Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen hydatidiform moles (complete moles) and lymphocytes from each parent were analyzed for human lymphocyte antigen (HLA-A and HLA-B specificities). It was demonstrated that molar tissues expressed homozygous A and B specificities which were identical to those of the father and not those of the mother. It was concluded that androgenesis was responsible for the pathogenesis of most cases of complete mole. There was homozygous expression of paternal HLA specificities which were heterozygous for A locus and/or B locus in eight of nine cases of complete mole. This suggests that these hydatidiform moles developed from an egg which was fertilized by a haploid sperm which duplicated its own chromosomes after meiosis.
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PMID:Human lymphocyte antigen expression in hydatidiform mole: androgenesis following fertilization by a haploid sperm. 9 96

Three hundred and seventeen patients with gestational trophoblastic tumors were investigated and treated between 1957-1973. The risk of trophoblastic tumor was influenced by the outcome of the antecedent pregnancy (hydatidiform mole, non-mole abortion, term delivery) and the ABO blood groups of the mating couple; it was also influenced by the patient's age. The response to treatment with chemotherapy and , where appropriate, with surgery and radiotherapy, was influenced prfoundly by several factors. These included 1) the outcome of the antecedent pregnancy, 2) the total body burden of tumor at the time treatment stated as reflected by the urinary output of human chorionic gonadotrophin (CG), 3) the interval between the antecedent pregnancy and the start of chemotherapy, 4) the ABO groups of the mating couple, 5) the extent of mononuclear cell infiltration in the tumor, 6) the immunological status of the patient at the start of treatment, 7) the size of tumor masses, 8) the site of metastases and particularly the presence of intracranial metastases, and possibly by 9) the age and 10) the parity of the patient. A detailed study of the HLA antigens of the patient, her husband, and antecedent child has shown no positive effect on risk or prognosis. These data provide a basis for a scoring system that allows the prognosis to be defined at the time of diagnosis and facilitates tisk of drug resistance. Applied retrospectively to the cases from which the scoring system was generated, prognostic groups with survival rates ranging from 0-100% can be defined. Unfavorable prognostic factors combine so as to increase the probability of drug resistance.
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PMID:Risk and prognostic factors in trophoblastic neoplasia. 18 54

There have been anecdotal reports of an association between coeliac disease and epilepsy with cerebral calcifications that resemble those of the Sturge-Weber syndrome. A series of patients who had epilepsy with calcifications, in whom coeliac disease (CD) was incidentally observed, prompted us to study this association. 43 patients (15 male, age range 4.6-30.7 years) were selected from two series. 31 patients with cerebral calcifications of unexplained origin and epilepsy (series A) underwent intestinal biopsy. 12 patients with CD and epilepsy (series B) underwent computed tomography. Antibodies to gluten, folic acid serum concentrations, were measured, and HLA typing was done in most patients. 24 of the series A patients were identified as having CD on the basis of a flat intestinal mucosa (15/22 with a high concentration of serum antigluten), and 5 series B patients showed cerebral calcifications, giving a total of 29 cases with the combination of CD, epilepsy, and cerebral calcifications (CEC). In 27 of these CEC patients, calcifications were located in the parieto-occipital regions. Only 2 of the series A patients had gastrointestinal symptoms at the time of intestinal biopsy; most patients had recurrent diarrhoea, anaemia, and other symptoms suggestive of CD in the first 3 years of life. The epilepsy in CEC patients was poorly responsive to antiepileptic drugs. Gluten-free diet beneficially affected the course of epilepsy only when started soon after epilepsy onset. Cases of "atypical Sturge-Weber syndrome" (characterised by serpiginous cerebral calcifications and epilepsy without facial port-wine naevus) should be reviewed, and CD should be ruled out in all cases of epilepsy and cerebral calcifications of unexplained origin.
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PMID:Coeliac disease, epilepsy, and cerebral calcifications. The Italian Working Group on Coeliac Disease and Epilepsy. 135 78

