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Affymetrix copy number data for melanoma cell line mapping

ABSTRACT: We searched for putative phenotypic and genotypic differences between primary lesions and melanoma metastasis. Therefore, we investigated melanoma cells derived either from the primary tumor or from lymph node metastasis of the same individual patient. In vitro studies revealed high migratory and anchorage-independent growth of metastasis-derived cells. Unexpectedly, whole genome DNA analysis displayed a total of 10 homozygous losses in the primum-derived cell line, whereas the metastasis–derived cell line only shared 5 of those losses. We further tested these cells in a mouse model for intradermal melanoma growth and detected fast growth of the metastasis-derived cell line and delayed growth of primum-derived cells. However, after re-grafting of primum-derived cells, tumor growth kinetic was accelerated and therefore comparable to metastasis-derived cells. Moreover, re-grafted primum-derived cells now also harboured the same reduced DNA deletion pattern, identical to human metastasis-derived cells. We conclude that our xenotransplantation model mimics clonal selection from a heterogeneous starting population, and we suggest that tumor cell progression at the metastatic niche can occur parallel and independently from the primary tumor. Therefore, we propose that for mutation-targeted therapy approaches, the genotyping procedure should include primary as well as metastatic melanoma biopsies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22461 | GEO | 2011/04/07

SECONDARY ACCESSION(S): PRJNA128607

REPOSITORIES: GEO

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Tissue samples from the same individual patient

Project description:We searched for putative phenotypic and genotypic differences between primary lesions and melanoma metastasis. Therefore we investigated melanoma cells derived either from the primary tumor or from lymph node metastasis of the same individual patient. In vitro studies revealed high migratory and anchorage independent growth of metastasis-derived cells. Unexpectedly, whole genome DNA analysis displayed a total of 10 homozygous losses in the primum-derived cell line, whereas the metastasis–derived cell line only shared 5 of those losses. We further tested these cells in a mouse model for intradermal melanoma growth and detected fast growth of the metastasis-derived cell line and no growth of primum-derived cells. Therefore we suggest that tumor cell progression at the metastatic niche can occur parallel and independently from the primary tumor. Additionally we screened melanoma samples isolated from patients and could identify one case were the primum harboured deletions not present in the metastatic lesion. We propose that for mutation-targeted therapy genotyping should be performed not only from primary, but foremost from metastatic melanoma cells.

2011-04-07 | GSE26053 | GEO

Tissue samples from the same individual patient

2011-04-07 | E-GEOD-26053 | biostudies-arrayexpress

Affymetrix copy number data for melanoma cell line mapping

Project description:We searched for putative phenotypic and genotypic differences between primary lesions and melanoma metastasis. Therefore, we investigated melanoma cells derived either from the primary tumor or from lymph node metastasis of the same individual patient. In vitro studies revealed high migratory and anchorage-independent growth of metastasis-derived cells. Unexpectedly, whole genome DNA analysis displayed a total of 10 homozygous losses in the primum-derived cell line, whereas the metastasis–derived cell line only shared 5 of those losses. We further tested these cells in a mouse model for intradermal melanoma growth and detected fast growth of the metastasis-derived cell line and delayed growth of primum-derived cells. However, after re-grafting of primum-derived cells, tumor growth kinetic was accelerated and therefore comparable to metastasis-derived cells. Moreover, re-grafted primum-derived cells now also harboured the same reduced DNA deletion pattern, identical to human metastasis-derived cells. We conclude that our xenotransplantation model mimics clonal selection from a heterogeneous starting population, and we suggest that tumor cell progression at the metastatic niche can occur parallel and independently from the primary tumor. Therefore, we propose that for mutation-targeted therapy approaches, the genotyping procedure should include primary as well as metastatic melanoma biopsies. DNA was extracted from in vitro grown cell lines, and Affymetrix SNP6.0 arrays were performed according to the manufacturer's instructions. Intensity Log2 ratios were used to manually search for homozygous deletions via the genotyping console.

2011-04-07 | E-GEOD-22461 | biostudies-arrayexpress

Emilin1 degradation and secretion in exosomes inactivate its tumor- and metastasis-suppressive role in melanoma mouse models

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Melanoma-derived small extracellular vesicles induce lymphangiogenesis and metastasis through a NGFR-dependent mechanism

Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in the establishment of lymph node pre-metastatic niches by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and were taken up by lymphatic endothelial cells, reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. We found that neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells, inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended the survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support the idea that NGFR secreted in sEVs favors lymph node pre-metastatic niche formation and lymph node metastasis in melanoma

2021-08-05 | PXD024852 | Pride

Melanoma-derived small extracellular vesicles induce lymphangiogenesis and metastasis by a NGFR-dependent mechanism

Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in establishing the lymph node pre-metastatic niche by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and are taken up by lymphatic endothelial cells reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. Analysis of involved factors demonstrated that the neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended mice survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support that NGFR is secreted in sEVs favoring lymph node pre-metastatic niche formation and lymph node metastasis in melanoma.

2021-07-16 | PXD024108 | Pride

Amyloid Beta Promotes Brain Metastasis

Project description:Brain metastasis is a significant cause of morbidity and mortality in multiple cancer types and represents an unmet clinical need. The mechanisms that mediate metastatic cancer growth in the brain parenchyma are largely unknown. Melanoma, which has the highest rate of brain metastasis among common cancer types, is an ideal model to study how cancer cells adapt to the brain parenchyma. We utilized pairs of brain metastasis-derived (BM) and non-brain metastasis-derived (NBM) melanoma short term cultures (STCs) obtained from the same patient. We performed TMT based multiplexed analysis of these cell lines using off-line fractionation to increase our proteomics coverage. Our unbiased proteomics analysis of these melanoma short-term cultures revealed that proteins implicated in neurodegenerative pathologies are differentially expressed in melanoma cells explanted from brain metastases compared to those derived from extracranial metastases. We showed that melanoma cells require amyloid beta for growth and survival in the brain parenchyma. Melanoma-secreted A beta activates surrounding astrocytes to a pro-metastatic, anti-inflammatory phenotype and prevents phagocytosis of melanoma by microglia. Finally, we demonstrate that pharmacological inhibition of Abeta decreases brain metastatic burden.

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Affymetrix SNP array data for a melanoma lesion and a cellline derived thereof

Project description:Here we report on a bulk culture termed MCM1, which was derived from a 61 year old male diagnosed with a nodular melanoma stage T2a, N0. At passage three of culturing, DNA was isolated and Affymetrix SNP6.0 array hybridizations were performed. Cultured MCM1 cells revealed overall identical copy number gains and losses as compared with the primary patient-derived lesion and were therefore used in this study. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA, which was extracted from a patient derived melanoma sample and from a cellline generated from the same melanoma sample at passage three.

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2008-05-07 | E-GEOD-5982 | biostudies-arrayexpress

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