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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biopsy samples obtained from 20 patients with human immunodeficiency virus (HIV)-associated non-Hodgkin lymphoma (NHL) were assessed for evidence of Epstein-Barr virus (EBV) and HIV sequences. DNA was extracted from formalin-fixed, paraffin-embedded NHL tissue and specific viral gene sequences were sought using the polymerase chain reaction (PCR). EBV sequences were found in 10 NHL samples (50%), with five tumors showing A-type and five B-type sequences. By serologic testing, 18 of 19 patients had antibodies to EBV, with 14 patients having antibodies to A-type EBV and 11 to B-type EBV. Serology confirmed the high prevalence of type B EBV in HIV-infected patients, but was not a reliable indicator of the EBV subtype present in the lymphomas. HIV sequences were present in biopsy tissue but at a level consistent with an origin from bystander HIV-infected cells. All 20 patients were negative by enzyme-linked immunosorbent assay for antibodies to human T-cell leukemia virus-type I. The high prevalence of type B EBV in these tumors is similar to the findings in endemic Burkitt's lymphoma, where 40% of the tumors have type B viral sequences. In normal populations, type B EBV is rarely found outside the nasopharynx. These studies support the hypothesis that EBV is an important cofactor in NHL in HIV-infected persons. The finding that B-type EBV is present in 25% of HIV-associated NHL suggests that this EBV subtype may be an important human pathogen with a wider geographic distribution than originally thought.
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PMID:Subtypes of Epstein-Barr virus in human immunodeficiency virus-associated non-Hodgkin lymphoma. 165 71

This review first considered some general problems in establishing causal links between a virus and a human cancer and offered some guidelines in the pursuit of this objective. Second, it reviewed the current causal associations for several candidate oncogenic viruses in relation to the tumors with which they are associated. These include Epstein-Barr virus in relation to Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and non-Hodgkin's lymphoma; hepatitis B and C viruses in relation to hepatocellular carcinoma; human T-cell leukemia/lymphoma virus type 1 and atypical leukemia/lymphoma; and human papilloma viruses in relation to cervical carcinoma. For some, the causal relationship is strong: hepatitis B virus with hepatocellular carcinoma, and human T-cell leukemia/lymphoma virus with adult T-cell leukemia/lymphoma. For one, the causal relationship is moderate: Epstein-Barr virus with African Burkitt's lymphoma. For others it is incomplete or inconclusive: Epstein-Barr virus with Hodgkin's disease and non-Hodgkin's lymphoma, and hepatitis C virus with hepatocellular carcinoma. Current techniques do not permit an answer for some: human papilloma virus with cervical carcinoma.
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PMID:Viruses and cancer. Causal associations. 166 91

We established two human plasma cell lines, FR4 and AD3, from ascitic fluid in a patient with IgA k plasmacytoma (PC). Aberrant amylase production was found in this patient. Both AD3 and FR4 were free of Epstein-Barr virus, and both produced Ig A k in vitro. They produced amylase of the salivary type in vitro. This was confirmed by the demonstration of amylase mRNA comigrating with salivary gland mRNA. These cell lines commonly had unusual chromosomal abnormalities der(14)t(8;14) and dic(8)t(1;8). AD3 had additional chromosomal abnormalities compared with FR4. This suggests that AD3 is a subline of FR4. The oncogene c-myc is rearranged in most case of Burkitt's lymphoma with t(8;14). However, neither rearrangement nor amplification of the c-myc allele was detected in our PC lines. These lines expressed c-myc of 2.4 kb. There were no structural changes in the amylase genes of AD3 and FR4 detectable with Southern blotting analysis. As these lines were authentic PC lines, they would be useful for the future study of the relationship between the mechanism of oncogenesis and the rare tumor aberration, amylase production.
Leukemia 1990 Aug
PMID:Amylase-producing plasmacytoma cell lines, AD3 and FR4, with der(14)t(8;14) and dic(8)t(1;8) established from ascites. 169 13

