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)

Nine halo nevi in various stages of regression were examined by electron microscopy for fine structural evidence of an immunological mechanism of tumor cell destruction and halo formation. Early regressing lesions (Stage I) showed nevus cells associated with infiltrating lymphocytes, monocytes, and plasma cells, but without nevus cell destruction. In later lesions (Stages II and III), vacuolar cytolysis was commonly observed in nevus cells. In Stage III lesions, portions of nevus cells are found within macrophages. The electron microscopic findings of lymphocyte, monocyte, and plasma cell infiltration of the tumor followed by vacuolar cytolysis support the concept of an immune reaction in regressing halo nevi.
Cancer Res 1975 Feb
PMID:Ultrastructural evidence for destruction in the halo nevus. 110 1

A series of Vinca alkaloids were found to block polymerization of crude tubulin extracts of porcine brain in a dose-dependent manner. This appears to be a specific effect occurring at low concentrations of drug. The concentration of vinblastine that prevents polymerization by 50% was 4.3 x 10(-7) mole/liter for a tubulin concentration of 3.0 mg/ml, and this concentration is consistent with levels achieved in vivo following routine pharmacological doses in humans.
Cancer Res 1976 Apr
PMID:Inhibition of tubulin-microtubule polymerization by drugs of the Vinca alkaloid class. 126 Jul 66

The objective of this study was to examine the binding of carcinogenic polycyclic aromatic hydrocarbons in well-characterized nuclear subfractions from transformable cells in culture. A cloned line of AKR mouse embryo cells was exposed to culture medium containing [3H]-3-methyl-cholanthrene (MC) (0.4 mug/ml) 670 Ci/mole). Cellular uptake and nuclear binding were determined after 4 hr of exposure. The addition of unlabeled MC up to 10 mug/ml did not cause reduction of [3H]MC cellular uptake or nuclear binding. From 2 to 5% of the total cellular MC was localized in the nuclei. All nuclear subfractions obtained from mechanically sheared nuclei and separated on sucrose gradients showed some MC binding; however, a high-affinity, high-specific-activity binding of MC was associated only with the slower-sedimenting component shown to represent that fraction of nuclear chromatin that is transcriptionally active. Conditions that caused the precipitation of this chromatin also resulted in the precipitation of the radioactive compound, thus suggesting that the MC was physically bound to the chromatin. Unlabeled MC (10 mug/ml) saturated this high-affinity MC binding to the transcripitionally active chromatin but did not saturate the binding to the other nuclear fractions. The binding of another potent carcinogen, [3H]-1,2,5,6-dibenzanthracene, and the "weak" carcinogen, [3H]-1,2,3,4-dibenzanthracene (3,4-DBA), to whole nuclei and nuclear subfractions was also determined. The concentration, specific activity, and time of treatment were identical with those used for MC. The level of binding of [3H]-1,2,5,6-dibenzanthracene was approximately 3-fold greater in whole nuclei on a per mass DNA basis than in those of either the MC or the 3,4-DBA. The binding of MC and 3,4-DBA to whole nuclei was approximately equal. As with MC, the [3H]-1,2,5,6-dibenzanthracene demonstrated a peak of high specific activity binding to the slower-sedimenting fraction of chromatin while the 3,4-DBA displayed considerably less binding to this fraction.
Cancer Res 1976 Aug
PMID:Binding of polycyclic aromatic hydrocarbons to transcriptionally active nuclear subfractions of AKR mouse embryo cells. 127 1

Twenty-one intradermal nevi were studied by morphometric methods in an attempt to morphologically characterize the two types of nevus cell--epithelioids, type A, and fusiforms, type C--and to quantify the differences between them. Morphometric parameters of the intradermal nevi were compared with similar parameters of melanocytes and melanoma cells so that the maturation rates of the nevi cells could be established and to see if the parameters might indicate the degree of malignancy. Superficial nevus cells were differentiated from deep cells by their larger size and larger nuclear area. Nuclear area appeared to have potential for differentiating benign from malignant tumors. Decrease in cellular area appeared to indicate maturation rather than atrophy. Melanoma cells were differentiated by their larger size. Cell nuclear perimeter appeared to have confirmatory value, while cell perimeter was inconclusive.
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PMID:Application of morphometric methods to the cytologic study of intradermal nevi. 129 28

