Meta-analysis of risk factors for cutaneous melanoma: III. Family history, actinic damage and phenotypic factors

Gandini, Sara; Sera, Francesco; Cattaruzza, Maria Sofia; Pasquini, Paolo; Zanetti, Roberto; Masini, Cinzia; Boyle, Peter; Melchi, Carmelo Francesco

doi:10.1016/j.ejca.2005.03.034

Cited by 666 publications

(600 citation statements)

References 99 publications

Supporting

Mentioning

536

Contrasting

Unclassified

Order By: Relevance

“…However, the distribution of pigmentation characteristics can vary within different populations, affecting risk estimates. Moreover, the ORs are lower after adjusting for phenotype, suggesting a significant correlation between these factors [3,18,20]. Similar to our findings, a previous study of 244 cases and 276 controls in an Australian Caucasian population showed that light hair and eye colors and the presence of ephelides in childhood did not have a relationship with CM [21].…”

Section: Characteristicsupporting

confidence: 79%

“…Several risk factors were identified as independent for development of CM, including atypical melanocytic nevi, multiple melanocytic nevi, personal history of non-melanoma skin cancer (NMSC), family history of CM, and significant occupational sun exposure. [18], or ephelides (OR: 1.99) [19] have been shown to be at greater risk of developing CM than people with dark phenotypes. However, the distribution of pigmentation characteristics can vary within different populations, affecting risk estimates.…”

Section: Characteristicmentioning

confidence: 99%

See 1 more Smart Citation

Risk Factors for Developing Cutaneous Melanoma in Santa Catarina, Brazil: A Case-Control Observational Study

Moreno¹,

Ciotta²,

Vedana³

et al. 2017

JDC

View full text Add to dashboard Cite

show abstract

Section: Characteristicsupporting

confidence: 79%

Section: Characteristicmentioning

confidence: 99%

Risk Factors for Developing Cutaneous Melanoma in Santa Catarina, Brazil: A Case-Control Observational Study

Moreno¹,

Ciotta²,

Vedana³

et al. 2017

JDC

View full text Add to dashboard Cite

show abstract

“…Older case-control studies of patients with familial atypical mole-melanoma (FAMM) syndrome suggested an elevated risk of ∼434-to 1000-fold over the general population (Greene et al 1985). A more recent metaanalysis of family history found that the presence of at least one first-degree relative with melanoma increases the risk by 2.24-fold (Ford et al 1995;Gandini et al 2005b). Genetic studies of this heritable trait in large melanoma-prone families ultimately led to the initial identification of CDKN2A as the familial melanoma gene.…”

Section: Cdkn2a the Familial Melanoma Locusmentioning

confidence: 99%

Malignant melanoma: genetics and therapeutics in the genomic era

2006

View full text Add to dashboard Cite

Cell for cell, probably no human cancer is as aggressive as melanoma. It is among a handful of cancers whose dimensions are reported in millimeters. Tumor thickness approaching 4 mm presents a high risk of metastasis, and a diagnosis of metastatic melanoma carries with it an abysmal median survival of 6-9 mo. What features of this malignancy account for such aggressive behavior? Is it the migratory history of its cell of origin or the programmed adaptation of its differentiated progeny to environmental stress, particularly ultraviolet radiation? While the answers to these questions are far from complete, major strides have been made in our understanding of the cellular, molecular, and genetic underpinnings of melanoma. More importantly, these discoveries carry profound implications for the development of therapies focused directly at the molecular engines driving melanoma, suggesting that we may have reached the brink of an unprecedented opportunity to translate basic science into clinical advances. In this review, we attempt to summarize our current understanding of the genetics and biology of this disease, drawing from expanding genomic information and lessons from development and genetically engineered mouse models. In addition, we look forward toward how these new insights will impact on therapeutic options for metastatic melanoma in the near future. The diseaseMelanomas most often arise within epidermal melanocytes of the skin, although they can also derive from noncutaneous melanocytes such as those lining the choroidal layer of the eye, GI and GU mucosal surfaces, or the meninges. Melanoma is also among the more common causes of "metastatic cancer of unknown primary," which may reflect either a propensity to arise in unexpected sites along the neural crest migratory route, or rapid growth of poorly differentiated lesions arising from indolent or unrecognized cutaneous primary lesions. Clinical staging for primary cutaneous melanoma employs measurements of thickness (in millimeters), presence of ulceration, penetration through cutaneous layers, mitotic rate, evidence of "in transit" metastasis, tumor spread to draining lymph nodes, and evidence of distant metastasis. Management issues in melanoma can be classified in terms of prevention, diagnosis, local disease management, and treatment of metastatic disease.In view of the epidemiological and emerging experimental evidence linking melanoma incidence to UV exposure and skin phototype, prevention and screening strategies represent key areas for reduction of disease incidence and severity. For most cutaneous melanomas in the so-called radial growth phase (e.g., thin melanomas), surgical removal affords curative treatment. In contrast, a significant fraction of patients diagnosed with intermediate-thickness (2-4 mm) cutaneous melanoma eventually succumb to recurrence at regional or distant sites.Critical biological questions facing the melanoma research community include: (1) What genetic and environmental factors contribute to and/or modulate risk of melanom...

show abstract

“…The incidence of melanoma has been increasing over decades, especially among fair-skinned people (1). Early-stage melanoma can be readily cured by surgical excision of the primary lesion, but advanced melanoma, often a metastatic disease, has a poor median survival, ranging from 2 to 8 months, with only 5% surviving Ͼ5 years (2).…”

mentioning

confidence: 99%

Acid Ceramidase Expression Modulates the Sensitivity of A375 Melanoma Cells to Dacarbazine

Bedia

Casas²,

Andrieu‐Abadie

et al. 2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

Dacarbazine (DTIC) is the treatment of choice for metastatic melanoma, but its response in patients remains very poor. Ceramide has been shown to be a death effector and to play an important role in regulating cancer cell growth upon chemotherapy. Among ceramidases, the enzymes that catabolize ceramide, acid ceramidase (aCDase) has been implicated in cancer progression. Here we show that DTIC elicits a time-and dosedependent decrease of aCDase activity and an increase of intracellular ceramide levels in human A375 melanoma cells. The loss of enzyme activity occurred as a consequence of reactive oxygen species-dependent activation of cathepsin B-mediated degradation of aCDase. These events preceded autophagic features and loss of cell viability. Down-regulation of acid but not neutral or alkaline ceramidase 2 resulted in elevated levels of ceramide and sensitization to the toxic effects of DTIC. Conversely, inducible overexpression of acid but not neutral ceramidase reduced ceramide levels and conferred resistance to DTIC. In conclusion, we report that increased levels of ceramide, due to enhanced degradation of aCDase, are in part responsible for the cell death effects of DTIC. These results suggest that downregulation of aCDase alone or in combination with DTIC may represent a useful tool in the treatment of metastatic melanoma.

show abstract

Meta-analysis of risk factors for cutaneous melanoma: III. Family history, actinic damage and phenotypic factors

Cited by 666 publications

References 99 publications

Risk Factors for Developing Cutaneous Melanoma in Santa Catarina, Brazil: A Case-Control Observational Study

Risk Factors for Developing Cutaneous Melanoma in Santa Catarina, Brazil: A Case-Control Observational Study

Malignant melanoma: genetics and therapeutics in the genomic era

Acid Ceramidase Expression Modulates the Sensitivity of A375 Melanoma Cells to Dacarbazine

Contact Info

Product

Resources

About