Yam 1B, a human B lymphoblastoid cell line, spontaneously produced an immunoregulatory factor, which suppresses blastogenesis and antibody formation by human lymphocytes. The Yam 1B cells, which were derived from the peripheral blood of an adult T-cell leukemia patient, have been established and maintained in our laboratory since 1985. This cell line expressed mature B-cell surface antigens including surface immunoglobulin M (IgM), CD23, and HLA-DR; had cytoplasmic IgM; and secreted small amounts of IgM in the culture supernatants. Yam 1B was positive for Epstein-Barr virus-associated antigen (EBNA) but negative for adult T-cell-associated antigen (ATLA). The serum-free Yam 1B culture supernatants (SN) inhibited the expression of transferrin R, but neither the expression of interleukin 2 (IL-2) R(CD25) nor the production of IL-2 in the lymphocytes stimulated with phytohemagglutin. Yam 1B SN also inhibited DNA synthesis by human T and B lymphocytes and immunoglobulin generation by normal B cells as well as by Epstein-Barr virus-transformed human B lymphoblastoid cell lines. The inhibitory activity of Yam 1B SN was inactivated at 56 degrees C and at pH 10 but was relatively stable at pH 2. It was abrogated by digestion with pronase and was partially stable by digestion with trypsin. Fractions collected from a Sephacryl S-300 gel filtration column (Pharmacia Fine Chemicals, Uppsala, Sweden) were found to have a peak of inhibitory activity of cell proliferation associated with molecules of apparent MWr of 43,000 to 67,000. The inhibitory activity of Yam 1B SN was not blocked by the anti-transforming growth factor beta antibody.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of lymphocyte blastogenesis and antibody production by soluble factor released by a human B-lymphoblastoid cell line. 179 Mar 7

Four leukemia cell lines; NALM-20, established at the onset of leukemia and NALM-21, -22 and -23 established at the relapse of the disease were found to be t(9;22)-positive leukemia lines having the biphenotypic feature of B cell and myeloid cell characteristics. In addition, a polyclonal Epstein-Barr virus-transformed normal B cell line, B250, was established from the peripheral blood at the onset of the disease.
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PMID:Bi-phenotypic t(9;22)-positive leukemia cell lines from a patient with acute leukemia: NALM-20, established at the onset; and NALM-21, NALM-22 and NALM-23, established after relapse. 181 49

Epstein-Barr virus (EBV) has been implicated in the development of lymphomas in immunocompromised patients. To test this hypothesis, 26 lymphomas involving the central nervous system (CNS) (11 primary, 15 systemic) were studied for the presence of EBV. In situ hybridization (ISH) was performed on formalin-fixed, paraffin-embedded tissue using a sulfur 35 (35S)-labeled EBV probe (EBV BAMH1-W). The results were interpreted without knowledge of the patients' immunologic status. The EBV sequences were detected in 11 lymphomas, nine of which were mixed or large cell subtypes. Review of the clinical information revealed that nine of the 26 lymphomas occurred in immunocompromised patients secondary to renal transplantation, human immunodeficiency virus infection, leukemia, and Wiskott-Aldrich syndrome. The EBV sequences were detected in all nine lymphomas occurring in immunocompromised patients, whereas two of the 17 lymphomas occurring in immunocompetent patients expressed EBV sequences. The authors conclude that the presence of EBV sequences in CNS lymphomas is highly correlated with a history of compromised immune status supporting a pathogenetic role of EBV in the development of CNS lymphomas in immunocompromised patients.
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PMID:In situ hybridization for the detection of Epstein-Barr virus in central nervous system lymphomas. 184 47

The Epstein-Barr virus (EBV) has been shown to be associated with posttransplant lymphoma, Hodgkin's disease, and T-cell lymphoma, in addition to African Burkitt's lymphoma. In a retrospective study of 56 consecutive cases of T-cell lymphoma, EBV DNA was found by Southern blot and in situ DNA hybridization in 10 (20%) of 50 peripheral T-cell lymphomas, but in none of six cases of T-lymphoblastic lymphoma. Peripheral T-cell lymphomas containing EBV DNA could be subclassified into three categories according to histology and immunophenotypic studies: (1) T-cell lymphoma of the helper phenotype, five cases. Two cases had histologic features resembling angioimmunoblastic lymphadenopathy (AILD). (2) T-cell lymphoma of the cytotoxic/suppressor phenotype, four cases. AILD-like features could also be recognized in two cases. Reed-Sternberg-like giant cells were identified in three cases designated Hodgkin-like T-cell lymphoma. (3) Angiocentric T-cell lymphoma or lymphomatoid granulomatosis in one case, initially affecting the skin and nose; no T-cell subset could be defined. Six of the eight EBV DNA-positive patients tested for serum EBV antibodies had elevated titers of IgG antiviral capsid antigen (greater than 640) and/or early antigen (greater than 10). From combined studies of Southern blot hybridization by using EBV termini fragment probe and in situ DNA hybridization, the EBV genomes appeared to be clonotypically proliferated in the neoplastic T cells. The patients in all three groups usually had prolonged fever preceding the diagnosis, hepatosplenomegaly, an aggressive clinical course, and poor response to chemotherapy; nine died with a median survival of only 8 months. We propose that these EBV-associated aggressive T-cell lymphomas, like human T-cell leukemia/lymphoma virus-positive T-cell lymphoma, have characteristic clinicopathologic features and should be treated as a separate disease entity.
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PMID:Aggressive peripheral T-cell lymphomas containing Epstein-Barr viral DNA: a clinicopathologic and molecular analysis. 184 84

