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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Etiological and epidemiological studies of triploid and hydatidiform molar conceptuses were done using HLA polymorphism. The segregation of HLA markers allowed to know the etiology of 25 triploidies and 19 hydatidiform moles. Five other moles and a post molar choriocarcinoma were also studied by molecular hybridization. This confirms that triploidies in about 3/4 of the cases involved two sets of paternal chromosomes mainly by di-sperm. Hydatidiform moles from Algeria, France and Senegal were all of androgenic origin excepted for one case. DNA analysis of the choriocarcinoma demonstrated the presence of a paternal marker suggesting for this case a direct cellular lineage from the mole. Positive associations with HLA A 28 and B 7 were found which could be related to gametogenesis-fecundation dysfunction. A slight excess of antigens shared by parents of triploidies was shown. This was not observed for parents of hydatidiform moles but when they shared HLA antigens a preferential inheritance in the mole of the shared specificities was observed. This relative compatibility of the molar conceptus with the mother may be an element of the process that prevent its early rejection.
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PMID:[HLA and molar pregnancies (triploidies, hydatidiform moles and choriocarcinoma). Etiological and epidemiological study]. 350 Dec 64

In 1977, Dr. Mark Greene and Dr. Wallace Clark examined members of the B. and K. families, in which several individuals had developed cutaneous malignant melanoma. They recognized that both families had nevi that were unusual in morphology, pattern, distribution, size, and number. These dysplastic nevi identify the individuals in melanoma-prone families who are at increased risk of melanoma; the cumulative risk of melanoma approaches 100% in affected members. Formal genetic analyses have revealed that the dysplastic nevus and melanoma traits appear to be pleiotropic effects of a single, highly penetrant, autosomal dominant gene. Linkage studies have revealed weak linkage with Rh on the short arm of chromosome 1 (1p), and excluded linkage with the HLA region on chromosome 6p, transferrin on 3q, H-ras on 11p, and Gm on 14q. The most promising location for the melanoma/dysplastic nevus susceptibility locus remains chromosome 1p. Future studies will focus on the localization of the melanoma gene, and then the characterization of the gene product to elucidate the etiology of melanoma.
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PMID:Where have dysplastic nevi led us? 350 42

The HLA and ABO systems were studied in patients with complete hydatidiform mole (CHM). The study confirmed that CHM can immunize the patient against paternally derived HLA-ABC antigens. In patients who required subsequent treatment for trophoblastic tumours the frequency of antibody detection was much higher (10/14) at the time of treatment than it had been at the time of evacuation (2/14). The source of immunogen was considered to be the stroma of the placental villi. It was demonstrated that in a series of 82 CHMs none of the 25 patients mated to a husband of the same ABO group as her own required treatment for postmole trophoblastic tumours. Among unlike matings 17 out of 57 of the patients required treatment. Thus it appears that trophoblastic proliferation after evacuation of mole is favoured by an ABO difference between maternal environment and the molar tissue.
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PMID:Immunogenicity of hydatidiform mole. 361 78

Complete mole is a form of natural allograft since it carries paternal genetic traits alone which differ antigenetically from those of the mother. Successful growth of mole is likely to be immunologically protected. Because the immune system is genetically controlled, the effect of HLA system on the development of androgenetic ova into moles is a subject of interest. In this study, HLA-A and -B specificities in the mole and its parent were compared with the ones of general population in Japan. Fifty-six molar tissues were used for absorption of HLA specificities determined by HLA typing of each patient and her husband. Results obtained were as follows. 1) HLA antigens were expressed on all molar tissues examined, and those antigen were derived selectively from paternal specificities, but not maternal one. 2) Fifty molar tissues had received the paternal haplotype and remaining six molar tissues had showed heterozygosity which were consistent with the paternal diplotype. Those suggested the fertilization of an empty egg by two spermatozoa. 3) A significant association was found with decreased frequency of HLA-Aw19 and HLA-Bw22 in the molar tissues (3.6% and 2.7%) compared with general population (16.4% and 11.5%). 4) The compatibility of HLA-A and -B types among moles with sequelae and the parents was higher(81%) than the estimated value(68%) in the control families. As a result, HLA analysis was useful for distinction of zygosity of molar tissues. Decreased frequencies of HLA-Aw19 and -Bw22 in the mole were assumed to be resulted from the wastage of androgenetic ova.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on HLA specificities in molar conceptions]. 367 84