Whereas the inflammatory infiltrates of malignant melanoma have been widely investigated, little is known about the infiltrates accompanying benign melanocytic naevi. Using monoclonal antibodies directed against HLA-DR antigens, the CD1 antigen, the transferrin receptor and functionally divergent macrophage subpopulations, frozen fresh material of 87 melanocytic naevi (MN), ten primary cutaneous melanomas (PCM) and ten samples of normal skin were studied. Compared with normal skin, abundant HLA-DR+ cells were found in the stroma of MN equivalent to the quantity present in PCM. In MN we found higher numbers of dermal CD1+ dendritic cells compared with PCM and normal skin. There were more macrophages that expressed the transferrin receptor or the antigens 27E10, RM3/1 and 25F9 in MN than in normal skin but fewer than in PCM. No significant differences were found between congenital MN (n = 40), common acquired MN (n = 27) and dysplastic MN (n = 20) macrophage subpopulations. Also, no correlations were evident between macrophage infiltrates and naevus location or patients' age. Our data show that potential melanoma precursors among melanocytic naevi cannot be identified by the pattern of macrophage infiltrates.
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PMID:Macrophages in melanocytic naevi. 138 Feb 30

HLA phenotypes were studied in 82 Chinese patients with myasthenia gravis (MG) and 202 healthy controls, using standard microcytotoxicity assay. The patients showed significant increase in HLA-Bw46 (46.3% vs 17.3%, chi 2 = 25.7, p less than 0.001), HLA-DR9 (56.1% vs 15%, chi 2 = 35.7, p less than 0.001) and HLA-DQw3 (89% vs 63.6%, chi 2 = 15.9, p less than 0.001). The HLA-DR3 was decreased (2.4% vs 32.7%, chi 2 = 27.0, p less than 0.001). Both HLA-Bw46 and -DR9 were increased in all subgroups except the over 40 at age of onset group. In thymectomised patients, no association with HLA antigen was found in the thymoma group, whereas both involuted and hyperplasic thymus groups had HLA DR9 association and only the hyperplasic thymus group showed HLA Bw46 association. No association with HLA antigens was noted in patients with low antibody titer, however, patients with antibody titers between 0.2 to 2 n mole/1, had an association with HLA Bw46 and DR9. The HLA DQw3 was associated with the group of female MG patients, age onset below 10 and with ocular myasthenia. Finally, the HLA A2, Bw46 and DR9 combination was also significantly increased in patients [24.3% (20/82) vs 7.4% (8/107), chi 2 = 10.5, p less than 0.001], especially in the subgroup of male MG, age onset below 10 and with ocular myasthenia.
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PMID:Association of HLA antigens with myasthenia gravis in Chinese on Taiwan. 239 79

Expression of beta 2 microglobulin (beta 2M), a light chain of class 1 HLA antigen, was studied in normal melanocytes and in benign and malignant melanocytic tumors by use of immunohistochemical methods. By immunoelectron microscopy, normal melanocytes were shown to express beta 2M on the cell surface. In lentigo maligna melanomas and acral lentiginous melanomas, the mean percentages of beta 2M-positive tumor cells were significantly lower in thick (greater than 1.50 mm) primary lesions and metastases than in thin (less than or equal to 1.50 mm) primary lesions. The evidence suggests that melanocyte-derived melanoma clones with a low grade of malignancy preserve class 1 HLA expression, and that the clones with a high grade of malignancy tend to lose the antigen expression. Nevus cells in common nevi have little or no expression of beta 2M. In halo nevi, however, beta 2M were detected on nevus cells in the lesions associated with inflammatory infiltration. Immunohistochemical analyses of the cellular composition of the inflammatory cells in halo nevi demonstrated the presence of cytotoxic T cells together with helper/inducer T cells, Langerhans cells, and macrophages. It appears that nevus cells of halo nevi are destroyed by cytotoxic T cells and that class 1 HLA antigens expressed on nevus cells play an important role in the target cell recognition and lysis by specific cytotoxic T cells.
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PMID:Beta 2 microglobulin expression in normal melanocytes, nevocellular nevi, and malignant melanomas. 265 98

