP2A interaction domain in sT, remain intact (40).Current data point toward MCV as the infectious cause for most Merkel cell cancers: the virus is associated with MCC tumors and, when present, expresses T antigen in tumor cells but not in healthy surrounding tissues (7,20,39). MCV is specific to MCC and is not detected at significant levels in other cancers or in healthy skin examined to date, despite widespread circulation of MCV among human populations (8,23,29,42). Clonal analysis of MCC tumors also supports the correct temporal relationship for causality; i.e., MCV infection occurs prior to MCC tumor development (18). If MCV is a direct cause of MCC tumorigenesis, it is expected that MCC tumors will require MCV protein expression to maintain the tumor ...

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“…Neuroendocrine tumors (NETs) are derived from neuroendocrine cells spread in the human body from the digestive and respiratory tracts, urinary and nervous systems (1) to the skin (2). These cells have similar features to the endocrine cells and express antigens that are also common in the nervous system (e.g.…”

mentioning

confidence: 99%

Surgical Treatment of Neuroendocrine Tumors of the Pancreas

Dobrowolski¹,

Śledziński²,

Sworczak³

et al. 2010

Polish Journal of Surgery

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Management of patients with neuroendocrine tumors (NETs) of the pancreas causes considerable controversy because rarity of this neoplasm. The aim of the study was to present our results of treatment of patients with NETs and to sum up our experience in surgical management. material and methods. Thirty four patients with neuroendocrine tumors of the pancreas were treated in Department of General, Endocrine and Transplant Surgery of Medical University in Gdańsk (24 inulinomas and 10 nonfunctioning neuroendocrine tumors). Insulinoma was present in the head of the pancreas in 3 cases, in the body in 8 cases, and 10 patients had lesion situated within the tail. Results. Localization of the tumor in patients with organic hyperinsulinism was possible in 21 out of 24 operated patients (17 patients with use of preoperative imaging studies, 4 patients with Intraoperative ultrasonography). In 3 remaining patients the localization of the pathologic mass was impossible with use of pre-and intraoperative techniques. conclusions. Treatment of choice of patients with neuroendocrine tumors of the pancreas is surgery. Management of patients with islet cells adenomatosis is still difficult clinical problem. Key words: insulinoma, neuroendocrine tumor, nesidioblastosis, pancreatic islet POLSKI PRZEGLĄD CHIRURGICZNY 10.2478/v10035-010-0058-1 2010 Neuroendocrine tumors (NETs) are derived from neuroendocrine cells spread in the human body from the digestive and respiratory tracts, urinary and nervous systems (1) to the skin (2). These cells have similar features to the endocrine cells and express antigens that are also common in the nervous system (e.g. synaptophysin, neuron-specific enolase, chromogranins), what led to the term of neuroendocrine cells. Neuroendocrine tumors has different morphology and clinical presentation, especially in ability to metastasis, what cause problems with their classification.There are 15 types of neuroendocrine cells being source of the neuroendocrine tumors in the digestive tract and pancreas, where the NETs are found most frequently (1). The World Health Organization 2000 classification of neuroendocrine tumors of the digestive tract and the pancreas identifies three tumors categories: 1) well-differentiated endocrine tumors with benign or uncertain behavior at the time of diagnosis, 2) well-differentiated endocrine tumors with low grade malignant behavior, 3) poorly differentiated endocrine carcinomas with high-grade malignant behavior. The classification was then subdivided on the basis of localization and biology of the tumors. For localization, the stomach, duodenum and jejunum, ileum, appendix, colon-rectum, and pancreas were distinguished. The biologic criteria employed were tumor size, angioinvasion, proliferative activity, histological differentiation, presence of metastases and hormonal activity. The WHO classification of neuroendocrine tumors of the pancreas is presented in tab. 1.

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Merkel cell carcinoma

Cited by 70 publications

References 55 publications

P53 mutation is a rare event in Merkel cell carcinoma of the head and neck

P53 mutation is a rare event in Merkel cell carcinoma of the head and neck

Merkel Cell Polyomavirus-Infected Merkel Cell Carcinoma Cells Require Expression of Viral T Antigens

Surgical Treatment of Neuroendocrine Tumors of the Pancreas

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