In a family displaying the familial atypical multiple-mole melanoma syndrome, linkage analyses were performed between HLA and an assumed dominant gene respectively determining each of the following affected phenotypes: precursor lesions; cutaneous malignant melanoma (CMM); and precursor lesions or CMM or both. The results suggest that there is a complex mechanism involving several factors, genetic and environmental interacting with the gene determining precursor lesions to cause the neoplastic transformation.
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PMID:HLA in familial malignant melanoma. 377 Feb 56

The dysplastic nevus (DN) was first described by Clark in 1976. It was subsequently recognized to be a precursor of melanoma. Dysplastic nevi present with typical clinical and histological criteria. The dysplastic nevus syndrome (DNS) can be considered when at least two other family members have been shown to have multiple dysplastic nevi. From our own experience of over 2000 non-selected patients with melanoma only 60 (3%) were shown to have the DNS. In these 60 we could prove direct genetic penetration even though no HLA phenotype preference could be seen. Evaluation of the biological activity of the DN in cell cultures, as well as T-lymphocyte analysis in the neighborhood of the DN have shown signs of incipient malignant transformation of the DN. The practical implications of these findings and observations are discussed.
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PMID:[Dysplastic nevus syndrome]. 378 85

The phenotypic changes in human melanoma cells during the course of tumor progression were studied with monoclonal antibodies (MAbs) against the melanoma-associated antigens (MAA) M.2.2.4, H.2.8.10, K.1.2, A.1.43, and A.10.33, and HLA-(A,B,C and D). Cryostat sections of 172 primary melanomas of the skin, 157 melanoma metastases and 56 nevi were investigated with an indirect immunoperoxidase method. Phenotypic heterogeneity was observed within lesions at all stages, and also within different tumors of the same patients. Despite this heterogeneity, principles of antigen expression were found. From the reaction pattern of MAbs, the following classifications of antigens were derived: "constitutive" markers of nevomelanocytic cells (M.2.2.4 and H.2.8.10) were found expressed over a wide range of local and systemic tumors. One MAA, K.1.2 (Suter et al., 1985), that declines with progression of melanoma, was classified as an "early" antigen, whereas MAA that appear in primary melanoma in proportion to invasiveness, and which are expressed in metastases of lymph nodes and visceral organs (A.1.43, and A.10.33), were classified as "late" markers of tumor progression. HLA-antigens were classified as "intermediate" markers, HLA-A,B,C, as an "early-intermediate", and HLA-DR as a "late-intermediate" marker. The occurrence of class II HLA, A.1.43-, and A.10.33-positive tumor cells in primary melanoma indicates a high metastatic potential of tumors, independent of tumor thickness. The data show that local and systemic progression of melanoma is associated with qualitative changes in tumor cells which can be recognized by MAbs.
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PMID:Phenotypic dynamics of tumor progression in human malignant melanoma. 386 Apr 79

The polymorphism of HLA antigens was used as a marker to investigate the genetic origin of hydatidiform moles in Senegal. An androgenetic etiology was demonstrated. When both parents shared HLA antigens a preferential inheritance in the mole of the shared specificities was observed. This relative compatibility of the molar conceptus with the mother may be an element of the process that prevents its early rejection.
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PMID:Androgenetic origin of African complete hydatidiform moles demonstrated by HLA markers. 386 46

Beta2 Microglobulin, the invariable light chain of the histocompatibility antigen, has proved to be absent on the cell surface of basal cell carcinoma. In actinically damaged skin and in patients with a past history of arsenic ingestion changes can be observed on the epidermal cell membrane which can predict malignancy before cell dysregulation is visible. The epidermis in the basal cell naevus syndrome behaves in this respect as normal epidermis and the spontaneous tumour growth cannot be explained by a predisposing defect in the HLA-antigens of the epidermal cell surface.
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PMID:The presence of beta2 microglobulin on the membrane of the keratinocyte in premalignant skin disorders. 616 73

Bleomycin (BLM), a potent anticancer glycopeptide antibiotic, was linked covalently to murine monoclonal anti-HLA IgG1 antibody (H-1) with the use of dextran T-40. As determined spectrophotometrically, the conjugate was composed of 57.5 moles BLM per mole antibody. Of the substituted BLM, 18.4% (10.6 moles BLM per mole antibody) exhibited antimicrobial activity. The BLM-(H-1) conjugate showed stronger cytotoxicity than BLM alone against HLA-bearing cells in cultivation after a 30-min exposure to the drugs. In the same experiment, the conjugate was less toxic than BLM against cells lacking HLA.
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PMID:Production of a monoclonal antibody-bleomycin conjugate utilizing dextran T-40 and the antigen-targeting cytotoxicity of the conjugate. 619 96


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