This article critically reviews the available methods for the assessment of cell proliferation in clinical practice, and evaluates their applications as diagnostic and prognostic variables in gynecological cancer. The mitotic count is not a standardised method and should not be considered to have inherent value as a measurement of cell proliferation in the clinical situation. In distinguishing benign and malignant uterine smooth muscle tumors, the degree of mitotic activity can only be interpreted in the context of the other pathological and clinical findings. Cytological atypia and the absence of stromal differentiation appear to be more accurate than mitotic activity in delineating high-grade endometrial stromal sarcomas. The potential biological behavior of placental site trophoblastic tumor cannot be reliably predicted on the basis of mitotic counts, and hysterectomy remains the treatment of choice for this condition. Flow cytometry produces accurate cell kinetic data and provides useful prognostic information in ovarian and endometrial tumors. The value of flow cytometry in cervical cancer is questionable and needs clarification. Complete and partial hydatidiform moles are generally distinguishable on the basis of ploidy studies. However, in view of the existence of a diploid partial mole, serial human chorionic gonadotrophin measurement is the only reliable method of establishing or excluding a diagnosis of persistent trophoblastic disease. The other clinical markers of cell proliferation do not have an established role as diagnostic or prognostic parameters in gynecological cancer and merit further critical evaluation. Estimation of mitotic activity is a simple, readily accessible method of assessing cell proliferation in routine histopathological practice and the role of an accurate mitotic index in diagnosis and prognosis must be investigated to determine the true value of counting mitotic figures in histological sections.
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PMID:The usefulness of clinical measurements of cell proliferation in gynecological cancer. 131 22

Mutations at the white spotting (w) locus in mice have deleterious effects on germ cells, melanocytes and hematopoietic stem cells. The w locus encodes the c-kit tyrosine-kinase receptor whose ligand is the product of the SI locus. Using monoclonal antibodies (MAb(s)) to the extracellular domain, we have evaluated the expression of c-kit in normal and transformed melanocytes. This cell lineage synthesizes a receptor with a mw of 145 kDa. The gene product is expressed in epidermal melanocytes and in a fraction of nevocytic and blue nevi. In primary melanomas, loss of the receptor is observed in more invasive lesions. Only 30% of the metastatic lesions express detectable levels of the receptor. These findings demonstrate that the c-kit product is down-regulated in melanocytes following malignant transformation. The functional relevance of this modulation remains to be evaluated.
Int J Cancer 1992 Sep 09
PMID:Progression of human cutaneous melanoma is associated with loss of expression of c-kit proto-oncogene receptor. 138 2

The anticarcinoma antibody BR64 was conjugated to a doxorubicin derivative, doxorubicin 13-[3-(2-pyridyldithio)propionyl]hydrazone, and the resulting conjugates (BR64-DOX) were evaluated for activity and immunological specificity in vitro and in human tumor xenograft models. The BR64-DOX immunoconjugates retained immunoreactivity and cytotoxicity and demonstrated antigen-specific cytotoxicity in vitro. The potency of BR64-DOX immunoconjugates in vitro was related to the drug:monoclonal antibody mole ratio of the conjugates. The antitumor activity of BR64-DOX conjugates was consistently superior to the maximal activity obtained with the parent drug, doxorubicin (DOX), in established human lung and human breast carcinoma xenograft models. The superior antitumor activity of BR64-DOX conjugates was reflected both in tumor growth inhibition and in regressions and cures of established tumors following the administration of tolerated doses of BR64-DOX. The antitumor activity of BR64-DOX conjugates was not the result of synergism between monoclonal antibody BR64 and DOX, because mixtures consisting of monoclonal antibody and optimized DOX were not more active than an equivalent dose of DOX administered alone. The antitumor activity of BR64-DOX conjugates was antigen specific; equivalent doses of nonbinding isotype-matched conjugates were not active against established tumor xenografts.
Cancer Res 1992 Oct 15
PMID:Antigen-specific activity of carcinoma-reactive BR64-doxorubicin conjugates evaluated in vitro and in human tumor xenograft models. 138 45