The reactivity of 12 surgically removed uveal melanoma lesions with monoclonal antibodies (MoAb) to 14 membrane-bound and 2 cytoplasmic cutaneous melanoma-associated antigens (MAA), to the 2 subunits of HLA Class I antigens and to the gene products of the HLA-D region was compared with that of cutaneous melanoma lesions and correlated with their histiotype. The membrane-bound determinants defined by the anti-Mr 92,000 and 45,000 MAA MoAb TP39.1, anti-Mr 110,000 MAA MoAb M111, anti-Mr 118,000 MAA MoAb TP36.1, anti-Mr 115,000 MAA MoAb 345.134, anti-ICAM-1 MoAb CL203.4 and anti-Mr 31,000 MAA MoAb M2590, and the cytoplasmic determinants defined by the anti-MAA MoAb 465.12 and 2G-10 display a distribution in uveal melanoma lesions similar to that in cutaneous melanoma lesions. On the other hand, membrane-bound determinants defined by the anti-Mr 100,000 MAA MoAb 376.96, anti-9-O-acetyl-GD3 ganglioside MoAb ME311 and anti-GD2-GD3 ganglioside MoAb ME361 were not detected in the uveal melanoma lesions tested. Furthermore, the membrane-bound determinants defined by the anti-GD3 MoAb R24, anti-nerve growth factor receptor MoAb ME20.4, anti-Mr 97,000 MAA MoAb 140.240, anti-carcinoembryonic antigen MoAb B1.1 and anti-HMW-MAA 149.53, 225.28, and 763.74 have a markedly lower expression in uveal than in cutaneous melanoma lesions. Incubation of uveal melanoma lesions with the pool of the MoAb 149.53, 225.28, and 763.74 recognizing distinct and spatially distant determinants of the HMW-MAA increased the intensity of staining of six lesions and stained four lesions which were not stained by the individual monoclonal antibodies. The distribution of HLA Class I antigens in uveal melanoma lesions resembles that in cutaneous melanoma lesions, since they are expressed in all the lesions of the mixed and epithelioid type but were not detected in those of the spindle type, i.e., the counterparts of nevocellular nevi. HLA Class II antigens are expressed with a lower frequency in uveal than in cutaneous melanoma lesions, since they were detected only in 2 of the 12 lesions. One of them is of the mixed type and the other one of the epithelioid type. Besides HLA antigens the determinants defined by the anti-carcinoembryonic MoAb B1.1, anti-ICAM-1 MoAb CL203.4, and anti-GD3 MoAb R24 displayed a differential distribution in the different histiotypes of uveal melanoma, since they are preferentially expressed in lesions of the mixed and epithelioid type.
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PMID:Analysis of the antigenic profile of uveal melanoma lesions with anti-cutaneous melanoma-associated antigen and anti-HLA monoclonal antibodies. 291 56

Complete hydatidiform moles may originate from either the fertilization of an empty egg by a haploid sperm followed by duplication (producing a monospermic, homozygous mole) or the fertilization of such an egg by 2 haploid sperm (producing a dispermic, heterozygous mole). This difference in the mechanism leading to the formation of complete moles raises the question of whether the risk of subsequent malignancy is influenced by the zygosity of the mole. In the research reported here, we compared the incidence of postmolar sequelae between patients with homozygous and heterozygous moles. Using chromosomal heteromorphism, HLA and PGM1 polymorphisms, we established the androgenetic origin of complete mole in 82 of 91 cases. Homozygosity was confirmed in 51 moles, and we found 10 heterozygous moles. Five of 10 patients with heterozygous moles developed postmolar trophoblastic disease, whereas only 2 of the 51 patients with homozygous moles had postmolar trophoblastic disease (an additional 5 patients showed signs of degenerating residual trophoblasts). A high incidence of sequelae after the expulsion of heterozygous moles suggests that the heterozygous constitution of allelic genes plays an important role in the process of malignant transformation of trophoblasts.
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PMID:[The propensity to malignancy of dispermic, heterozygous moles]. 296 Jun 1

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.
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PMID:Immunobiology of complete molar pregnancy and gestational trophoblastic tumor. 303 May 77

We describe a 13-year-old girl with multiple pigmented nodules and plaques arranged in a cluster in the right lumbar region, which had developed since infancy. Eleven of 15 lesions which were examined histologically were found to be Spitz naevi. The remaining four lesions were compound naevocellular naevi, and two of them showed focal dysplasia. Eight Spitz naevi were investigated immunohistologically with monoclonal antibodies against HLA-antigens and malignancy-associated melanocytic antigens which are rarely present in common naevi. Naevus cells in all lesions expressed HLA-ABC antigens, but lacked HLA-DR antigens in seven of the eight lesions. All naevi were positive for 'constitutive' (KG-6-56) and 'early' (K-1-2) markers of naevomelanocytic cells. In five of the eight Spitz naevi, at least one of the three malignancy-associated melanocytic antigens PAL-M1, A-1-43 and A-10-33 was found. The expression of malignancy-associated antigens in multiple agminate Spitz naevi is at variance with their benign clinical course.
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PMID:Multiple agminate Spitz naevi: review of the literature and report of a case with distinctive immunohistological features. 331 74


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