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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the occurrence and type of malignant tumors in 148 patients with sarcoidosis followed at the Okayama University Hospital. Nine patients had malignancies; in 2 of 9 patients the development of malignancy preceded that of sarcoidosis, and one patient presented with sarcoidosis and malignancy at the same time. Six patients developed six types of malignancy following the development sarcoidosis; one case each of stomach cancer, lung cancer, breast cancer, thyroid cancer, testicular tumor, laryngeal cancer, and chronic lymphocytic leukemia. There was no significant difference between sexes (3 males and 3 females). The mean age of the cancer group at the onset of sarcoidosis was 56 years, which was significantly higher (p less than 0.05) than that of the control group. In these 6 patients, the mean interval from onset of sarcoidosis to detection of cancer was 11.7 years (range 1.5 to 30.2 years). The relative risk of malignancy was calculated based on the data for 148 patients with sarcoidosis with a total of 1371 person-years. The expected incidences of cancer for all sites and specific sites were estimated by applying age- and sex-adjusted person-years. The observed incidence of cancer was significantly (p less than 0.05) greater than the expected incidence for thyroid cancer, laryngeal cancer, and leukemia. No significant difference in incidence was found for all sites or for the other sites of cancer. The increased cancer incidence in sarcoidosis may be secondary to immunological abnormalities associated with this disease.
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PMID:[Malignancies in patients with sarcoidosis]. 140 74

Multiple myeloma (MM) and chronic lymphocytic leukemia (CLL) are closely related B-cell cancers. Parallel and divergent features of these diseases are reviewed. In MM, expression of multiple hemopoietic lineage-associated antigens on the malignant cells and the substantial likelihood of progression to acute myelogenous leukemia suggest transformation of a pluripotent stem cell. In CLL, transformation more likely involves a committed B-cell progenitor. Another difference is that clonal evolution with associated cytogenetic progression is common in MM but not CLL. Other data, including studies of proto-oncogenes and tumor suppressor genes, suggest that MM results both from increased proliferation and accumulation of tumor cells, whereas tumor cell accumulation is the predominant feature of CLL. These differences may be reflected in the seemingly greater role of cytokine abnormalities in MM progression. For example, osteoclast-activating properties of some cytokines account for bone involvement in MM but not in CLL. MM and CLL share common features such as stage-dependent anemia and immune deficiency. Both diseases respond to alkylating agents but vary markedly in their sensitivity to fludarabine (CLL greater than MM) and glucocorticoids (MM greater than CLL). Differences between these diseases in progression-free interval and survival may reflect different definitions of premalignant and malignant phases rather than biologic differences. Detailed comparisons between MM and CLL may provide additional insights into these and related B-cell cancers.
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PMID:Multiple myeloma and chronic lymphocytic leukemia: parallels and contrasts. 141 9

The use of immunohistochemical staining with the DiSC assay is described. This modified staining procedure allows differentiation of viable human tumor cells from normal cells in biopsy preparations, facilitating the evaluation of slides from chemosensitivity assays. Samples from ALL and CLL patients were processed using both the DiSC and modified MoAb-DiSC procedure. The predictive results were compared and found to be identical. This procedure is advantageous in determining the chemosensitivity of tumor cells in a highly heterogeneous biopsy specimen.
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PMID:Modification of the DiSC assay by the incorporation of monoclonal antibody staining. 143 46

Cytogenetic analysis using banding techniques of B-chronic lymphocytic leukemia (CLL) is hampered by the difficult in vitro proliferation of these tumor cells. For detection of specific cytogenetic aberrations these problems can be overcome with non-radioactive in situ hybridization (ISH). ISH may especially be applied for the detection of trisomy 12, which is the most frequent cytogenetic aberration in CLL. Sixty-seven patients with CLL, four normal controls and one lymphoblastoid B-cell line with a trisomy 12 were studied using a chromosome 12 specific probe. To determine the hybridization properties of the CLL cells, all samples were also hybridized with probes specific for chromosomes 1 and 8. All leukemias were analyzed by immunocytochemistry to determine the proportion of tumor cells. Eight cases (11%) showed a trisomy 12. After correction for the number of tumor cells, it was demonstrated that in almost all cases (7 out of 8), the aberration was present in a proportion of the tumor cells (between 30 and 72%). Except for one patient this mosaicism persisted with long-term follow-up. We conclude that the in vivo incidence of trisomy 12 in CLL is approximately 11%, and that trisomy 12 occurs in most instances in only a subpopulation of the leukemic cells. Both findings suggest that trisomy 12 in CLL is a late event.
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PMID:Mosaicism of trisomy 12 in chronic lymphocytic leukemia detected by non-radioactive in situ hybridization. 143 7

A fluorometric microculture cytotoxicity assay was employed for the study of cyclosporin A induced cytotoxicity in tumor samples from patients with B type chronic lymphocytic leukemia (B-CLL). Tumor cells from patients with B-CLL were found to be significantly more sensitive to the cytotoxic actions of cyclosporin A than normal blood mononuclear cells and tumor cells obtained from patients with different types of acute leukemia and solid tumors. The effect of cyclosporin A on B-CLL samples could be reproduced by a non-immunosuppressive cyclosporin A analogue. One B-CLL patient treated with cyclosporin A responded with a significant decrease in tumor mass and alleviation of anemia and B symptoms. The results show that cyclosporin A and its non-immunosuppressive analogues appear selectively toxic to B-CLL cells, an observation which may have clinical implications.
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PMID:Selective cytotoxic activity of cyclosporins against tumor cells from patients with B cell chronic lymphocytic leukemia. 147 73

