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)

Apoptosis-related genes and proteins and proliferation activity and their relationship with Epstein-Barr virus (EBV) is a contemporary issue. In this study, prognostic or pathogenetic roles of EBV latent infection, proliferating activity, and apoptosis-regulating proteins in pediatric Hodgkin lymphomas were explored. EBV-EBER, lmp-1, ki-67, bcl-2, survivin, Bax, fas, c-myc, and p53, and apoptotic index were analyzed in 63 pediatric Hodgkin lymphoma cases. The results were evaluated by chi-square, Mann Whitney U test, Pearson correlation analysis, and Kaplan Meier survival analysis. Thirty-two cases were stage I or II, whereas 31 cases were stage III or IV. The mean age was 8.4 +/- 63.54 years. EBV was positive in 52 (82.5%) cases. Overall survival was 94% and event-free survival 83.6%. Bax expression was observed 74.6%, bcl-2 47.6%, survivin 43%, p53 33.3%, fas 54%, and c-myc 25.4%. The mean apoptotic index was 18.22%. The mean proliferation index was 57.83%. The proliferation index was positively related with EBV but not with prognosis. None of the parameters were related with prognosis. EBV was negatively related with the apoptotic index. There were no relationships between bax, bcl-2, survivin, p53, fas, and c-myc with EBV. These results suggest that EBV might play a role in Hodgkin lymphoma pathogenesis by inducing proliferative activity and inhibiting apoptosis. Apoptosis-related proteins were not correlated with EBV. None of the parameters was found to predict prognosis.
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PMID:Prognostic significance of cell proliferation and apoptosis-regulating proteins in Epstein-Barr virus positive and negative pediatric Hodgkin lymphoma. 1803 36

Although treatment of Hodgkin's lymphoma (HL) with a multi-drug approach has been very successful, its toxicity becomes evident after several years as secondary malignancies and cardiovascular disease. Therefore, the current goal in HL treatment is to find new therapies that specifically target the deregulated signaling cascades, such as NF-kappaB and STAT3, which cause Hodgkin and Reed-Sternberg (H-RS) cell proliferation and resistance of apoptosis. Based on the above information, we investigated the capacity of curcumin to inhibit NF-kappaB and STAT3 in H-RS cells, characterizing the functional consequences. Curcumin is incorporated into H-RS cells and acts inhibiting both NF-kappaB and STAT3 activation, leading to a decreased expression of proteins involved in cell proliferation and apoptosis, e.g. Bcl-2, Bcl-xL, cFLIP, XIAP, c-IAP1, survivin, c-myc and cyclin D1. Interestingly, curcumin caused cell cycle arrest in G2-M and a significant reduction (80-97%) in H-RS cell viability. Furthermore, curcumin triggered cell death by apoptosis, as evidenced by the activation of caspase-3 and caspase-9, changes in nuclear morphology and phosphatidylserine translocation. The above findings provide a mechanistic rationale for the potential use of curcumin as a therapeutic agent for patients with HL.
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PMID:Curcumin induces cell-arrest and apoptosis in association with the inhibition of constitutively active NF-kappaB and STAT3 pathways in Hodgkin's lymphoma cells. 1838 90

Dual translocated (or "dual hit") lymphomas are highly aggressive B cell neoplasms associated with an extremely poor prognosis. The optimal treatment for these lymphomas remains undefined. We present two cases of follicular lymphoma with transformation to Burkitt-like lymphoma. In both cases dual translocations involving both the bcl-2 and c-myc loci were present. Each patient underwent intensive induction immunochemotherapy followed by autologous stem cell transplantation and radiation therapy. The first patient received post-transplant mediastinal radiation and developed recurrence in multiple areas outside of the radiation field. The second patient received total body irradiation as part of the conditioning regimen, and is without recurrence 18 months after transplant, and 24 months after diagnosis of the dual translocated lymphoma. We review dual translocation B cell lymphoma in the setting of transformation from follicular lymphoma, and suggest a potential role for total body irradiation in the management of this highly aggressive non-Hodgkin lymphoma.
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PMID:Follicular lymphoma transformation to dual translocated Burkitt-like lymphoma: improved disease control associated with radiation therapy. 1993 65