Although sun exposure is believed to be associated causally with cutaneous melanoma, the high incidence on less sun-exposed areas such as the back, as well as on chronically exposed sites such as the face, suggests that the association with sunlight is less straightforward than for other skin cancers. To explain this enigmatic site distribution, a theory of site-dependent susceptibility of melanocytes to malignant transformation is proposed. As possible evidence, all melanomas diagnosed in the state of Queensland, Australia, over a one-year period were surveyed for histologic evidence of benign melanocytic nevus cells adjacent to the melanoma, and analyzed according to anatomic distribution. Results showed a regional variation in the proportion of melanomas with adjacent nevi not explicable by regional variation in nevus density, which suggests that there is a varying susceptibility of nevi to malignant change. Given that nevus cells are equivalent to melanocytes, this finding would support the hypothesis that melanocytes at-large have a differential response to the mitogenic stimulus of sunlight according to anatomic site.
Cancer Causes Control 1992 Nov
PMID:A theory of site distribution of melanomas: Queensland, Australia. 142 Aug 53

A retrospective review of 891 patients with newly diagnosed primary cutaneous malignant melanoma (CMM) registered at the British Columbia Cancer Agency from 1972 to 1981 is presented. Age-standardized incidence rates in British Columbia have increased markedly over that time. The female-to-male ratio was 1.13:1 and the median age overall was 47 years. A change in the size of a mole was the most common presenting sign (in 43% of patients) and the median duration of signs was 5.9 months. Predominant tumour sites were the trunk for males and the lower limbs for females. Dominant growth patterns were superficial spreading melanoma (65%), nodular melanoma (25%), lentigo maligna melanoma (5%) and acral lentiginous melanoma (2%). On staging of the primary tumour, 90% of patients had local disease, 9% of patients had regional disease and 1% of patients had distant disease at presentation. Median depths of tumours were 1.45 mm for males and 1.10 mm for females; no T1 tumours (tumours 0.75 mm or less in depth [TNM classification]) were staged beyond the local area. Disease recurred in 44% of males and 32% of females. The 15-year survival rate was 55.5% for males and 70.3% for females. These findings are compared with those of recent international series. It is apparent that earlier diagnosis improves survival and that more education is needed in view of the increasing incidence and death from CMM.
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PMID:Primary cutaneous malignant melanoma: experience of the British Columbia Cancer Agency from 1972 to 1981. 145 84

B cells derived from peripheral-blood lymphocytes (PBL) and tumor-infiltrating lymphocytes (TIL) from a patient with a high serum antibody titer to autologous melanoma were transformed with Epstein-Barr virus (EBV) and evaluated for reactivity against autologous tumor. B cells producing antibody reactive with autologous tumor and unreactive with normal fibroblasts were detected both in TIL and in PBL. One cell line derived from PBL and another derived from TIL sustained production of tumor-reactive antibody for 10 weeks and over 15 months respectively. The cell line derived from PBL, 2D11, produced an antibody reactive with a trypsin-resistant antigen expressed on the cell membrane of autologous and allogeneic melanoma cell lines. The cell line derived from TIL, 1F6, produced an antibody reactive with a cell-surface glycoprotein expressed by 5 autologous melanoma cell lines derived from 5 different metastases and 16/19 allogeneic melanoma cell lines. 1F6 also showed reactivity with cell lines derived from a blue nevus, a congenital nevus, an astrocytoma, and 1/4 renal-cell carcinomas; but it was not reactive with 5 foreskin melanocyte cell lines, 2 normal fibroblast lines, 5 leukemia/lymphoma lines, 8 lung-cancer lines, 8 glioblastoma lines, or lines derived from 1 ovarian carcinoma, 1 colon carcinoma, 1 vulvar carcinoma, 1 fibrosarcoma, 1 murine melanoma, or 4 murine leukemia/lymphomas. We describe here an antibody that detects a new melanoma specificity obtained by EBV transformation of tumor-infiltrating B cells.
Int J Cancer 1992 Dec 02
PMID:Analysis of two human monoclonal antibodies against melanoma. 145 38


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