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)

We report two patients with low-grade malignant primary cutaneous B cell lymphoma in association with Borrelia burgdorferi infection. Extracutaneous manifestations were ruled out by standard staging procedures. Infection with Borrelia burgdorferi was confirmed by cultivation from lesional skin in both patients. In the first patient skin lesions cleared completely after pulse therapy with cefotaxime, whereas in the second patient antibiotic treatment failed. In this patient, however, skin lesions completely cleared after intralesional injection of interferon alfa-2a. Antibiotic treatment or intralesional injection of interferon alfa-2a should be considered as a first-line treatment of Borrelia burgdorferi-associated primary cutaneous B cell lymphoma before more aggressive conventional therapeutic modalities (e.g., radiation therapy) are applied.
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PMID:Borrelia burgdorferi-associated primary cutaneous B cell lymphoma: complete clearing of skin lesions after antibiotic pulse therapy or intralesional injection of interferon alfa-2a. 903 7

Infection of 10 day-old chicken embryos with the recombinant avian leukosis virus (ALV) EU-8 induces a high incidence of rapid-onset B-cell lymphoma by insertional activation of the c-myb gene. LR-9, a related ALV with differences from EU-8 in the gag and pol genes, induces rapid-onset lymphoma at only a low incidence. To localize the viral determinant(s) responsible for this biologic difference, we constructed and tested a series of reciprocal chimeras between EU-8 and LR-9 ALVs. The ability to induce rapid-onset lymphoma efficiently was localized to a 925-nucleotide (nt) region of the EU-8 gag gene. Sequence analysis of the region revealed a 42-nt deletion in EU-8 relative to LR-9, as well as some single-nucleotide changes. A mutant virus, delta LR-9, constructed by deleting these 42 nt from LR-9, also induced rapid-onset lymphoma at a high frequency, confirming the biologic significance of this deletion. This deletion removed nt 735 to 776, which lies within a cis-acting RNA element that negatively regulates splicing (NRS). The deletion was shown to cause an increase in splicing efficiency, which may lead to increased production of a truncated myb gene product from an ALV-myb readthrough RNA.
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PMID:Genetic determinant of rapid-onset B-cell lymphoma by avian leukosis virus. 926 73

The authors assess clinical and radiographic findings of pulmonary nodules and masses after lung and heart-lung transplantation. One hundred and fifty nine patients who survived at least 3 months after lung and heart-lung transplantation were followed by serial chest radiographs for a median of 27 months. Single or multiple lung nodules or masses were noted at chest radiography in 15 (9.4%) of 159 patients. Imaging findings and causes of these nodules and masses were reviewed retrospectively. Infection was found in 10 (6%) of 159 patients. Specific pathogens (11 pathogens in 10 patients) were Aspergillus (n = 4), Mycobacteria (n = 4), and other bacteria (n = 3). Noninfectious causes were found in 5 (3%) of patients and included B-cell lymphoma (n = 2), bronchogenic carcinoma (n = 2), and pulmonary infarcts (n = 1). Nodules and masses appeared a median of 11 months after transplantation (range: 0.2 to 36 months). Five patients (33%) had single lesions; the other 10 (67%) patients had multiple lesions (range 2 to 50). Aspergillus lesions were most commonly located in the upper lobes, were cavitary in three of four patients, and all were fatal. Nodules and masses arose in the transplanted lung in 12 (80%) of the patients, and in the native lung in 3 (20%) of the patients (2 bronchogenic carcinoma, 1 M. tuberculosis simulating bronchogenic carcinoma). Nodules and masses detected by chest radiography are not uncommon (9.4%) after lung and heart-lung transplantation. Infections are more common than noninfectious causes of posttransplant nodules and masses. Specific clinical and imaging characteristics may provide clues to etiology.
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PMID:Pulmonary nodules and masses after lung and heart-lung transplantation. 1092 9

This reviews discusses the recent progress in the development of a vaccine against Helicobacter pylori. To date, this gram-negative, spiral-shaped bacterium is one of the most common infections of mankind. Infection usually occurs during childhood, and when left untreated results in lifelong colonization of the stomach. Helicobacter pylori infection is a chronic gastritis that can lead to peptic ulcer disease, gastric adenocarcinoma and gastric B-cell lymphoma. Antimicrobial therapy is currently the method of choice for curing H. pylori infection, but complex dosing, inconsistent efficiency, development of antibiotic resistance, costs and various side effects compromise widespread use. As a consequence, new strategies for the prevention and eradication of H. pylori infections are being explored. Vaccines are an attractive option, because they are both effective and economic in use. Natural infection with H. pylori usually results in a strong inflammatory Th1-type CD4(+)T-cell response that does not seem to have any protective effects. Successful vaccination studies indicate that a Th2-type response is required for protection, but the exact mechanisms involved in protective immunization are still poorly understood. Although commercial development of products for clinical trial is underway, many important issues, such as lack of a suitable mucosal adjuvant, and prevention of potential side effects, such as postimmunization gastritis, need to be resolved.
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PMID:Recent developments in Helicobacter pylori vaccination. 1176 56

