Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The IgG1 monoclonal antibody, 44-3A6, was raised against the human lung adenocarcinoma cell line, A549. It has been shown to react with a 40,000 MW protein found on the cell surface, which is preserved in formalin-fixed paraffin-embedded tissues. A recent study of pulmonary carcinomas utilizing immunohistochemical methods showed exclusive binding to lung adenocarcinomas, subsets of neuroendocrine tumors, some carcinoids and a subset of large cell carcinomas. Reactivity was not seen in squamous cell carcinomas and small cell neuroendocrine carcinomas. In addition, melanomas, sarcomas and hematologic malignancies do not express this antigen. We now report on the reactivity pattern of 44-3A6 in adenocarcinomas of nonpulmonary primary sites and in normal adults organs. Strong diffuse staining of neoplastic cells in adenocarcinomas of the stomach, colon, pancreas, gallbladder and breast was noted. Adenocarcinomas arising in the endometrium, ovary, kidney, prostate, thyroid and liver were either negative or showed weak and/or focal reactivity. Strong staining patterns were even noted in adenocarcinomas which had an 'undifferentiated' component; i.e., lacking well-defined glandular elements. Immunoreactivity was noted in epithelial cells in several tissues from which these adenocarcinomas arose including the bronchial tract, stomach, small intestine, pancreas and colon, whereas epithelial cells from the endometrium, kidney, ovary, prostate and thyroid were negative or showed diffuse weak immunoreactivity. Our finding indicate that monoclonal antibody 44-3A6 recognizes an epithelial antigen on subsets of normal as well as transformed glandular epithelia. The differential pattern of expression of its target antigen probably reflects differences in tumor genesis and/or differentiation.
Tumour Biol 1988
PMID:Expression of the antigenic determinant recognized by the monoclonal antibody 44-3A6 on select human adenocarcinomas and normal human tissues. 245 98

In the past decade, interferon, the first of a new class of biologic response modifiers, has undergone extensive Phase I and II clinical evaluation in a broad spectrum of cancers, including hematologic malignancies, lymphomas, and solid tumors. Interferon has been found to have important clinical activity in hairy-cell leukemia, low-grade non-Hodgkin's lymphoma, cutaneous T cell lymphoma, chronic myelogenous leukemia, previously untreated multiple myeloma, acquired immunodeficiency syndrome-related Kaposi's sarcoma, malignant carcinoid tumors, intravesically treated superficial bladder cancer, intraperitoneally treated ovarian carcinoma, renal cell carcinoma, and malignant melanoma. Recombinant DNA technology has produced molecules such as the interferons, which are antigenic and can induce antibody formation as part of a generalized immune response. The frequency of antibody occurrence, the magnitude of the antibody response, and the type of antibody induced by the interferons is thought to be related to several factors. These include the specific type of neoplasm for which interferon was administered; the specie of interferon administered; the dose, route, schedule, and duration of interferon administered; and the assay method and sampling time used to determine the antibody titer. Opinions and clinical observations about how these antibodies affect the clinical course of a disease vary among investigators. Some studies have demonstrated that antibody formation is associated with an abrogation of the clinical response, while others have not found any effects on the clinical course of a disease due to antibody presence.
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PMID:Biotherapy with interferon--1988. 246 49

Evaluation of double-stranded RNA by flow cytometric analysis is an important parameter for discriminating quantitatively between human tumoral and normal cells. We studied double-stranded RNA (ds-RNA) measurements using propidium-iodide after DNase treatment in bone marrow and in peripheral blood cells from patients with acute lymphoblastic leukemia, acute myeloid leukemia, chronic myeloid leukemia and multiple myeloma. The highest incidence of ds-RNA excess (greater than 30%) was observed in patients with acute leukemia (75%), while those displaying it in complete remission phase were 20-25% and in relapse about 80%. A high incidence was also noted in patients with chronic myeloid leukemia in blastic crisis (100%) and in patients with multiple myeloma with heavy tumor stage myeloma (78%). We never observed an elevated ds-RNA excess in the control group, formed by normal peripheral blood lymphocytes. Indeed the specificity of this tumor marker is attested to not only by its high levels in various hematologic malignancies, but also by its absence in normal cells. Hence the importance of its clinical implications in malignant hematologic diseases is confirmed.
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PMID:Double-stranded RNA excess in hematologic diseases: clinical implications. 263 84

