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Lymphocytic Lymphoma (lymphocytic + lymphoma)

Distribution by Scientific Domains

Medical Sciences	100%

Distribution within Medical Sciences

Hematology	40%

Kinds of Lymphocytic Lymphoma

chronic lymphocytic small lymphocytic lymphoma

lymphocytic small lymphocytic lymphoma

small lymphocytic lymphoma

Selected Abstracts

MUM1/IRF4 Expression Is an Unfavorable Prognostic Factor in B-Cell Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Lymphoma (SLL)

CANCER SCIENCE, Issue 6 2002
Masato Ito
B-Cell chronic lymphocytic leukemia (B-CLL)/small lymphocytic lymphoma (SLL) consists of heterogeneous diseases that are distinguished by morphological, immunophenotypic and molecular features. MUM1 (multiple myeloma oncogene 1) is a protooncogene that is deregulated as a result of (6;14)(p25;q32) chromosomal translocation in multiple myeloma, and is also expressed in a variety of malignant lymphoma entities. We examined the expression of MUM1 in B-CLL/SLL, and found that 2 of 4 B-CLL-derived cell lines and 14 of 29 patients' specimens expressed MUM1 by immunohistochemical analysis. MUM1 expression was not associated with CD38 expression, somatic hypermutation of immunoglobulin heavy chain gene variable region (IgVH), or any other clinical characteristics of the patients. Interestingly, the patients who were positive for MUM1 showed shorter overall survival tunes than those who were negative for MUM1 (50% survival: 22 months vs. 82 months) (P=0.0008, log-rank test). Multivariate analysis by Cox's proportional-hazards regression model showed that MUM1 expression and unmutated IgVH status were independent unfavorable prognostic factors in patients with B-CLL/SLL. These findings suggest that MUM1 expression is a useful prognostic factor in B-CLL/SLL. The biological role and mechanism of action of MUM1 in B-CLL/SLL need to be clarified for the development of therapies for patients with the poor prognostic subtype. [source]

Cytologic features of mixed papillary carcinoma and chronic lymphocytic leukemia/small lymphocytic lymphoma of the thyroid gland

DIAGNOSTIC CYTOPATHOLOGY, Issue 11 2008
Michelle Reid-Nicholson M.D.
Abstract We report a case of papillary thyroid carcinoma (PTC) and chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma of the thyroid gland. To the best of our knowledge, this is the first such case to be reported in the cytology literature. An 81-year-old male with known CLL presented for routine physical examination and was found to have a left-sided thyroid nodule. Thyroid ultrasound showed a calcified nodule. Fine-needle aspiration biopsy (FNAB) was performed and revealed PTC and an atypical lymphoid infiltrate that was suspicious for lymphoma. A partial thyroidectomy was performed and confirmed PTC with concurrent gland involvement by chronic lymphocytic leukemia/small lymphocytic lymphoma (SLL). Diagn. Cytopathol. 2008;36:813,817. © 2008 Wiley-Liss, Inc. [source]

Genetic polymorphisms in the metabolic pathway and non-Hodgkin lymphoma survival,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 1 2010
Xuesong Han
Metabolic pathway enzymes, such as Cytochrome P450 (CYP), glutathione S-transferase (GST), and N -acetyltransferases (NAT) are involved in activation and detoxification of environmental carcinogens as well as drug metabolism. We hypothesized that the genetic variations in such metabolic pathways may affect NHL prognosis and survival. Follow-up information of 496 female NHL incident cases diagnosed during 1996,2000 in Connecticut were abstracted from the Connecticut Tumor Registry in 2008; survival analyses were conducted by comparing the Kaplan-Meier curves, and hazard ratios (HR) were computed from the Cox Proportional Hazard models adjusting for demographic and tumor characteristics which were suggested by previous studies to be determinants of NHL survival. We identified six SNPs from four metabolism genes (CYP2E1, GSTP1, GSTT1, and NAT1) that were associated with NHL survival. Specifically, polymorphisms in GSTT1 were associated with follicular lymphoma survival; and polymorphisms in CYP2E1, GSTP1, and NAT1 were associated with survival of chronic lymphocytic leukemia/small lymphocytic lymphoma. Our study suggests that genetic polymorphisms in metabolic pathways may help improve the prediction of NHL survival and prognosis. Am. J. Hematol., 2010. © 2009 Wiley-Liss, Inc. [source]

