Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Classic Hodgkin's lymphoma (cHL) most often involves lymph nodes, and gastric involvement is rare. Hodgkin's and Reed-Sternberg (H-RS) cells in cHL are known to often lack expression of several B-lineage markers, such as CD20, CD79a, Oct-2, and Bob-1. We present an extremely rare case of mixed-cellularity cHL in the stomach in which expression of these B-cells was detected immunohistochemically. The patient was an 83-year-old Japanese woman who developed a sensation of abdominal fullness and appetite loss. Endoscopic and abdominal computed tomography examinations revealed a gastric ulcer lesion and swelling of para-aortic lymph nodes, respectively. A subtotal gastrectomy was performed, and the histopathologic diagnosis was established as a typical cHL compatible with stomach origin. The patient underwent postoperative chemotherapy of 3 cycles of ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) and has since been in complete remission. Immunohistochemically, the H-RS cells in the cHL were positive not only for CD30 but also for CD20, CD79a, Oct-2, and Bob-1, whereas they were negative for CD3, CD15, CD45, EMA, and ALK1. Our patient may have had an intermediate cHL disease overlapping that of non-Hodgkin's peripheral B-cell lymphoma, possibly reflecting derivation from germinal-center B-cells.
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PMID:Primary gastric Hodgkin's lymphoma expressing a B-Cell profile including Oct-2 and Bob-1 proteins. 1756 19

The presumed involvement of paired box gene 5 (PAX5) in B-lymphomagenesis is based largely on the discovery of Pax5-specific translocations and somatic hypermutations in non-Hodgkin lymphomas. Yet mechanistically, the contribution of Pax5 to neoplastic growth remains undeciphered. Here we used 2 Myc-induced mouse B lymphoma cell lines, Myc5-M5 and Myc5-M12, which spontaneously silence Pax5. Reconstitution of these cells with Pax5-tamoxifen receptor fusion protein (Pax5ER(TAM)) increased neoplastic growth in a hormone-dependent manner. Conversely, expression of dominant-negative Pax5 in murine lymphomas and Pax5 knockdown in human lymphomas negatively affected cell expansion. Expression profiling revealed that Pax5 was required to maintain mRNA levels of several crucial components of B cell receptor (BCR) signaling, including CD79a, a protein with the immunoreceptor tyrosine-based activation motif (ITAM). In contrast, expression of 2 known ITAM antagonists, CD22 and PIR-B, was suppressed. The key role of BCR/ITAM signaling in Pax5-dependent lymphomagenesis was corroborated in Syk, an ITAM-associated tyrosine kinase. Moreover, we observed consistent expression of phosphorylated BLNK, an activated BCR adaptor protein, in human B cell lymphomas. Thus, stimulation of neoplastic growth by Pax5 occurs through BCR and is sensitive to genetic and pharmacological inhibitors of this pathway.
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PMID:B cell activator PAX5 promotes lymphomagenesis through stimulation of B cell receptor signaling. 1771

We describe a 10-month-old, intact female American Cocker Spaniel with pulmonary lymphomatoid granulomatosis (PLG). On clinical examination, this dog presented with nonproductive dry cough, serous nasal discharge, dyspnea, and lack of appetite. Radiography showed a consolidated lesion in the left cranial lung lobe. Histopathologic examination showed a mixed population of atypical lymphoid cells that had infiltrated into the pulmonary blood vessels angiocentrically. The lymphocytes were CD3 positive, consistent with a pan-T-cell phenotype. The lymphoid cells in the lesion were also positive for CD20cy and CD79a, indicative of the presence of B cells. We also observed large Reed-Sternberg-like cells that were positive for CD15 and CD30, similar to observations in human pulmonary Hodgkin's disease (PHD). In conclusion, canine PLG in this Cocker Spaniel was associated with B and T cells, which is first identified in a case of canine PLG. It was histopathologically similar to human lymphomatoid granulomatosis and immunophenotypically similar to human PHD.
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PMID:Pulmonary lymphomatoid granulomatosis in a dog: evidence of immunophenotypic diversity and relationship to human pulmonary lymphomatoid granulomatosis and pulmonary Hodgkin's disease. 1803 6

