Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been proposed that the pathogenesis of melanoma proceeds through multiple stages, ranging from benign proliferation of melanocytic cells to acquisition of the capacity to invade tissues and metastasize. During investigations of cell surface antigens expressed by melanocytes and melanoma, we identified an antigen system that was expressed by cultured normal melanocytes but not by melanoma cell lines. mAbs against this antigen detected a 120-kD cell surface glycoprotein on melanocytes. This molecule had been identified previously as the binding protein for adenosine deaminase (ADAbp). ADAbp was expressed by 51 melanocyte cell lines derived from normal fetal, newborn, and adult skin and adult choroid, but not by 102 melanoma cell lines derived from primary and metastatic lesions. Studies with radiolabeled bovine adenosine deaminase, confirmed that melanocytes expressed binding sites for adenosine deaminase, but no binding sites were detected on cultured melanoma cells. Further studies showed that ADAbp+ melanocytes became ADAbp- upon malignant transformation in vitro. Immunohistochemical studies on a panel of frozen tissues demonstrated reactivity of anti-ADAbp mAbs with epidermal melanocytes and benign junctional nevi, but not with potentially premalignant dysplastic nevi or primary/metastatic melanoma lesions. These studies demonstrate that ADAbp expression is lost with malignant transformation of melanocytes, presumably at an early stage in the transformation process.
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PMID:Cell surface antigens of human melanocytes and melanoma. Expression of adenosine deaminase binding protein is extinguished with melanocyte transformation. 289 80

We report a clinical and histologic study of 70 patients, each with a single melanocytic lesion termed "deep penetrating nevus" (DPN). The lesions are most commonly found on the face, upper trunk, or proximal extremities of patients between the ages of 10 and 30 years. Typically they are darkly pigmented. Histologically they are characterized by loosely organized nests of pleomorphic pigmented cells that penetrate deep into the reticular dermis and often to the subcutaneous fat. Follow-up was obtained from 48 patients. It ranged from 1 to 23 years (mean, 7 years). Despite an initial histologic diagnosis of malignant melanoma in 29% of the cases, there were no local recurrences and no distant metastases. It is important to differentiate DPN from malignant melanoma. The characteristic histologic features of DPN also allow its differentiation from spindle cell and epithelioid cell nevi and blue nevi.
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PMID:Deep penetrating nevus. 290 96

The unique curability of gestational trophoblastic tumors may in part be attributable to a host immunologic response. The occurrence of rapidly progressive and fatal choriocarcinoma may be favored by histocompatibility between patients and their partners. However, histocompatibility is not a prerequisite for the development and persistence of gestational choriocarcinoma. The expression of HLA by choriocarcinoma cells in culture is enhanced following incubation with gamma-interferon and this may be of both biologic and clinical significance. Complete molar pregnancy is a complete allograft because all molar chromosomes are of paternal origin. Patients with complete mole are sensitized to paternal HLA antigen which is expressed in molar tissue. Other polymorphic antigen systems including trophoblast-leukocyte common antigens and placental-type alkaline phosphatase are also expressed in molar tissue. We have studied the immunopathology of the molar implantation site to investigate possible humoral and cellular immune responses. The relationships among normal placenta, complete mole and choriocarcinoma are not clearly understood. The pattern of expression of oncofetal antigens in these three gestational tissues may be used to assess trophoblastic differentiation. In studies to date, molar trophoblast has the same pattern of expression of oncofetal antigens as normal placental trophoblast. We will review recent advances in our understanding of the immunobiology of gestational trophoblastic disease and suggest new directions for further research.
Cancer Metastasis Rev 1986
PMID:Immunobiology of complete molar pregnancy and gestational trophoblastic tumor. 303 May 77

We examined 2,227 lymph nodes from 100 patients with clinical Stage I cutaneous melanoma for the presence of microscopic deposits of tumor. On examination of hematoxylin-and-eosin-stained sections, none had melanoma. Sixteen nodes from 14 patients had melanoma detectable by an antiserum to S-100 protein in a peroxidase-antiperoxidase (PAP) assay. The melanomatous nature of these cells was confirmed by their reaction with the melanoma-directed monoclonal antibody NKl/C3. The incidence of occult nodal metastases was highest in patients with deeply invasive and micrometrically thick primary tumors. The incidence of occult melanoma was not increased where additional serial sections were cut and semiserial sections examined. Pitfalls in the identification of occult melanoma cells (OMC) include S-100 protein-positive interdigitating dendritic cells, capsular nevus cells, a minority of sinus "macrophages," and the Schwann cells of node-associated nerves. Thus, we conclude that the incidence of early melanoma metastases in the regional lymph nodes of patients with clinical Stage I melanoma is greater than has previously been appreciated on the basis of assessment of routine hematoxylin-and-eosin-stained sections. Six of the 14 patients with OMC died of melanoma (41%), as compared to only 18 of 86 patients without OMC (21%; 0.10 greater than P greater than 0.05).
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PMID:Occult tumor cells in the lymph nodes of patients with pathological stage I malignant melanoma. An immunohistological study. 271 94