Autoimmune cytopenia does not predict poor prognosis in chronic lymphocytic leukemia/small lymphocytic lymphoma,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 1 2003
Mouhammed J. Kyasa
Abstract Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is characterized by an acquired immune defect that can cause autoimmune complications, including anemia and thrombocytopenia. We conducted an observational study of the epidemiology, clinical presentation and significance of autoimmune complications of CLL/SLL in 132 patients from a large population (>45,000 veterans), in which at least 90% of patients with CLL/SLL have been previously identified. Over a period of 12.5 years, 12 patients (9.1%) had autoimmune complications; of these, 6 (4.5%) had autoimmune hemolytic anemia (AIHA), 5 (3.8%) had immune thrombocytopenia (ITP), and 1 (0.8%) had pure red blood cell aplasia (PRBA). All 6 cases of AIHA had a positive direct immunoglobulin test for IgG and C3d. In 6 patients, CLL/SLL was an incidental finding at the time of presentation with autoimmune cytopenia. Nine out of 10 patients responded to immunosuppressive therapy, which was complicated by serious infection in 7 cases, one of which was fatal. The major cause of mortality in patients with autoimmune complications of CLL/SLL was secondary malignancy. Survival of patients with immune cytopenia was not significantly different from CLL/SLL patients without immune cytopenia. Among patients with anemia or thrombocytopenia, mortality was significantly higher in those with bone marrow failure compared to an autoimmune etiology. We show that in a non-referred population with a high incidence of CLL/SLL, autoimmune cytopenia can occur early in the natural history of the disease. These data suggest that the Rai and Binet classifications for CLL need to be modified for patients with autoimmune cytopenia. Am. J. Hematol. 74:1,8, 2003. Published 2003 Wiley-Liss, Inc. [source]

Endothelial stimulation by small lymphocytic lymphoma correlates with secreted levels of basic fibroblastic growth factor

BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2003
Lisa Rimsza
Summary. Lymph nodes (LN) involved with small lympho- cytic lymphoma (SLL) reportedly contain increased numbers of microvessels that may constitute a therapeutic target in this disease. We investigated the secretion of the angiogenic growth factor, basic fibroblastic growth factor (bFGF), from primary tissue cultures of 15 LN with SLL and 10 reactive LN. bFGF was detected from the resulting conditioned media (CM) in 13/15 SLL samples (mean 92 ± 30, range 5,420 pg/ml) but was undetectable in CM from all reactive lymph nodes. CM was also used in a 72-h human umbilical vein endothelial cell (HUVEC) proliferation assay. HUVEC proliferation increased in the presence of SLL CM (70 ± 17%, range ,4,194%), proportional to secreted levels of bFGF (R2 = 0·95), and was reversed by depleting bFGF from CM. Previous SLL studies have examined either patient serum samples or paraffin-embedded lymph node tissue sections. This is the first study to examine the secretion of an angiogenic growth factor from primary cultures of lymph node cells. Our results indicate that bFGF is probably the primary mediator responsible for increased angiogenesis in involved nodes. These findings may be pertinent to future investigation into the mechanisms of increased angiogenesis in SLL. [source]

Combination therapy with fludarabine and rituximab followed by alemtuzumab in the first-line treatment of patients with chronic lymphocytic leukemia or small lymphocytic lymphoma

CANCER, Issue 6 2008
A phase 2 trial of the Minnie Pearl Cancer Research Network
Abstract BACKGROUND The purpose of the current study was to evaluate the efficacy and toxicity of the combination of fludarabine and rituximab, followed by alemtuzumab, as first-line treatment for patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL). METHODS In a nonrandomized phase 2 trial, 41 patients who had previously untreated CLL or SLL and required treatment received 4 cycles of the fludarabine and rituximab combination followed 5 weeks later by 4 weeks (12 doses) of intravenous alemtuzumab therapy. The response to treatment was evaluated after completion of treatment with fludarabine and rituximab, and again after the completion of alemtuzumab consolidation. RESULTS Initial treatment with the combination of fludarabine and rituximab was well tolerated, and produced a 71% overall response rate (13% complete response). Thirty-four patients began treatment with intravenous alemtuzumab, but this drug was relatively poorly tolerated when given at a short interval after fludarabine and rituximab, and only 20 patients (49% of total) were able to complete the prescribed course. Five patients had an improvement in their response with alemtuzumab; the final complete response rate was 21%. The median progression-free survival for the entire group was 42 months. Toxicity with alemtuzumab included infusion-related toxicity, myelosuppression, and opportunistic infections. CONCLUSIONS The intravenous schedule of alemtuzumab employed in the trial was relatively poorly tolerated in this community-based trial. The relatively low complete response rates after treatment with the combination of fludarabine and rituximab and after the completion of treatment suggest that these abbreviated courses may compromise efficacy. The generalized use of alemtuzumab as consolidation therapy cannot yet be recommended for community practice. However, optimization of the route of administration, duration of treatment, and interval after completion of induction therapy may improve efficacy, and further investigation is ongoing. Cancer 2008. © 2008 American Cancer Society. [source]