Notch-signalling has been implicated as a pathogenetic factor and a therapeutical target in T-cell leukaemias and in some lymphomas of B-cell origin. Our aim was to investigate the role of Notch-signalling in apoptosis regulation in human non-Hodgkin B-cell lymphoma (B-NHL) cell lines and in primary chronic lymhocytic leukaemia (CLL) cells using Delta-like 4 (Dll4) ligand mediated Notch activation and gamma-secretase inhibitor (GSI) mediated Notch inhibition in vitro. The potential cross-talk of Notch with the transforming growth factor-beta (TGFb) pathway in apoptosis induction was also explored, and the effect of GSI on drug-induced apoptosis was assessed. Modulation of Notch-signalling by itself did not change the rate of apoptosis in B-NHL cell lines and in CLL cells. TGFb-induced apoptosis was decreased - but not completely abolished - by GSI in TGFb-sensitive cell lines, but resistance to the apoptotic effects of TGFb were not reversed by Notch activation or inhibition. Drug-induced apoptosis was not modified by GSI. We identified Hairy/Enhancer of Split (HES)-1 as a TGFb target gene in selected - TGFb-sensitive - B-NHL cell lines. TGFb-induced HES-1 was only partially Notch-dependent in later phases. Apoptosis regulation by TGFb and GSI was not dependent on the transcriptional regulation of c-myc. In conclusion, our data does not support a unifying role of Notch in regulating apoptosis in B-NHL, but warns that gamma-secretase inhibitors may actually counteract apoptosis in some cases.
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PMID:Notch-regulation upon Dll4-stimulation of TGFb-induced apoptosis and gene expression in human B-cell non-Hodgkin lymphomas. 2001 7

We investigated the role of the histone deacetylase inhibitor, romidepsin, in Epstein-Barr virus (EBV)-positive diffuse large B-cell lymphoma (DLBCL), an aggressive non-Hodgkin lymphoma with poor clinical outcomes. We used EBV-positive and EBV-negative DLBCL cell lines and generated two EBV-transfected cell lines, LY7/EBV and U2932/EBV. Romidepsin was cytotoxic to cultured EBV-positive cells via the activation of the caspase cascade. Moreover, in vivo mice xenograft models demonstrated the cytotoxicity of romidepsin to EBV-positive DLBCL cells. Romidepsin induced cytotoxicity via the reduction of LMP1 and c-myc expression in EBV-positive cells. Inhibiting either LMP1 or c-myc using small inhibitory RNAs caused partial cytotoxicity in EBV-positive Farage and U2932/EBV lines. The dual inhibition of LMP1 and c-myc showed a synergistic cytotoxic effect in EBV-positive cells similar in magnitude to that of romidepsin alone. In addition, either double blockade of LMP1 and c-myc activity or romidepsin single treatment activated EBV lytic cycle in EBV-positive cells. In conclusion, romidepsin exerts strong anti-tumor activity in EBV-positive DLBCL via the inhibition of both LMP1 and c-myc. Our findings indicate that romidepsin might be a promising treatment for EBV-positive DLBCL.
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PMID:Histone deacetylase inhibitor romidepsin induces efficient tumor cell lysis via selective down-regulation of LMP1 and c-myc expression in EBV-positive diffuse large B-cell lymphoma. 2579 Sep 7

Burkitt lymphoma belongs to the B cell non-Hodgkin tumors and is known as the fastest growing human tumor. It is mostly seen in children and young adults. Typically for this type of lymphoma is the chromosomal translocation that leads to a deregulated expression of the c-myc oncogene. Our case report describes a 17 year old patient who presents with atypical right lower quadrant pain. He underwent an explorative laparoscopy and a Burkitt lymphoma was discovered. Subsequently several imaging studies were performed to stage the disease. Intensive systemic chemotherapy is the choice of treatment. Surgery can have a role in early stages and acute complications of the tumor but frequently the role of surgery is restricted to histological biopsy.
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PMID:Burkitt Lymphoma Mimicking an Acute Appendicitis in a 17 Years Old Boy: a Case Report. 2632 34