Age-related Epstein-Barr virus-positive (EBV(+)) B-cell lymphoproliferative disorder (ALPD) is a disease entity identified from a large-scale re-survey of cases diagnosed as diffuse large B-cell lymphoma. ALPD is a group of EBV(+) polymorphic B-cell lymphoma typically seen in elderly patients. An age-associated decline in host immunity against EBV might be partly responsible for the pathogenesis of ALPD. Histologically, ALPD is often characterized by a minor proportion of EBV-encoded RNA-positive tumor cells in a background of extensive cellular infiltration, similar to that of classical Hodgkin's lymphoma. In contrast to Hodgkin and Reed-Sternberg cells, ALPD tumor cells are clearly positive for B cell markers CD20 and/or CD79a. Hodgkin and Reed-Sternberg cells produce various chemokines, including CCL17 and CCL22, that attract chemokine receptor CCR4-expressing Th2 cells and regulatory T cells. Previously, we have shown that EBV-immortalized B cells also produce CCL17 and CCL22 through latent membrane protein 1 (LMP1)-mediated activation of nuclear factor kappaB. Here we examined expression of CCL17 and CCL22 in ALPD. ALPD tumor cells were often heterogeneous in size in accordance with the differential expression of EBV latent genes at the single cell level. LMP1-expressing tumor cells were typically large in size and selectively positive for CCL17 and CCL22. CCR4(+) cells and forkhead box protein 3(+) regulatory T cells were abundantly present, and the majority of forkhead box protein 3(+) cells were CCR4(+). Collectively, our data show production of CCL17 and CCL22 by LMP1(+) large-sized tumor cells and accumulation of CCR4-expressing cells including regulatory T cells in ALPD.
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PMID:Expression of CCL17 and CCL22 by latent membrane protein 1-positive tumor cells in age-related Epstein-Barr virus-associated B-cell lymphoproliferative disorder. 1827 28

Although the latent membrane protein-1 (LMP1) of the Epstein-Barr virus (EBV) is believed to be important for the transformation of germinal centre (GC) B cells, the precise contribution of this viral oncogene to lymphoma development is poorly understood. In this study, we used a non-viral vector-based method to express LMP1 in primary human GC B cells. Gene expression profiling revealed that LMP1 induced in GC B cells transcriptional changes characteristic of Hodgkin's lymphoma cell lines. Strikingly, LMP1 down-regulated the expression of B-cell-specific genes including B-cell receptor components such as CD79A, CD79B, CD19, CD20, CD22, and BLNK. LMP1 also induced the expression of ID2, a negative regulator of B-cell differentiation. Our data suggest that in EBV-positive cases, LMP1 is likely to be a major contributor to the altered transcriptional pattern characteristic of Hodgkin/Reed-Sternberg cells, including the loss of B-cell identity.
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PMID:The Epstein-Barr virus oncoprotein, latent membrane protein-1, reprograms germinal centre B cells towards a Hodgkin's Reed-Sternberg-like phenotype. 1856 61

Non-Hodgkin lymphoma is a rare cause of biliary obstruction. To the best of our knowledge, non-Hodgkin lymphoma in the peripancreatic region causing obstructive jaundice with simultaneous portal vein (PV) invasion has not yet been reported. We present a 50-year-old patient with obstructive jaundice whose extrahepatic portal vein was obstructed by the invasion of a peripancreatic non-Hodgkin lymphoma. The patient denied any other symptoms such as recurrent fever, night sweat and loss of body weight. Computed tomography (CT) revealed a 10 cm mass in the retroperitoneal space behind the head of the pancreas causing obstruction of the distal bile duct and the PV. A pylorus-preserving pancreaticoduodenectomy combined with a PV resection was performed. The PV was reconstructed using an autologous right internal jugular vein graft. The resected specimen showed endoluminal invasion of both the bile duct and the PV. Histological examination showed the mass consisting of diffuse sheets of large malignant lymphoid cells. These cells were positive for CD20 and CD79a, partially positive for CD10, and negative for CD3, CD4, CD5, CD8 and CD30. The pathologic diagnosis was diffuse large B-cell type non-Hodgkin lymphoma and the patient was transferred to the Department of Hematology and Oncology for chemotherapy. He received four cycles of combined chemotherapy including cyclophosphamide, doxorubicin, vincristine and prednisone plus rituximab, and three cycles of intrathecal chemoprophylaxis including methotorexate, cytosine arbinoside and prednisone. The patient is alive with no evidence of the disease for 7 mo after operation and will receive additional courses of chemotherapy.
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PMID:Non-Hodgkin lymphoma as a cause of obstructive jaundice with simultaneous extrahepatic portal vein obstruction: a case report. 1860 98