Infection with immunosuppressive lentiviruses is associated with increased cancer risk,but most studies have implicated indirect mechanisms as the tumor cells generally lack integrated viral sequences. An exception wasfound in a B-cell lymphoma (Q254) where the tumor cells contained a single integrated feline immunodeficiency virus genome. Additional analysis now indicates that feline immunodeficiency virus integration in lymphoma Q254 resulted in promoter insertion and truncation of a conserved gene on feline chromosome B3, whereas the unaffected allele of the gene appeared to be transcriptionally down-regulated. The orthologous human gene (FLJ12973), is expressed ubiquitously and encodes a WD-repeat protein with structural similarity to DDB2, the small subunit of the xeroderma pigmentosum XP-E complex. Moreover, the gene is located within a region of frequent tumor-specific deletions on chromosome 15q15. These observations demonstrate the direct mutagenic potential of the lentiviruses and identify a new candidate tumor suppressor gene.
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PMID:Feline immunodeficiency virus integration in B-cell lymphoma identifies a candidate tumor suppressor gene on human chromosome 15q15. 1249 53

Primary non-Hodgkin's lymphomas of the stomach are associated with Helicobacter pylori infection. We analyzed gastric lymphoma onset data with respect to prior H. pylori infections based on the multistage theory of carcinogenesis. This theory provides a link between epidemiological data and biological processes. The study involved 133 patients, aged 29-75 years, diagnosed with marginal zone B-cell lymphoma (MZBL) and diffuse large cell B-cell lymphoma (DLBL). A 2-parametric Weibull model was applied to MZBL and DLBL onset data. Median age of diagnosis of MZBL (DLBL) was 59 years (55 years) in males and 65.5 years (64 years) in females. Infection with H. pylori was found in 81.3% (59.5%) of the patients diagnosed with MZBL (DLBL). Lymphoma latency data were fitted to Weibull distributions with a shape parameter of 5.7 for MZBL cases and 4.2 for DLBL. The shape parameter that indicates the number of steps in carcinogenesis was approximately independent of the status of infection with H. pylori in DLBL in contrast to MZBL. It was shown that gastric lymphoma onset data can be described by Weibull distribution functions. The findings support the hypothesis that MZBL and DLBL have different lines of development. There is indication of stronger antigen dependency in the carcinogenesis of MZBL in comparison to DLBL.
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PMID:Helicobacter pylori and carcinogenesis of gastric B-cell lymphomas. 1259 22

Human T-lymphotropic virus type I (HTLV-I) is closely associated with T-cell lymphoma/leukaemia, which always shows monoclonal HTLV-1 provirus DNA integration. HTLV-1 is not associated with B-cell lymphoma. The relationship between B-cell lymphoma and HTLV-1 was analysed retrospectively in early stage B-cell non-Hodgkin's lymphoma (NHL) according to HTLV-1 infection and pathological features. We analysed 198 cases of head and neck B-cell NHL treated with radiotherapy and/or chemotherapy; 21 were seropositive and 177 were seronegative for HTLV-1. We also immunostained 26 cases of diffuse large B-cell lymphoma (DLBL), including 12 seropositive and 14 seronegative for HTLV-1 respectively, for CD20, CD3, CD4, CD8, CD56, MIB-1 and T-cell-restricted intracellular antigen (TIA-1) to examine the phenotype, immunity and proliferation activity. The 5-year overall survival rates were 78% and 49% (P = 0.007, log rank test) for HTLV-1 seronegative and seropositive cases respectively. Infection with HTLV-1 was significantly associated with poor survival in patients with B-cell lymphoma by multivariate analysis. For DLBL, HTLV-1 infection was not a significant factor, but the overall survival curve was similar to that of the 21 seropositive B-cell lymphoma cases. Lymphoma cells were negative for TIA-1, but the background lymphocytes were positive for this marker. The number of TIA-1-positive cells was higher in HTLV-1-negative cases than in-positive cases. In conclusion, patients with B-cell-NHL (B-NHL) who are also HTLV-1 carriers have a poorer prognosis than non-carriers. HTLV-1 does not seem to be associated with lymphomagenesis of the B phenotype itself, but correlates with host immunity by reducing the number of cytotoxic T-cells.
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PMID:HTLV-1 carriers with B-cell lymphoma of localized stage head and neck: prognosis, clinical and immunopathological features. 1461 63

