Establishment and Characterization of Two Merkel Cell Tumor Cultures

Moll, Ingrid; Bohnert, E.; Herbst, Curt; Förster, W.; Moll, Roland; Franke, Werner W.

doi:10.1111/1523-1747.ep12371794

Cited by 28 publications

(23 citation statements)

References 29 publications

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“…Trisomy of chromosome 6 is widely considered as recurrent chromosomal aberration in MCC, [26][27][28] which was the case also in our study. In 42% of the primary MCC samples analyzed by CGH, overrepresentation of all genomic material of chromosome 6 was observed.…”

Section: Discussionsupporting

confidence: 77%

Recurrent DNA copy number changes revealed by comparative genomic hybridization in primary Merkel cell carcinomas

et al. 2004

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Comparative genomic hybridization (CGH) was used to search for gains, high-level amplifications and losses of DNA sequences along all chromosome arms in 19 primary Merkel cell carcinomas (MCC). Extensive genetic aberrations, with a mean value of 5.571.1 changes per tumor were detected in 13 out of the 19 samples analyzed. Our CGH results reveal several new and other previously known chromosomal regions that are involved in the pathogenesis of MCC. The majority of the alterations were gains of whole chromosomes or whole chromosome arms. Compared to losses, the frequency of DNA copy number gains was two-fold. DNA sequence copy number gains were most common in chromosomes 6 (42%), 1 (37%), and 5 (32%). The most frequent minimal common regions of gains were 6pterqter (42%), 1q11q31 (32%), and 5p (32%). No recurrent high-level amplifications were observed. High-level amplifications of small chromosomal regions were found in four samples out of the 19 tumors analyzed (21%). Amplifications affected 1q22q24 (5%), 4p (5%), and 5p (5%). Losses most frequently affected chromosomes 13 (21%) and 4 (16%). Minimal common regions with the most frequent losses were 13q13q31 (21%), 4q (16%), and 16q (11%). No significant statistical correlation between genomic aberrations and clinicopathological factors was revealed, despite the fact that there was an obvious tendency towards it. Primary MCC expressing DNA alterations were predominantly distinguished in large tumors, and risk of metastatic dissemination was three-fold compared to tumors with no DNA alterations.

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Section: Discussionsupporting

confidence: 77%

Recurrent DNA copy number changes revealed by comparative genomic hybridization in primary Merkel cell carcinomas

et al. 2004

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“…MCC cells form clusters on tumor stromal cell feeder layers (Figure S1-A, B). Morphologically, MCC cells contained large, round to oval, vesicular nuclei with loosely textured chromatin as well as scant cytoplasm, a classic feature of MCC (Figure S1-C,D) [30]. CK20 is an intermediate filament and expressed in the epidermal Merkel cells.…”

Section: Resultsmentioning

confidence: 99%

“…In accordance with institutional approvals for human study protocol, fresh MCC tumor tissues from a patient with lymph node metastasis were finely minced and mechanically dissociated tumor materials were passing through a nylon sieve [30]. The resultant cell suspension obtained was seeded in RPMI medium with 10% fetal bovine serum (FBS), penicillin and streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Chronic mTOR activation promotes cell survival in Merkel cell carcinoma

Lin¹,

McDermott²,

Shao³

et al. 2014

Cancer Letters

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Merkel cell carcinoma (MCC) is an aggressive skin cancer with rising incidence. In this study, we demonstrate that mTOR activation and suppressed autophagy is common in MCCs. mTOR inhibition in two primary human MCC cell lines induces autophagy and cell death that is independent of caspase activation but can be attenuated by autophagy inhibition. This is the first study to evaluate mTOR and autophagy in MCC. Our data suggests a potential role of autophagic cell death upon mTOR inhibition and thus uncovers a previously underappreciated role of mTOR signaling and cell survival, and merits further studies for potential therapeutic targets.

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“…Tumour cell lines derived from Merkel cells have been shown to express CKs 8, 18, 19, and 20. 10 This observation has led to the use of antibodies to specific CKs in an attempt to find a discriminatory marker, of which CK20 appears to be the most specific. 3 5 CK8/18 is as sensitive for MCC as CK20, staining a similar proportion of cells, but it is not as specific because it also stained half of the SCCs.…”

Section: Discussionmentioning

confidence: 99%

Merkel cell carcinoma can be distinguished from metastatic small cell carcinoma using antibodies to cytokeratin 20 and thyroid transcription factor 1

Leech¹,

Kolar²,

Barrett³

et al. 2001

Journal of Clinical Pathology

133

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Aim-To investigate whether immunohistochemical staining for cytokeratin 20 (CK20) and thyroid transcription factor 1 (TTF-1) is useful in distinguishing Merkel cell carcinomas (MCCs) from metastatic small cell carcinomas (SCCs). Methods-Eleven cases of MCC and 10 of lung SCC were stained for CK20 and TTF-1. Results-Ten of 11 MCCs stained with the antibody to CK20. None was positive for TTF-1. No SCC stained with anti-CK20 and all stained strongly with anti-TTF-1. Conclusions-The use of both anti-CK20 and anti-TTF-1 can reliably distinguish between MCC and metastatic SCC, thus avoiding the need for a detailed clinical investigation of patients with MCC in whom metastatic SCC must be excluded. (J Clin Pathol 2001;54:727-729)

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Establishment and Characterization of Two Merkel Cell Tumor Cultures

Cited by 28 publications

References 29 publications

Recurrent DNA copy number changes revealed by comparative genomic hybridization in primary Merkel cell carcinomas

Recurrent DNA copy number changes revealed by comparative genomic hybridization in primary Merkel cell carcinomas

Chronic mTOR activation promotes cell survival in Merkel cell carcinoma

Merkel cell carcinoma can be distinguished from metastatic small cell carcinoma using antibodies to cytokeratin 20 and thyroid transcription factor 1

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