The expression of c-myc oncogene in neoplastic and non-neoplastic lymphoid tissue was studied using the specific monoclonal antibody myc 1-9E10 and the 3 step streptavidin-biotin immunoperoxidase method in paraffin sections. Twelve samples of non-neoplastic reactive lymph nodes of various etiology, 181 of non-Hodgkin's lymphomas (NHL), and five of hairy cell leukemia (HCL) were studied. The staining pattern was mainly nuclear but cytoplasmic reactions were also occasionally observed. The percentage of positive cells per total, cell population was estimated and all cases were classified into four groups: 0.-15%, 16-.30%, 31-45% and more than 45% positive cells. In the reactive lymph nodes, mainly germinal center cells were stained, but the percentage in eleven of the 12 cases was less than 15%. All cases of HCL were negative. In NHL lymphoma, only malignant cells were evaluated. Fifty-six per cent of cases of NHL had more than 15% positive cells. The percentage of positive cells was greater in high grade than in intermediate and low grade NHL (80.6x, 47.6%, and 10.6 respectively had more than 30:< positive cells). This correlation proved to be statistically significant (p < 0.001). The above findings suggest a relation between the expression of the c-myc oncogene and lymphomagenesis and indicate that (evaluation of the expression of c-myc in NHL may be helpful in determining the grade of malignancy.
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PMID:Expression of c-myc p62 Protein in Non-Hodgkin's Lymphomas. 2746 92

Plasmablastic lymphoma (PBL) is a rare, highly aggressive subtype of non-Hodgkin lymphoma with plasma-cell differentiation occurring typically in immune-suppressed patients such as those with AIDS. This study reports the establishment and characterization of a new cell line, PBL-1, derived from a patient with AIDS-associated PBL. Morphological assessment of PBL-1 indicated plasma-cell differentiation with a CD20(-) CD38(+) CD138(+) immunophenotype and IgH/c-myc translocation. The cell line harbours Epstein-Barr virus, but a 52.7-kbp length defect was identified in its genome, resulting in no expression of viral microRNAs encoded in the BamHI-A Rightward Transcript region. Importantly, supplementation of culture medium with >5 ng/mL of interleukin-6 (IL-6) was required for PBL-1 growth. Starvation of IL-6 or addition of tocilizumab, an inhibitory antibody for the IL-6 receptor, induced apoptosis of PBL-1. Transduction of IL-6 into PBL-1 by lentivirus vector induced autologous growth without IL-6 supplementation of culture medium. These data indicate the IL-6 dependency of PBL-1 for proliferation and survival. mTOR inhibitors induced cell death effectively, suggesting mTOR in the IL-6 signalling pathway is a potential therapeutic target for PBL. This established PBL cell line will be a useful tool to further understand the pathophysiology of PBL and aid the future development of PBL treatment.
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PMID:Interleukin-6-dependent growth in a newly established plasmablastic lymphoma cell line and its therapeutic targets. 2886 May 65

Rheumatoid arthritis (RA) is a common rheumatological condition affecting the joints and has a wide range of extra-articular manifestations. A 69 year old male, known case of rheumatoid arthritis presented to our OPD with right lower limb redness and swelling, and left axillary lymph node swelling. Lymph node biopsy revealed a high grade diffuse large B-cell lymphoma with co-expression of c-myc and bcl-2 (double expressor). RA increases the risk of both Hodgkin's lymphoma (HL) and non-Hodgkin's Lymphoma (NHL). The association with diffuse large B-cell lymphoma (DLBCL) has been found to be particularly strong, however double expressor DLBCL is an extremely uncommon occurrence. High disease activity of rheumatoid arthritis is a major determinant in development of lymphomas.
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PMID:Lymphoma in Rheumatoid Arthritis - Catastrophic Sequela of a Common Disease. 3132 74


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