In a blind study, chromosome aberrations in tumor cells were analyzed by conventional cytogenetic techniques (G banding) and nonradioactive in situ hybridization with chromosome-specific probes. The material was obtained directly from patients with hematologic diseases and from colon tumor derived cell lines. The cytogenetic data obtained with G banding were in accord with those obtained by in situ hybridization to metaphase chromosomes. Most importantly, in situ hybridization to interphase nuclei gave reliable results and even allowed detection of cell subpopulations that were not detected by analyzing metaphase chromosomes. Furthermore, in retrospect, even structural aberrations could be detected in interphase nuclei; abnormal cells with either an i(1q) or a translocation der(1)t(1;7) could be identified. Our results show that the application of in situ hybridization in combination with routine cytogenetic techniques offers significant advantages for cytogenetic analysis of solid tumors and hematologic malignancies.
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PMID:Detection of chromosome aberrations in interphase tumor nuclei by nonradioactive in situ hybridization. 255 85

Autocrine production of growth factors may contribute to the rapid and fatal proliferation of acute hematologic malignancies. We have investigated whether the more controlled growth of less aggressive malignancies such as chronic myeloid leukemia (CML) may be associated with autocrine production of growth inhibitory factors. TNF inhibits the growth of both normal and leukemic hemopoietic progenitor cells. We find that exogenous TNF reduces the viability and DNA synthesis of purified myeloid cells from patients with CML and inhibits myeloid colony formation by patient progenitor cells. However, unlike progenitor cells from normal donors, patient myeloid progenitor cells also constitutively express mRNA for TNF and secrete functional TNF protein in culture. This endogenous TNF impedes the growth of CML cells because anti-TNF mAb shown to neutralize bioactive human TNF increases CML cell DNA synthesis whereas non-neutralizing anti-TNF mAb has no effect. Production of TNF by CML cells is not associated with production of lymphotoxin (TNF-beta), IL-1 or IL-6. TNF-mediated autocrine growth inhibition may contribute to the maintenance of the stable, chronic phase of this disease and similar mechanisms may operate in other malignancies to limit tumor proliferation. Competition between autocrine growth promoting and inhibiting factors may underlie the observed differences in biologic behavior between acute and chronic malignancies.
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PMID:Tumor necrosis factor mediates autocrine growth inhibition in a chronic leukemia. 258 19

Bone marrow transplantation (BMT) offers potentially curable treatment for patients with high-risk hematologic malignancies. However, relapse remains the major cause for failure of autologous BMT in these diseases and of allogeneic BMT in subsets of patients with these diseases. With our current preparative regimens, relapse rates following autologous BMT are over 30% for patients with intermediate or high-grade non-Hodgkin lymphoma and relapsed Hodgkin's disease in sensitive relapse and over 50% following autologous BMT for patients with acute non-lymphoblastic leukemia (ANLL) and acute lymphoblastic leukemia (ALL). Relapse rates exceed 80% in patients treated with autologous BMT for non-Hodgkin lymphomas and Hodgkin's disease in drug-resistant relapse. We also see a relapse rate over 50% in patients given allogeneic BMT for ANLL in second or third remission or early relapse, for ALL in third or subsequent remission or early relapse, and for chronic myelogenous leukemia (CML) in accelerated phase or blast crisis. We have explored two new approaches for improving the anti-tumor activity of our BMT preparative regimens. One involves combining etoposide, a chemotherapeutic agent that has excellent activity against leukemias and lymphomas, has shown synergistic activity with cyclophosphamide in vitro, and can be substantially dose-escalated, with busulfan and cyclophosphamide. The other approach attempts to induce graft-versus-host disease (GVHD), which appears to provide a clinical anti-tumor effect following allogeneic BMT, in recipients of autologous BMT. A syndrome similar to mild GVHD has been reported to occur spontaneously in a small number of patients receiving autologous or syngeneic transplants. GVHD can also be induced in rats undergoing syngeneic BMT by treatment with cyclosporine (CSA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New conditioning regimens for high risk marrow transplants. 262 18

