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)

Two cases of renal lymphoma were reported. Case 1 was a 73-year-old, and case 2 was a 59-year-old female. Their chief complaint was flank pain. The findings obtained by CT and angiography were not compatible with renal cancer. The tentative diagnosis of case 1 was inflammatory disease or soft tissue tumor, and that of case 2 was renal subcapsular tumor. Histological specimen was obtained by open biopsy from case 1, and by nephrectomy from case 2. Immunohistochemical surface marker study revealed both tumors were B cell lymphoma. Chemotherapy (CHOP-Bleo, or PPA) in both cases and additional radiotherapy in case 2 markedly reduced the tumor size. Nevertheless, case 1 died 5 months later from recurrence, and case 2 died 14 months later of gastrointestinal bleeding. At autopsy, the renal subcapsular layer was infiltrated by lymphoma cells in both cases, and lymphadenopathy was not observed. Reviewing 16 cases previously reported as renal lymphoma, the capsular or subcapsular diffuse infiltration to the kidney is considered to be a characteristic feature of renal lymphoma.
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PMID:[Renal lymphoma. Report of 2 cases and review of the literature]. 143 94

The BC-1 cell line, derived from a body cavity-based, B-cell lymphoma, is dually infected with Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV). In these studies, the relationships between these two gammaherpesviruses and BC-1 cells were characterized and compared. Single-cell cloning experiments suggested that all BC-1 cells contain both genomes. In more than 98% of cells, both viruses were latent. The two viruses could be differentially induced into their lytic cycles by chemicals. EBV was activated into DNA replication and late-gene expression by the phorbol ester tetradecanoyl phorbol acetate (TPA). KSHV was induced into DNA replication and late-gene expression by n-butyrate. Amplification of both EBV and KSHV DNAs was inhibited by phosphonoacetic acid. Induction of the KSHV lytic cycle by n-butyrate was accompanied by the disappearance of host-cell beta-actin mRNA. Induction of EBV by TPA was not accompanied by such an effect on host-cell gene expression. Induction of the KSHV lytic cycle by n-butyrate was associated with the expression of several novel polypeptides. Recognition of one of these, p40, served as the basis of development of an assay for antibodies to KSHV in the sera of infected patients. BC-1 cells released infectious EBV; however, there was no evidence for the release of encapsidated KSHV genomes by BC-1 cells, even though n-butyrate-treated cells contained numerous intranuclear nucleocapsids. The differential inducibility of these two herpesviruses in the same cell line points to the importance of viral factors in the switch from latency to lytic cycle.
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PMID:Selective switch between latency and lytic replication of Kaposi's sarcoma herpesvirus and Epstein-Barr virus in dually infected body cavity lymphoma cells. 898 52