Issues in the epidemiology of melanoma

Oliveria, Susan A.; Dusza, Stephen W.; Berwick, Marianne

doi:10.1586/14737140.1.3.453

Cited by 27 publications

(21 citation statements)

References 45 publications

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“…In addition, the final pathology diagnosis, whether correct or not, is ultimately responsible for determining which lesions enter into cancer registry databases [1]. This in turn may influence the results of epidemiological investigations of cancer, diagnostic studies, or comparative studies that rely upon evaluations provided by pathologists [2,3,4,5]. …”

Section: Introductionmentioning

confidence: 99%

Agreement of Dermatopathologists in the Evaluation of Clinically Difficult Melanocytic Lesions: How Golden Is the ‘Gold Standard’?

et al. 2012

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Background: The ‘gold standard’ for the diagnosis of melanocytic lesions is dermatopathology. Although most of the diagnostic criteria are clearly defined, the interpretation of histopathology slides may be subject to interobserver variability. Objectives: The aim of this study was to determine the variability among dermatopathologists in the interpretation of clinically difficult melanocytic lesions. Methods: This study used the database of MelaFind®, a computer-vision system for the diagnosis of melanoma. All lesions were surgically removed and sent for independent evaluation by four dermatopathologists. Agreement was calculated using kappa statistics. Results: A total of 1,249 pigmented melanocytic lesions were included. There was a substantial agreement among expert dermatopathologists: two-category kappa was 0.80 (melanoma vs. non-melanoma) and three-category kappa was 0.62 (malignant vs. borderline vs. benign melanocytic lesions). The agreement was significantly greater for patients ≥40 years (three-category kappa = 0.67) than for younger patients (kappa = 0.49). In addition, the agreement was significantly lower for patients with atypical mole syndrome (AMS) (kappa = 0.31) than for patients without AMS (kappa = 0.76). Limitations: The data were limited by the inclusion/exclusion criteria of the MelaFind® study. This might represent a selection bias. The agreement was evaluated using kappa statistics. This is a standard method for evaluating agreement among pathologists, but might be considered controversial by some statisticians. Conclusions: Expert dermatopathologists have a high level of agreement when diagnosing clinically difficult melanocytic lesions. However, even among expert dermatopathologists, the current ‘gold standard’ is not perfect. Our results indicate that lesions from younger patients and patients with AMS may be more problematic for the dermatopathologists, suggesting that improved diagnostic criteria are needed for such patients.

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Section: Introductionmentioning

confidence: 99%

Agreement of Dermatopathologists in the Evaluation of Clinically Difficult Melanocytic Lesions: How Golden Is the ‘Gold Standard’?

et al. 2012

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“…The incidence of melanoma has increased during the past 50 years at a rate that exceeds any other solid tumor, with substantially increased mortality rates as well (1,2). Although melanoma accounts for only 10% of all skin cancers, it is responsible for 80% of all skin cancer deaths (3).…”

Section: Introductionmentioning

confidence: 99%

Topical Treatment with Inhibitors of the Phosphatidylinositol 3′-Kinase/Akt and Raf/Mitogen-Activated Protein Kinase Kinase/Extracellular Signal-Regulated Kinase Pathways Reduces Melanoma Development in Severe Combined Immunodeficient Mice

Bedogni¹,

O'Neill²,

Welford³

et al. 2004

Cancer Research

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Topical treatment with inhibitors of the phosphatidylinositol 3-kinase/ Akt and Raf/mitogen-activated protein kinase kinase/extracellular signalregulated kinase pathways inhibited the growth of TPras transgenic melanomas in severe combined immunodeficient mice, blocked invasive behavior, and reduced angiogenesis. The inhibitor Ly294002, which is specific for phosphatidylinositol 3-kinase, effectively reduced melanoma cell growth both in vitro and in vivo. Both Ly294002 and U0126, a mitogen-activated protein kinase kinase 1/2 inhibitor, reduced invasion, which correlated with reduction of the metalloproteinase matrix metalloproteinase 2. Tumor angiogenesis was disrupted through inhibition of vascular endothelial growth factor production from the tumor cells and antiangiogenic effects on endothelial cells. Observations with TPras melanoma cells that express dominant negative ⌬p85 or kinase-inactive Raf 301 supported the specificity of the phenomena observed with the chemical inhibitors. These studies demonstrate that topical treatment targeting Ras effectors is efficacious, without systemic toxicities, and may prove to be useful in treating and preventing the progression of cutaneous melanoma.

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“…Metastatic disease is estimated to have caused 7600 deaths in 2003 and is the second cause of lost productive years among cancers (1,2). Melanoma is highly resistant to conventional chemotherapy with dacarbazine or its derivative temozolomide (TMZ) having the best single agent activity with a response rate of only 15-20% and a short 4-month median response duration.…”

Section: Introductionmentioning

confidence: 99%

Augmenting Chemosensitivity of Malignant Melanoma Tumors via Proteasome Inhibition

Horton²,

et al. 2004

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Melanoma poses a great challenge to patients, oncologists, and biologists because of its nearly universal resistance to chemotherapy. Many studies have shown that nuclear factor B is constitutively activated in melanoma, thereby promoting the proliferation of melanoma cells by inhibiting the apoptotic responses to chemotherapy. Nuclear factor B activity is regulated by phosphorylation and subsequent degradation of inhibitor of nuclear factor B by the ubiquitin-proteasome pathway. In this study, we show that the novel proteasome inhibitor, bortezomib, inhibited the growth of melanoma cells in vitro at a concentration range of 0.1-10 nM and in combination with the chemotherapeutic agent temozolomide, the inhibitory effect on melanoma cell growth was even more prominent. Data from a murine model showed reduced tumor growth when bortezomib was administered to human melanoma tumors. Strikingly, animals receiving bortezomib in combination with temozolomide achieved complete remission of palpable tumors after only 30 days of therapy, lasting >200 days. Our data indicate strongly that bortezomib in combination with chemotherapeutic agents should be studied additionally for the treatment of melanoma.

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Issues in the epidemiology of melanoma

Cited by 27 publications

References 45 publications

Agreement of Dermatopathologists in the Evaluation of Clinically Difficult Melanocytic Lesions: How Golden Is the ‘Gold Standard’?

Agreement of Dermatopathologists in the Evaluation of Clinically Difficult Melanocytic Lesions: How Golden Is the ‘Gold Standard’?

Topical Treatment with Inhibitors of the Phosphatidylinositol 3′-Kinase/Akt and Raf/Mitogen-Activated Protein Kinase Kinase/Extracellular Signal-Regulated Kinase Pathways Reduces Melanoma Development in Severe Combined Immunodeficient Mice

Augmenting Chemosensitivity of Malignant Melanoma Tumors via Proteasome Inhibition

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