Molecular biology of melanoma

Swick, Julie M.; Maize, John C.

doi:10.1016/j.jaad.2011.06.047

Cited by 35 publications

(30 citation statements)

References 20 publications

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“…35 As BRAF belongs to the MAPK pathway, its increased activation ultimately stimulates MM cellular proliferation. [36][37][38] BRAF mutations have been associated with activation of AKT or loss of PTEN. [39][40][41] Furthermore, aberrations in the G proteins, GNAQ and GNA11, stimulate BRAF and its downstream effector, MEK.…”

Section: Pathophysiology: Sharing Of Signal Transduction Pathways mentioning

confidence: 99%

“…44 Finally, BRAF overactivation in association with CCND1/cyclin D1 overexpression may contribute to melanoma metastasis. 45 Mutations of NRAS, a small GTPase directly upstream of BRAF, are observed in B20% of melanomas 35,36,40,46 and are mutually exclusive from BRAF mutations. 39 Abnormalities in KIT, the receptor tyrosine kinase immediately upstream of RAS and PI3K, are found in roughly 27% of mucosal, 24% of acral, and 21% of melanomas on chronically sun-damaged skin, but are seldom found in melanomas on skin without chronic sun damage.…”

Section: Pathophysiology: Sharing Of Signal Transduction Pathways mentioning

confidence: 99%

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Melanoma genotypes and phenotypes get personal

Pimiento

Larkin

Smalley

et al. 2013

Laboratory Investigation

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Section: Pathophysiology: Sharing Of Signal Transduction Pathways mentioning

confidence: 99%

Section: Pathophysiology: Sharing Of Signal Transduction Pathways mentioning

confidence: 99%

Melanoma genotypes and phenotypes get personal

Pimiento

Larkin

Smalley

et al. 2013

Laboratory Investigation

View full text Add to dashboard Cite

“…Pathogenesis of melanoma is characterized by mutations of MAPK pathway components, N-RAS, B-RAF, PTEN and p53, while metastatic transition is accompanied by gain of functions of transcription factors like NF-kB and STATs and loss of TFAP2 family members (2,3). Given the complexity of networks and pathways involved, disclosing the molecular mechanisms underlying melanoma formation and progression is crucial to provide novel therapeutic strategies (4,5).…”

Section: Introductionmentioning

confidence: 99%

miR-146a Exerts Differential Effects on Melanoma Growth and Metastatization

Raimo¹,

Orso²,

Grassi³

et al. 2016

Molecular Cancer Research

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Malignant melanoma is the most aggressive form of skin cancer; therefore, it is crucial to disclose its underlying molecular mechanisms. MicroRNAs (miRNAs) are small endogenous noncoding RNAs able to posttranscriptionally downregulate the expression of direct target genes. Using a melanoma progression model, miR-146a was identified as a key double-acting player in melanoma malignancy. In fact, miR-146a is able to enhance tumor growth, while it suppresses dissemination. It was determined that miR-146a coordinated melanoma cell growth by its direct targets lunatic fringe (LFNG) and NUMB, which operate on the NOTCH/PTEN/Akt pathway; while inhibition of metastasis formation was linked to decreased expression of ITGAV and ROCK1. Relevantly, miR-146a expression correlated with melanoma recurrence and was enriched in both patient-derived melanoma and cutaneous metastasis specimens, while its direct targets were depleted. However, miR-146a levels drop in circulating tumor cells (CTCs), suggesting the necessity for miR-146a expression to fluctuate during tumor progression in order to favor tumor growth and allow dissemination. This study reconciles the contradictory biologic functions of miR-146a in melanoma progression and unravels distinct molecular mechanisms that need to be considered for therapeutic interventions.

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“…They are focused on mutations in DNA, RNA and proteins. Such specific and sensitive procedures applied to CMM help refining the diagnosis, classification, outcome prediction, as well as selection and monitoring of therapy [14][15][16][17][18][19][20][21][22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Streamlining Molecular Pathobiology of Malignant Melanoma

Pierard¹

2016

CRDOA

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Currently, regular histopathology and immunohistochemistry are commonly taken for granted in the diagnosis of Cutaneous Malignant Melanoma (CMM). In addition, attempts at molecular diagnosis in dermatopathology have benefited from advances in pathobiology genomics and proteomics. They provide utmost information for optimal patient care. Sensitive techniques detect specific DNA and RNA sequences, and molecular methods were refined in the field of polypeptides. This review aims at covering on an overall glance about molecular genetics available as diagnostic supports in CMM. Laboratory methods have disclosed and highlighted some pathogenic pathways of atypical melanocytic neoplasms with particular emphasis on the activation of the Mitogen-Activated Protein Kinase (MAPK) signalling pathway (including BRAF and KIT) during the initiation step of the neoplasms. Many familial CMM contain mutations of the tumor suppressor gene p16 or CDKN2A. In addition, mutations in p53 are found in distinct CMM types. Many CMM are likely related to a variety of common low penetrance genes. Molecular dermatopathology represents a promising tool for both research and diagnosis. Knowledge of tumor mutation status is becoming increasingly important. The expected benefit of molecular dermatopathology tends to ultimately improve the targeted patient management. Such method evolution points to a need for improving the routine training requirements for dermatopathologists involved in cancer diagnostic responsibilities.

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Molecular biology of melanoma

Cited by 35 publications

References 20 publications

Melanoma genotypes and phenotypes get personal

Melanoma genotypes and phenotypes get personal

miR-146a Exerts Differential Effects on Melanoma Growth and Metastatization

Streamlining Molecular Pathobiology of Malignant Melanoma

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