Cutaneous malignant melanoma (CMM) rates have been increasing in the United States at an average rate of about 4% per year. In 1987, it was estimated that there would be 25,800 cases and 5,800 deaths from CMM in the United States. The exact cause of the increase in unknown, but there is evidence to suggest that increasing exposure to the ultraviolet B (UVB) radiation present in sunlight may be partly responsible. The evidence includes: 1. the fact that higher CMM incidence rates are observed in people with lesser amounts of skin pigment (which blocks penetration of UV); 2. a correlation of higher CMM rates with decreasing latitude and increasing UVB levels; 3. the observation that freckles and nevi (precursors to CMM) are induced by solar exposure; 4. differences in CMM rates between natives and immigrants to sunny climates; 5. high rates of CMM in patients who cannot repair UVB-induced DNA damage; and 6. the indication that sun exposure at early ages and of an intermittent nature results in higher CMM risks. With the concern that depletion of stratospheric ozone could result in increasing levels of UVB, it has become important to understand the relationship between UVB and CMM in order to estimate the increases in CMM that would be expected with ozone depletion. When empirical relationships between UVB and CMM incidence and mortality rates were derived and used to estimate the impact of stratospheric ozone depletion, a 1% depletion of ozone was predicted to result in increases of 1%-2% in CMM incidence and 0.8%-1.5% in CMM mortality.
Cancer Metastasis Rev 1988 Dec
PMID:Cutaneous malignant melanoma and ultraviolet radiation: a review. 306 76

In vivo ultrasound examination has been introduced into dermatology as a non-invasive diagnostic technique. The resolution capacity, however, has been limited so far, and the in vivo ultrasonic features have not been fully understood. Using high frequencies (GHz range) in acoustic microscopy, we have been able to achieve a resolution comparable to that in light microscopy. In a first step, we examined normal human skin sections and compared them to histological specimens. The following study on melanocytic nevi, malignant melanoma, and metastases of melanoma showed that their acoustic images were more pronounced than those of the surrounding tissue. The echo intensity of solid basal cell carcinoma and squamous cell carcinoma resembled that of the epithelium. The structures found in acoustic microscopy can be correlated to those seen in light microscopy.
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PMID:[Ultrasound microscopy of skin sections]. 307 Sep 95

In 1979 a registry of large (20 cm or more in diameter) congenital nevocytic nevi was established at the NYU Medical Center. To date, 56 patients have been entered. Seven were lost to follow-up. An additional two patients had melanoma on entry into the study and were therefore excluded from the results of prospective following such patients for the development of melanoma. Thus, this report concerns 47 individuals who were followed prospectively for a mean of 53 months, only 1 of whom developed melanoma. This was a 2-month-old girl at entry into the study who subsequently developed Touraine's syndrome. She eventually developed a primary melanoma in the central nervous system and died of metastatic disease at the age of 21 months.
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PMID:Melanomas arising in large congenital nevocytic nevi: a prospective study. 320 54

We describe an experimental model for the induction of cutaneous melanomas in albino guinea pigs by means of repeated topical application of 7,12-dimethyl-benzanthracene over 13 consecutive months. At the end of the experiment 87.5% of the animals presented multiple lesions of a melanocytic nature. The most frequent and the earliest detected was melanocytic hyperplasia, followed by dysplasia. These lesions occurred in 75% of animals and were observed from the 4th month onward. Nevus-type lesions appeared from the 12th month and affected 70% of animals, whilst melanomas occurred in 65%. Metastases were observed in 45% of animals, in lungs, lymph nodes, kidney, and adrenal gland.
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PMID:Melanocytic carcinogenesis in albino guinea pigs. 323 6

A monoclonal antibody, NKI/beteb, was prepared against membranes from a human melanoma metastasis, and in immunoprecipitates of melanoma cell lysates specific 100- and 7-kd glycoproteins were found. The large glycoproteins were also present in conditioned medium of melanoma cell lines. The antigen is located on the inner side of membranes of (pre)melanosomes and premelanosomelike vesicles. The antibody reacted in the immunoperoxidase test on frozen tissue sections with 27 of 28 nevocellular nevi (15/16 common, 12/12 dysplastic), 39/39 primary melanomas (3 intraepidermal, 24 cutaneous, 12 choroidal), 56/63 melanoma metastases, and 4/4 clear-cell sarcomas (melanoma of soft tissue). With sections of formalin-fixed paraffin-embedded tissues, the reaction was less sensitive. No reactivity was detected with frozen sections of 185 other tumors, except for 1 case of non-Hodgkin's lymphoma in which macrophages were positive. With the exception of melanocytes, all frozen sections of adult tissues that were tested were negative with NKI/beteb. On the basis of its tissue distribution so far, the antigen recognized by NKI/beteb seems to be a specific and sensitive diagnostic marker for cells of the melanocyte lineage.
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PMID:A monoclonal antibody specific for cells of the melanocyte lineage. 327 9

Cutaneous melanoma is rapidly becoming a potentially curable cancer if it is detected and properly treated in an early phase of development. Unlike other cancers, which are usually hidden from detection until they are relatively large or metastatic disease has occurred, cutaneous melanoma is readily detectable simply by examining the skin. Information is now available that will be useful in selecting individuals at greatest risk. The most important melanoma risk factors (in decreasing order of importance) for a given individual are as follows: a persistently changed or changing mole, adulthood, irregular varieties of pigmented lesions (including dysplastic moles and lentigo maligna), a congenital mole, Caucasian race, a previous cutaneous melanoma, a family history of cutaneous melanoma, immunosuppression, sun sensitivity, and excessive sun exposure. Selective screening and appropriate treatment of individuals who have these risk factors may reduce the morbidity and mortality of cutaneous melanoma.
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PMID:Risk factors for cutaneous melanoma. A practical method of recognizing predisposed individuals. 331 89


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