Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nevus cell components have been observed in up to 40% of melanomas, but little is known of the pathobiology of these components in relation to their malignant potential. We studied 44 nevi of the typical, dysplastic, congenital, and Spitz types with a battery of monoclonal and polyclonal antibodies that react on formalin-fixed, paraffin-embedded tissues (HMB.45, S-100 protein, RAP-5, epithelial membrane antigen [EMA], and neuron-specific enolase [NSE]) by avidin-biotin immunohistochemical methods. EMA and RAP-5 (which detects the ras oncogene-associated P21 protein) were negative in all cases. Melanoma-specific HMB.45 was strongly reactive with the epidermal component and had a weak to negative reaction with the dermal component in the typical nevi. However, the reaction seen with HMB.45 in the junctional component of dysplastic nevi, congenital nevi, and some Spitz nevi was heterogeneous. One Spitz nevi showed HMB.45 staining in a pattern near to that of melanoma. In contrast to HMB.45, S-100 protein labeled nevomelanocytes, regardless of whether they were within the epidermis or dermis, although, in half of the dysplastic nevi, the reaction was heterogeneous, with some atypical cells failing to stain. But, with cytologically atypical junctional component (dysplastic-appearing), congenital nevi also stained heterogeneously for S-100 protein compared with the dermal component. NSE stained the central component of some Spitz nevi more intensely than the lateral component. Junctional nevomelanocytic subsets of some congenital nevi revealed HMB.45 and S-100 reactivity similar to dysplastic nevi.
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PMID:Typical, dysplastic, congenital, and Spitz nevi: a comparative immunohistochemical study. 229 3

Melanoma may present a great variety of cell morphology and mimic virtually almost all other neoplasms, and metastatic lesions pose major diagnostic difficulties. A typical immunoreactive profile of melanoma is: S-100p- and HMB-45-positivity, but these markers are not always present. Other new antigens for melanoma are NKIC3 and Anti-Melan-A (MART-1). This tumor may also present expression of unspecific markers, as cytokeratin, CEA, EMA, desmin, NFP, GFAP, CD68 and actins. We present here unusual features of two metastatic melanomas, showing the anaplastic pattern, immunopositive for desmin.
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PMID:Rhabdomyosarcomatous (myoblastic?) phenotype of metastatic malignant melanoma. A case report. 1214 Aug 74

Benign melanotic lesions of the vagina are uncommon and only a few cases have been reported in the literature. A 34-year-old woman was referred because of a Vaginal Intraepithelial Neoplasia 1 biopsy result. On the gynecological examination, two different hyperpigmented areas were noted in the vagina. The colposcopic visualization of the cervix and vagina found an aceto-white lesion at the right lateral wall of the upper third of the vagina. Biopsies from three areas were taken. Histological study reported a melanosis of the vagina and HPV infection. An immunohistochemical panel of epithelial markers was performed in vaginal samples, such as Cytokeratin AE1/AE3 and epithelial membrane antigen, mesenchymal marker: vimentin; melanocytic makers: protein S-100 and HMB45 (Human Melanoma Black); proliferating cell marker: proliferating cell nuclear antigen (PCNA), and P-53 oncoprotein. High Risk (16, 18, 31, 45) and Low Risk (6, 11) HPV types were studied by In Situ Hybridization using the same vaginal samples. CK, EMA and Vimentin were 2+. Melanocytic markers, HMB45 and S100, and PCNA were 1+ in basal cell layer. P-53 was negative. The melanotic tissue and acetowhite lesion were positives to HPV Types 6,11. In conclusion, melanosis of the vagina is a uncommon benign pathology. Usually, melanosis is present in women over 40 years old. We present a case of melanosis of the vagina in a young woman infected with low-risk HPV types and review the literature.
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PMID:Melanosis of the vagina and human papillomavirus infection, an uncommon pathology: case report. 2195 Jan 98

Melanoma is a tumour derived from melanocytes, cells of neuroectodermal origin. Melanoma treatment represents a challenge to oncologists due to its aggressive course and early and multiple metastases. Surgical excision of lesions is a highly effective intervention, but only in early stages. In contrast, median survival of patients with metastatic melanoma is still below one year. In 2011 the FDA and EMA have approved new drugs, ipilimumab and vemurafenib, that might be a major breakthrough in treating patients with advanced melanoma. However, time is needed to conclude whether they replace dacarbazine, a drug used for over 30 years in the therapy of metastatic melanoma, even if the response rate was only 10-15%. The mechanism of dacarbazine action is not clear but it is probably based on methylation of purine bases in DNA. The low therapeutic efficacy of dacarbazine might be the consequence of rapid removal of DNA lesions by repair systems. A high melanoma chemoresistance is also driven by the extent and nature of alterations in signal transductions in tumour cells. None of the previously conducted trials proved superiority of any treatment modality over monotherapy with dacarbazine. Higher response rates did not correlate with survival benefit, and more intense adverse effects were frequently observed. There are some expectations for targeted therapy and immunotherapy, which have already demonstrated some efficacy in clinical studies. This review aims at providing the current knowledge on dacarbazine and its analogue, temozolomide, including the latest results of clinical studies combining these drugs with other treatment protocols.
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PMID:[Dacarbazine, a chemotherapeutic against metastatic melanoma and a reference drug for new treatment modalities]. 2217 38

Melanoma is a malignant tumor which is inclined to metastasize promptly into the lymphatic system and other organs such as lung, liver, brain or bone. Therefore early diagnosis remains crucial for improving clinical outcome for melanoma patients. Current chemotherapy and chemo-immunotherapy regimes have shown little clinical benefit with no improvement in overall survival. However, new advances in melanoma biology such as the discovery of predisposed gene signatures and key somatic events have changed clinical practice. New therapeutic approaches are being tested or have been approved by the FDA/EMA recently including targeted therapies, such as BRAF- and MEK-inhibitors, and novel immunotherapies, such as anti-CTLA4 or anti-PD1 therapies. For these therapies an improvement of progression-free and overall survival has been seen in patients with advanced non-resectable melanoma. The following review summarizes recent therapeutic options after the ASCO and ESMO annual meetings 2014 for the treatment of malignant melanoma.
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PMID:New therapeutic options for advanced non-resectable malignant melanoma. 2559 40