The specificity and sensitivity of CD19, CD20, CD79a, and PAX5 for detection of B-cell lineage lymphoma/leukemia derivation was determined on tissue microarrays containing 148 Hodgkin lymphomas, 358 B-cell and 16 T-cell lymphomas, 50 myelomas, and 69 acute leukemias. In mature lymphoid neoplasms, receiver-operating characteristic curve analysis showed CD20 to be the most sensitive, and CD20 and CD79a the most specific markers for B-lineage derivation. CD19 had the weakest specificity, because it was expressed in 3 T-cell lymphomas, but its sensitivity was better than CD79a. In Hodgkin lymphoma cases, the presence of B-cell markers in Hodgkin and Reed-Sternberg cells decreased in the following order: PAX5>CD20>CD79a>CD19. CD19 and PAX5 were not detectable in myelomas. In acute leukemia, CD20 turned to be the most specific, and PAX5 and CD19 the most sensitive markers for B-lineage derivation. In conclusion, an optimal B-cell lineage panel for daily routine on paraffin-embedded tissues should consist of CD20 and CD79a, and eventually, PAX5 for mature lymphoid neoplasms and PAX5 and CD19, and eventually, CD20 in (acute) precursor cell leukemias, because they cover most of the sensitivity and specificity needed.
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PMID:Diagnostic utility of the B-cell lineage markers CD20, CD79a, PAX5, and CD19 in paraffin-embedded tissues from lymphoid neoplasms. 1883 17

The Pax5 gene encodes the B-cell specific activator protein (BSAP), a member of the highly conserved paired box (PAX)-domain family of transcription factors and a key regulator in the development and differentiation of B-cells. Pax5 serves as a valuable B-cell marker in the classification of human lymphoma patients as it is restricted to lymphomas of B-cell lineage. In dogs, detection of Pax5 protein in lymphoma tissue has not been reported. Therefore, we have investigated the expression and detection of BSAP using a monoclonal anti-Pax5 antibody (anti-BSAP, clone 24) in canine lymphoma tissue samples to evaluate its diagnostic relevance as a B-cell marker. A series of 25 lymph nodes from 23 canine non-Hodgkin lymphoma patients, a reactive canine lymph node, and a normal non-reactive canine lymph node, were evaluated. All B-cell non-Hodgkin lymphomas (15) were found to express Pax5 protein. In addition, there was a strong correlation between Pax5 and CD79a expression. Three CD3 positive and five CD3 and CD79a positive lymphomas were immunophenotypically negative for anti-Pax5, indicating a T-cell lineage. In conclusion, anti-Pax5 antibody may offer an excellent B-cell marker in canine lymphomas.
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PMID:Pax5 immunostaining in paraffin-embedded sections of canine non-Hodgkin lymphoma: a novel canine pan pre-B- and B-cell marker. 1910 Jun 28

Follicular lymphoid hyperplasia (FLH) of the palate is a very rare benign, proliferative process, with only 20 cases published so far in the English language literature. We describe a case, in a 55-year-old Caucasian female, who developed a swelling in the left posterior hard palate. Bony involvement was absent. Importantly, the medical history was positive for a previous non-Hodgkin lymphoma. Following incisional biopsy, histological examination revealed a vaguely nodular lymphoid proliferation composed of small well-differentiated lymphocytes. The lymphoid follicles were positive for CD20, CD79a, CD10, CD21 and BCL6, while negative for BCL2. The parafollicular areas revealed positivity for CD3, CD5, CD30, and CD15. Both areas were CD45 positive. Subsequent immunoglobulin heavy chain gene rearrangement analysis revealed a polyclonal lesion. No further treatment was instituted, and the patient is currently being followed-up every three months. This report demonstrates that FLHs are especially important due to their clinical and, occasionally, microscopic resemblance to follicular lymphomas. Morphologic and immunohistochemical analyses and molecular studies are essential to achieve accurate diagnosis and to implement appropriate management.
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PMID:Follicular lymphoid hyperplasia of the palate: case report and literature review. 1913 28

Epstein-Barr virus positive diffuse large B-cell lymphoma (EBV+ DLBCL) of the elderly is a rare B-cell lymphoproliferative disorder (B-LPD) that occurs in patients > 50 years with no known history of immunodeficiency or lymphoma. Patients present with moderate to severe clinical B-symptoms. These lesions show complete effacement of normal tissue/nodal architecture by large atypical lymphoid cells/immunoblasts and Hodgkin/Reed-Sternberg-like giant cells with variable amounts of inflammatory cells in the background. The ratio of neoplastic to inflammatory cells, degree of mitoses and necrosis can be quite variable; hence EBV+ DLBCL of the elderly was historically divided into low grade polymorphic and high grade monomorphic types. Further studies have shown both types to be different points in the spectrum of disease, and are all high grade lymphomas. The neoplastic large lymphoid cells show expression of CD20/CD79a and PAX-5, with variable expression of CD30, LMP-1 and EBNA-2, but CD15, CD10 and BCL6 are generally negative. Neoplastic cells show EBER positivity and high Ki-67 expression. Differential diagnoses include EBV+ B-LPD, classical Hodgkin lymphoma and EBV-DLBCL. EBV+ DLBCL of the elderly is highly aggressive with a median survival of 2 years. These patients are less responsive to standard chemotherapy compared with other B-LPD.
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PMID:Epstein-Barr virus positive diffuse large B-cell lymphoma of the elderly. 1925 22


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