The authors report two cases of malignant melanoma associated with hairy cell leukemia. Skin neoplasia preceded hematological malignancy in the first observation. Among reports concerning the association of malignant melanoma with hematological diseases, chronic lymphocytic leukemia, Hodgkin's lymphoma and non Hodgkin's lymphoma are preponderant. Epidemiological studies would be of value to predict the expected risk of malignant melanoma in hairy cell leukemia.
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PMID:Malignant melanoma and hairy cell leukemia. Two cases. 150 30

Cases of leukemia in more than one family member occur rarely. Family members of patients with chronic lymphocytic leukemia (CLL) may, however, be at increased risk of hematologic malignancy. The charts of all patients with CLL (29) seen by the author from 1987 through 1989 were reviewed and living patients specifically questioned about family history of malignancy. Ten of the 29 (34%) had a first-degree relative with a hematologic malignancy. Three patients had a first-degree relative with CLL including a pair of identical twins. Two additional patients had a spouse with a lymphoid malignancy. No differences were found in serum immunoglobulin levels between those patients with a family history of hematologic neoplasia and those without. The lymphocytes of the majority of patients with a family history of hematologic neoplasia (60%) expressed kappa light chains as did those without (70%). An increased incidence of lymphoid malignancy has been reported in western Ashkenazi Jews and in particular those of Russian descent. The majority of our cases were of Jewish origin and came from Eastern Europe. Seven of 10 patients with a family history of hematologic neoplasia were from Eastern Europe. In contrast only one of three patients with CLL who had a first-degree relative with CLL was of Jewish origin.
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PMID:Increased incidence of hematologic malignancies in first-degree relatives of patients with chronic lymphocytic leukemia. 155 Oct 21

To investigate the issue of clonality in Richter's syndrome, phenotypic, molecular genetic, and cytogenetic studies were performed on tumor tissue from a patient with concurrent chronic lymphocytic leukemia and diffuse large cell lymphoma in a single lymph node specimen. The tumor was biphenotypic for immunoglobulin (Ig) expression with surface Ig lambda-positive chronic lymphocytic leukemia and surface and cytoplasmic Ig kappa-positive diffuse large cell lymphoma. DNA samples prepared from areas of the lymph node rich in chronic lymphocytic leukemia cells and diffuse large cell lymphoma cells were examined in parallel. Identical Ig heavy chain gene rearrangements were detected in the BamHI and EcoRI digests of the two samples, but the patterns of rearrangement were different in the HindIII and PstI digests. Because it is very unlikely that multiple rearranged Ig heavy chain gene fragments of identical size would be found in more than one enzyme digest from two independently derived B-cell clones, it is probable that the two processes originated from a single clone. Modifications after rearrangement probably accounted for the differing band sizes seen in the HindIII and PstI digests. These conclusions are supported by cytogenetic analysis, which revealed two clones with a common primary abnormality (trisomy 12), one of which also exhibited secondary abnormalities. Therefore, Richter's syndrome may represent a composite tumor of common clonal origin, even when differences in light chain expression are identified.
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PMID:Richter's syndrome with different immunoglobulin light chain types. Molecular and cytogenetic features indicate a common clonal origin. 157 10

Mutations of exons 5 to 8 of the p53 gene were looked for in 39 cases of B-cell chronic lymphocytic leukemia (CLL) using polymerase chain reaction single-strand conformation polymorphism analysis and DNA sequencing. All patients also had cytogenetic analysis. A point mutation, leading to an amino acid change in the p53 protein was found in four cases, involving exon 7 (one case) or exon 8 (three cases). Mutations seemed to predominate in advanced clinical stages (Binet's stage C). All four patients with 17p monosomy had a mutation whereas no mutation was found in the 35 patients with cytogenetically normal 17p. These findings suggest that p53 mutations are relatively rare in B-cell CLL, and largely predominate or may even be restricted to patients with 17p monosomy (who constitute about 5% of all B-cell CLL patients in large published series). In those patients, the mutations may play a role in leukemogenesis through loss of tumor suppressive activity of normal p53 genes.
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PMID:Mutations of the p53 gene in B-cell chronic lymphocytic leukemia: a report on 39 cases with cytogenetic analysis. 158 88

Cytogenetic analysis was performed on peripheral blood cells stimulated with interleukin 6 (IL-6), lipopolysaccharide from Escherichia coli (LPS), phytohemagglutinin (PHA), pokeweed mitogen (PWM) and tetradecanoyl-phorbol-acetate (TPA), in a patient with B-chronic lymphocytic leukemia, showing a t(1;19;?) translocation as the sole abnormality. To our knowledge, this translocation has not been described before in any human neoplasia. In this case, the poor response to therapy (survival time 4 months) suggested that t(1;19;?) could be related to an aggressive course of the disease.
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PMID:New chromosomal abnormality. t(1;19;?) in a case of B-chronic lymphocytic leukemia. 160 55


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