Although the association of malignancies and systemic mast cell disease (SMCD) is well established, the nature of this relationship is poorly understood. The observation of 19 malignancies in 17 of 60 patients with SMCD raised several questions regarding the chronological relationship of onset of SMCD and the malignancies, whether these patients are at increased risk for developing malignancy, and whether the distribution of solid vs hematologic malignancies indicates a relationship between SMCD and a particular tumor. The following malignancies were observed: eight solid tumors, seven acute nonlymphocytic leukemias, three malignant lymphomas, and one refractory anemia with excess blasts in transformation. The majority (13/17) of patients were found to have malignancies before, or within 12 months of, SMCD diagnosis. Statistical analysis suggested that patients with SMCD are not at increased risk for malignancies subsequent to the diagnosis of SMCD. The varied types of solid malignancies observed indicated a random distribution, in contrast to the hematologic malignancies that appeared to primarily affect the myeloid cells.
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PMID:Solid and hematologic malignancies in 60 patients with systemic mast cell disease. 265 Jun 53

Most hematologic malignancies can present with or later develop cutaneous lesions. The proper diagnosis of such patients through the evaluation of their cutaneous lesions is complicated both by the confusing variety of clinical findings and by the shifting classifications of hematologic malignancies in the face of evolving knowledge. The spectrum of T-cell malignancies continues to increase and now includes several disorders formerly attributed to B-cells or macrophages. The cutaneous findings of malignant and malignant behaving hematologic disorders are grouped by the presumed cellular etiology and by the clinical subset of tumor. Clinical and histopathologic features unique to individual disorders are emphasized, as well as those features that may be shared by otherwise quite dissimilar malignancies.
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PMID:An approach to cutaneous changes caused by hematologic malignancies. 266 81

A high incidence of multiple primary neoplasms has been observed in our patients with ATL in comparison to persons with other forms of hematologic malignancy who we have observed during the past 24 years (1963-1985). Five of 15 patients with ATL (33.3%) have had at least one other associated neoplasm in comparison to only 44 of 1156 patients with other forms of hematological malignancy (3.8%). The incidence figures for secondary neoplasms associated with the other hematologic malignancies were 4.3% (16/370) for acute non-lymphocytic leukemia (ANLL), 2.2% (2/90) for acute lymphocytic leukemia (ALL), 4.8% (1/21) for acute unclassifiable leukemia, 2.2% (5/225) for chronic myelogenous leukemia, 4.7% (2/43) for chronic lymphocytic leukemia, 5.9% (8/136) for malignant monoclonal gammopathy and 3.7% (10/271) for malignant lymphoma. The incidence of multiple neoplasms in patients with ATL in comparison to those with other hematological malignancies was significant (p less than 0.01 or p less than 0.001). The neoplasms associated with ATL have been adenocarcinoma of the thyroid or lung, and squamous cell carcinoma of the larynx, lip or lung. We identified ATL-derived factor (ADF) in the cytoplasm of the secondary neoplasms of the ATL patients by means of indirect immunofluoroscopy and immunohistochemical techniques utilizing anti-ADF antibody. We also identified ras p21 products in these neoplasms by means of p21 ras monoclonal antibody studies. The possibility that HTLV-I was the cause of the secondary neoplasms thus was investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on association between the ATL and the development of multiple malignant neoplasms--analysis of 1171 cases of hematological malignancies during the past 24 years]. 268 7

Like most hematologic malignancies, solid cancers may be associated with non-random chromosomal abnormalities. Heterogeneity in the cell population in solid cancers and the chromosomal variations occurring among primary, explant, and passaged cells of a given tumor, however, present a major difficulty in assessment of their cytogenetic changes. Alternative approaches to identifying specific somatic changes in subtypes of solid cancers, without cell culture manipulations, must be developed. This report describes preliminary evidence indicating that oligonucleotide probes, homologous to short tandem repeats, that can determine individual identity, may also be useful tools with which to examine somatic changes in DNA which has been isolated directly from a tumor mass. Two, of the four, bladder tumors (transitional cell carcinomas) analyzed, exhibited oligonucleotide-based DNA fingerprint patterns that differed from those of corresponding constitutive or uninvolved tissue DNA. The changes that were observed included gain or loss of hypervariable DNA fragments or shifts in band intensities.
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PMID:Analysis of somatic changes in human tumor DNA using synthetic oligonucleotide probes. 270 36


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