Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant human growth hormone (rhGH) previously has been demonstrated to promote human or mouse T-cell engraftment in immunodeficient mice. We then wanted to examine long-term effects of rhGH on human cell engraftment in these mice. Mice with severe combined immune deficiency (SCID) were given human peripheral blood lymphocytes or human bone marrow cells and daily injections of rhGH (20 micrograms ip every other day). Upon later assessment for engraftment by flow cytometric analysis, it was determined that rhGH strongly promoted human T-cell engraftment in the thymus and spleens of these mice. However, there was considerable variability in both the incidence and extent of engraftment which appears to be due to donor-to-donor variation. Additionally, rhGH promoted B lymphomagenesis in these mice since long-term treatment of these xenogeneic chimeras with rhGH resulted in the increased incidence of human Epstein-Barr virus (EBV)-infected B-cell lymphoma. Thus, while rhGH can be used to optimize human T-cell engraftment in SCID mice, it also increases the likelihood of B-cell lymphoma generation when the donor is EBV infected. The results suggest that the activation of human T cells by rhGH results in an increased ability of these cells to traffic to the peripheral lymphoid organs of the SCID mice and results in a lymphoid microenvironment conducive to the outgrowth of EBV-transformed B lymphocytes.
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PMID:Recombinant human growth hormone promotes human lymphocyte engraftment in immunodeficient mice and results in an increased incidence of human Epstein Barr virus-induced B-cell lymphoma. 133 93

AKR mice are highly susceptible to spontaneous T cell lymphomagenesis and thymus removal at the age of 1 to 3 mo greatly reduces its development. Twelve-mo-old AKR mice thymectomized at young age were shown previously to carry potential lymphoma cells that could be triggered to develop into B cell lymphomas (80 to 100%) after removal from their host "restrictive" environment into young histocompatible hosts. Additional attempts were made to terminate the potential lymphoma cell dormant state in 12-mo-old thymectomized AKR mice. Replenishment of some deficiencies caused by thymectomy at a young age, including a s.c. syngeneic thymus graft or a single injection of the dual tropic recombinant virus isolates DTV-71 or MCF-247 into 12-mo-old thymectomized AKR mice resulted in Ly-1+ pre-B or B cell lymphoma development in 80 to 98% of these treated mice. In vivo elimination of T cell subsets by administration of cyclosporin A or by mAb expressed on Th cells (anti-CD4) or cytotoxic T cells (anti-CD8) stimulated the progression of dormant potential lymphoma cells towards B cell lymphoma development. The most striking results were observed after administration of anti-CD8 mAb: 90 to 100% of these treated mice developed Ly-1+ B cell lymphomas within 80 days. The effect of rIL-2 on dormant PLC was also tested. Administration of rIL-2 to 12-mo-old thymectomized mice terminated tumor dormancy in 94% of the treated mice within 66 days. Tests of the resulting B lymphomas for dual tropic recombinant virus/mink cell focus-inducing virus infection indicated that the breakdown of tumor dormancy did not result from development of pathogenic class I mink cell focus-inducing viruses. These results suggest that T cell subsets and/or their products are involved in the proliferation arrest of potential lymphoma cells present in thymectomized AKR mice.
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PMID:Termination of the B cell lymphoma dormant state in thymectomized AKR mice. 134 24

The proto-oncogene PRAD1 (parathyroid adenoma 1) on chromosome 11q13 was found to be overexpressed in all five B-cell lines with t(11;14)(q13;q32) translocation tested. One B-cell lymphoma and four myeloma cell lines with this translocation demonstrated more than 10-fold overexpression as determined by Northern blot analysis, when compared with normal lymphoid tissues such as thymus, spleen and lymph node. Hematopoietic cell lines without the translocation were also examined, but none of these demonstrated the overexpression, confirming that overexpression of the PRAD1 gene is associated with t(11;14) translocation. A truncated form of mRNA was seen in one of five cell lines with the translocation, SP-49. Hybridization with different regions of the PRAD1 cDNA revealed that the truncated form of mRNA retained the coding region but had lost the 3' untranslated region. Southern blot analysis demonstrated a gene rearrangement in this SP-49 cell line. To study the genetic alteration responsible for the truncated form of mRNA in this cell line, the rearranged allele as well as the germline allele were cloned. The restriction map revealed that the rearranged portion was at the 3' end of the PRAD1 gene, eliminating the mRNA-destabilizing signal AUUUA. Human-rodent hybrid cell analysis demonstrated that the region introduced 3' of PRAD1 was derived from chromosome 11, suggesting that the PRAD1 gene region is deleted at the 3' end. Over-expression of the PRAD1 gene in association with t(11;14)(q13;q32) translocation suggested that in these cases the regulation of PRAD1 was altered by the juxtaposed gene, most likely the immunoglobulin heavy-chain gene from chromosome 14.
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PMID:Gene rearrangement and overexpression of PRAD1 in lymphoid malignancy with t(11;14)(q13;q32) translocation. 153 1