Rickettsia rickettsii, a gram-negative and obligate intracellular bacterium, is the causative agent of Rocky Mountain spotted fever. In human infections, the primary target of R. rickettsii infection is vascular endothelium. Our laboratory has shown that activation of nuclear transcription factor-kappa B (NF-kappaB) during R. rickettsii infection of cultured human endothelial cells protects against apoptosis by preventing the activation of apical caspases-8 and -9, and the effector caspase-3. To understand upstream signaling mechanisms, we have determined the effect of NF-kappaB blockade on the status of different Bcl-2 (B-cell lymphoma 2) proteins in this study. Quantitative analysis following TUNEL and Hoechst staining confirmed that infection of endothelial cells with R. rickettsii for 6 h in the presence of a specific NF-kappaB inhibitor, MG132, resulted in induction of apoptosis. Infection-induced apoptosis of EC was associated with decreased level of Bid and accumulation of Bad, while cytosolic level of Bax remained relatively unchanged. Further, the cellular levels of apoptosis antagonist Bcl-2 were found to be down-regulated and apoptogenic mitochondrial proteins Smac and cytochrome c were released into cytoplasm. These results implicate an important regulatory role for NF-kappaB in controlling the intracellular levels and/or localization of pro- as well as anti-apoptotic proteins of Bcl-2 family, the intricate balance of which is a critical determinant of downstream signaling mechanisms governing cell fate during intracellular infection.
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PMID:NF-kappaB activation suppresses host cell apoptosis during Rickettsia rickettsii infection via regulatory effects on intracellular localization or levels of apoptogenic and anti-apoptotic proteins. 1513 41

Some B cell lymphomas lack important costimulatory properties that could prevent them from being used as cell based vaccines. Infection of A20 B lymphoma cells with a replication-defective adenovirus encoding murine (m) CD40L, but not mIL-2, produces an antigen presentation phenotype with upregulation of MHC Class I/II, induction of B7-1/2 molecules and production of MIL-12 and MIP-1alpha. Subcutaneous vaccination with irradiated Ad-mCD40L-infected- or Ad-mIL-2-infected-A20 cells generated A20-specific CD8+ T cell responses and cross reactive A20 Ig antibodies. Only vaccination with Ad-mCD40L-infected A20 cells produced a significant delay in tumor growth and long-term survival (p = 0.0039). Stronger protective immunity to A20 challenge was generated by intravenous priming with A20 cells infected with Ad-mCD40L, Ad-mIL-2 or their combination followed by a boost immunization with A20 cells activated with syngeneic fibroblasts expressing CD40L. Compared to Ad-LacZ-infected A20 priming, the combination priming was most effective followed by Ad-mCD40L and Ad-mIL-2 (p = 0.0027, p = 0.0027, p = 0.0163 respectively). Significant A20-specific CD8+ T cell-mediated cytotoxicity was only demonstrated in splenocytes from these groups of vaccinated animals. By contrast, ELISPOT assay of splenocytes from all A20 prime/boosted vaccinated groups demonstrated increases in gamma-interferon release by T cells elicited by in vitro stimulation either with A20 cells or another syngeneic 2PK-3 lymphoma, indicating the presence of cross reactive immunity. Similarly anti-A20 immunoglobulin antibodies generated after vaccination were not necessarily A20 idiotype-specific. Direct therapy of pre-established tumors was achieved with the combination of Ad-mCD40L and Ad-mIL-2 given at Days 4 and 8 at the tumor site with a significant long-term survival of 85% of tumor-bearing mice (p = 0.0001). Our study strongly supports the use of Ad-CD40L and Ad-IL-2 combination therapy for the treatment of patients with B cell lymphoma.
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PMID:Use of adenoviruses encoding CD40L or IL-2 against B cell lymphoma. 1530 Aug 3

Patients who have common variable immunodeficiency (CVID) and granulomatous/lymphocytic interstitial lung disease (GLILD) are at high risk for early mortality and B cell lymphomas. Infection with human herpes virus type 8 (HHV8), a B cell lymphotrophic virus, is linked to lymphoproliferative disorders in people who have secondary immunodeficiencies. Therefore, we determined the prevalence of HHV8 infection in CVID patients with GLILD. Genomic DNA isolated from peripheral blood mononuclear cells was screened by nested- and real time-quantitative PCR (QRT-PCR) for the presence of HHV8 genome. It was positive in 6/9 CVID patients with GLILD (CVID-GLILD), 1/21 CVID patients without GLILD (CVID-control), and no patients receiving intravenous gamma globulin (n = 13) or normal blood donors (n = 20). Immunohistochemistry (IHC) demonstrated expression of the latency-associated nuclear antigen-1 (LANA-1) in the biopsies of the lung, liver, and bone marrow of four patients with CVID-GLILD. One CVID-GLILD patient developed a B cell lymphoma during the course of the study. QRT-PCR demonstrated high copy number of HHV8 genome and IHC showed diffuse staining for LANA-1 in the malignant lymph node. HHV8 infection may be an important factor in the pathogenesis of the interstitial lung disease and lymphoproliferative disorders in patients with CVID.
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PMID:Possible role of human herpesvirus 8 in the lymphoproliferative disorders in common variable immunodeficiency. 1610 7


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