Using separated lymphocytes from 95 male patients with B-cell lymphoproliferative disorders, we have established both Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and short-term cultures with polyclonal B-cell mitogens. Cytogenetic studies of these patients revealed an extra Y chromosome in 4 of 71 male cell lines examined. An extra Y chromosome appeared to be the sole karyotype change (47,XY, + Y) in 2 of these 4 patients. The extra Y chromosome was accompanied by extra copies of chromosomes 12 and 21 (48,XY, + Y, + 12 and 48,XY, + Y, + 21) in the other 2 patients, respectively. The possible oncological role of the extra Y chromosome in the initiation of leukemia is discussed.
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PMID:Extra Y chromosome in chronic lymphoproliferative disorders. 184 90

A lymphoblastoid cell line (SD-1) has been established by Epstein-Barr virus immortalisation of Philadelphia chromosome positive acute lymphoblastic leukaemia (ALL) cells. Using newly derived anti-bcr monoclonal and anti-abl polyclonal antibodies it was demonstrated that both the original leukaemic cells and the derived cell line expressed the p190 form of the bcr-abl protein found in a proportion of cases of Philadelphia chromosome positive ALL. Interestingly, the leukaemia and the derived cell line each displayed different, clonal patterns of immunoglobulin gene rearrangements providing direct evidence that the t(9;22) translocation which results in the expression of the p190 bcr-abl protein must occur before immunoglobulin heavy chain gene rearrangement. In contrast to the leukaemia, which had multiple chromosome abnormalities in addition to the t(9;22), the cell line had the t(9;22) translocation as its sole abnormality. Although SD-1 cells were demonstrated to express continuously the p190 bcr-abl protein, they were unable to form colonies in soft agar and did not cause tumours in splenectomised nude mice. This cell line therefore represents an appropriate target cell line in which to examine the cooperativity of the p190 bcr-abl protein with other activated oncogene products.
Leukemia 1991 Jan
PMID:Establishment of a lymphoblastoid cell line, SD-1, expressing the p190 bcr-abl chimaeric protein. 184 83

Directly growing Epstein-Barr virus (EBV)-carrying cell lines were established from a chronic lymphocytic leukemia (CLL) patient (PG) on repeated occasions. The lines carried the same ring chromosome 15 as the leukemia cells in vivo and were similarly trisomic for chromosome 12. They all showed the same JH rearrangement, indicating that they had arisen from the same B-cell progenitor. They also had the same single EBV-terminal repeat (TR), indicating that they had been generated by a single EBV infection event. It may be surmised that a single CLL cell had been infected by EBV in vivo and established itself subsequently as a subclone within the CLL population. This subpopulation persists in vivo but does not appear to expand with time. After explantation, it transforms into lymphoblastoid cells and proliferates selectively as immortalized lines. The leukemia-representative CLL lines were phenotypically indistinguishable from the B95-8 virus-transformed normal diploid cells of the patient, established in parallel by in vitro infection. They grew as typical LCL clusters and expressed the same B-cell activation markers. The methylation status of EBV-DNA was different in the CLL lines and the B95-8-virus-transformed LCLs. When Hpall- and Mspl- digested DNA was probed with BamHI C, E, H and W fragments, the CLL lines showed a mixture of methylated and unmethylated restriction fragments as in certain EBV-carrying Burkitt lymphoma (BL) lines. In contrast, the EBV-DNA of B95-8 virus-transformed normal diploid cells was completely unmethylated, as in other LCLs.
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PMID:Clonality and methylation status of the Epstein-Barr virus (EBV) genomes in in vivo-infected EBV-carrying chronic lymphocytic leukemia (CLL) cell lines. 185 Mar 84


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