Injection of a nonlymphomagenic ecotropic virus 24-666 isolated from a B cell lymphoma of AKR origin into young AKR mice (1-60 days old) inhibited spontaneous T cell lymphoma development. The reduction in T cell lymphoma incidence (16/106-15%) was accompanied with the appearance of B cell lymphomas (16/106-34%) in older mice (500 days mean latency). Infection of newborn to 60-day-old AKR mice with 24-666 prevented changes in thymus subpopulations and expression of MuLV-related cell surface antigens, normally observed in the thymus of 5- to 6-month-old AKR mice prior to lymphoma development. Thymuses of 24-666-infected 9- to 12-month-old mice lacked recombinant dual tropic virus (DTV) expression and retained the thymus pattern of 2-month-old AKR mice. At 12 months after 24-666 administration a striking decrease in Thy1.1 level and in the CD4+ CD8+ population and an increase in CD4- CD8- cells and in mu+ B cells, predominantly Ly1+, were observed. The presence of B cells in these thymuses was also reflected in the high response of thymocytes to LPS blastogenesis accompanied by a decreased response to PHA. Although T cell lymphoma development was markedly reduced by 24-666 administration, the establishment of potential lymphoma cells (PLC) was not affected. Transfer of lymphoid cells from 12-month-old grossly normal 24-666-infected mice to the appropriate recipients resulted in a high incidence (64-80%) of B cell lymphoma development. Thus, 24-666 seems to act through interference with the establishment of DTV in the thymus, thereby preventing PLC promotion to overt T cell lymphomas. Lack of the favorable microenvironment for PLC development in the T cell pathway enables PLC development in the B cell pathway in older mice.
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PMID:Prevention of spontaneous AKR T cell lymphomagenesis by 24-666, a virus isolated from an AKR B cell lymphoma. 167 38

We describe two cases of primary low-grade B-cell lymphoma of the thymus that showed histological features of low-grade B-cell lymphoma arising in mucosa-associated lymphoid tissue (MALT). The appearances most closely resembled MALT lymphoma arising in myoepithelial sialadenitis (MESA). In both cases, the tumor was excised. In one case, there has been no recurrence in 4 years of follow-up without further treatment; in the second case, the tumor has involved an axillary lymph node. Immunohistochemistry showed light-chain restriction in both cases, and the B-cell phenotype was similar to that previously described in MALT lymphomas. The occurrence of MALT lymphoma in the thymus is consistent with the presence of mucosal structures (Hassall's corpuscles) and with recent descriptions of a native B-cell population in this organ. The relationship of this previously undescribed thymic low-grade B-cell MALT lymphoma arising in the thymus has not yet been clarified.
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PMID:Low-grade B-cell lymphoma of mucosa-associated lymphoid tissue arising in the thymus. A thymic lymphoma mimicking myoepithelial sialadenitis. 169 Sep 52

109 malignant lymphomas were surveyed by Southern blot analysis and polymerase chain reaction (PCR) for Epstein-Barr virus (EBV) DNA and compared with 16 examples of non-neoplastic lymphadenopathy and 4 normal thymuses. In specimens positive by the method of Southern and PCR, in situ hybridization studies were performed on formalin-fixed, paraffin-embedded sections. By Southern blot analysis, two of seven Hodgkin's disease samples (29%) (one of mixed cellularity and the other of lymphocyte predominance type), three of 56 B-cell lymphomas (5.6%) and five of 46 T-cell lymphomas (11%) demonstrated EBV DNA. However, the 16 examples of lymphadenitis and the 4 normal thymuses showed no EBV DNA. With PCR, EBV DNA was identified in one B-cell lymphoma, nine T-cell lymphomas, ten lymphadenitis specimens and two of the normal thymus, in addition to the positive specimens determined by the Southern blotting method. These results indicate that the presence of EBV DNA is not related to lymphoid malignancy, but enhancement of the DNA is demonstrated in some neoplastic conditions. By in situ hybridization, EBV genomes were not detected in all PCR-positive cases, but only in those positive by Southern blot analysis.
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PMID:Analysis of Epstein-Barr viral genomes in lymphoid malignancy using Southern blotting, polymerase chain reaction and in situ hybridization. 198 7

Mediastinal B-cell malignant lymphoma of a 22-year-old female was successfully treated by combination chemotherapy including Adriamycin, Vincristine and Cyclophosphamide. She suffered from dyspnea and axillary tumor in September 1984. Roentgenological examination revealed a large anterior mediastinal tumor. Biopsy of the axillary tumor yielded a diagnosis of metastatic undifferentiated carcinoma from thymus by hematoxylin and eosin. Radiotherapy and chemotherapy including CDDP and ACNU resulted in a symptom-free period of only 2 months. Superior vena cava syndrome and massive pleural effusion recurred. Salvage chemotherapy including Adriamycin, Vincristine and Cyclophosphamide resulted in rapid therapeutic effect. Six courses of chemotherapy were administered, and she is alive and well 4 years after the first salvage chemotherapy. A definitive diagnosis of B-cell lymphoma was made after review of biopsy specimens using immunohistochemical procedures. To select adequate treatment for mediastinal malignant lymphoma, reliable diagnostic procedures including immunohistochemistry are needed. Intensive chemotherapy with appropriate drugs may obtain good response even in advanced cases, such as this.
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PMID:[A case report of mediastinal malignant lymphoma with long survival following combination chemotherapy using adriamycin, vincristine and cyclophosphamide]. 221 91

Injection of a dual tropic virus (DTV) isolated from a T cell lymphoma AKR/J mice into the thymus of 14 day old AKR/J puppies accelerates lymphoma development; 90-100% of the injected mice develop the disease within 120 days. In contrast a cell free centrifuge CFC-666 prepared B cell lymphoma of AKR/J origin injected into the thymus of 14 day old AKR/J mice failed to accelerate T cell lymphomagenesis and actually prevented the spontaneous T cell lymphoma development. However, 50% of the treated mice developed B cell lymphoma with a latency of 417 + 18 days. DTV injection induces amplification of thymic expression of MuLV related antigens, besides changes in thymus subpopulation. Such changes emerge spontaneously in 5-6 month preleukemic AKR/J mice (at the time of spontaneous DTV formation in the thymus). These changes in the thymus were not observed following CFC-666 injection. We assume therefore that CFC-666 interferes with spontaneous DTV formation that contributes to T cell lymphomagenesis.
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PMID:Prevention of T-cell lymphoma in AKR/J mice. 284 90

A non-neoplastic T cell population associated with a murine monoclonal B cell malignancy, CH44, was analyzed. Immunofluorescence on cell suspensions and immunoperoxidase staining on tissue sections using monoclonal antibodies to the antigens Thy1.2, Ly-1, L3T4, and Lyt-2 confirmed the presence of both TH (Ly-1/L3T4+, Lyt-2-) and Tc/s (Ly-1/L3T4-, Lyt-2+) T cell subpopulations. The non-neoplastic T cells were present in both a 0.6 and 2.1 g CH44-bearing spleen. T cells, not normally in liver in significant numbers, were found in liver tissue when the CH44 tumor cells were present. These data implied an active proliferation of the T cell populations within tissues containing the malignant B cells. Supernatant from an in-vitro-adapted cell line of CH44 (CH44.LX) was tested for its ability to induce proliferation of normal murine splenocytes and thymocytes. As assayed by tritiated thymidine incorporation, both spleen and thymus cells proliferated in the presence of CH44.LX supernatant. Although supernatant from two of nine other B cell lines was able to stimulate the proliferation of spleen cells, only CH44.LX could induce proliferation of thymus cells. Supernatant from the seven other B cell lines and three hybridomas had no measurable effect on either splenocytes or thymocytes in this assay. It is hypothesized that the presence of a non-neoplastic proliferating T cell population associated with a neoplastic B cell lymphoma during in vivo passaging of the tumor is the result of effects derived from a secreted product of the malignant B cells. Whether the T cells have any effect on the growth of the malignant B cells is not known.
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PMID:Analysis of a murine B cell lymphoma, CH44, with an associated non-neoplastic T cell population. I. Proliferation of normal T lymphocytes is induced by a secreted product of the malignant B cells. 297 41

A case of B-cell lymphoma of probable thymic origin is reported. A 34-year-old woman was found to have an anterior mediastinal tumor in November 1986. The surface lymph nodes were not palpable. A total resection of the tumor mass was performed. The tumor invaded the right pleura, the right lung and the pericardium. Histologically, normal thymus was found at the margin of the tumor tissue. The neoplasm was predominantly composed of large lymphoid cells, separated by rather thick fibrous bands of nodular fashion in some areas. Immunohistochemical staining demonstrated monoclonal cytoplasmic IgG and kappa chains in a small portion of the neoplastic cells in fixed tissue. The cells showed positive staining with cluster of differentiation (CD) 20 (B1) but negative staining with antibodies reactive with T-cells in unfixed tissue. "Malignant lymphoma, diffuse, large cell type (B)" was the diagnosis. The arrangements of immunoglobulin (Ig) and T cell receptor (TCR) beta genes were studied. Clonal rearrangement bands of IgH and Ig kappa genes were observed in the same sizes in both the tumor and the peripheral blood before chemotherapy. The patient received chemotherapy until September 1987, and is in complete remission at present (January 1988). The peripheral blood showed germ line patterns of IgH and Ig kappa genes in complete remission. No rearrangement bands of TCR beta genes were detected throughout. The B-cell lineage was proved both from gene arrangement analysis and with immunohistochemistry.
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PMID:B-cell lymphoma of probable thymic origin: case report. 326 89


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