14q deletions are associated with trisomy 12,NOTCH1mutations and unmutatedIGHVgenes in chronic lymphocytic leukemia and small lymphocytic lymphoma

2014 ◽  
Vol 53 (8) ◽  
pp. 657-666 ◽  
Author(s):  
Adrien Cosson ◽  
Elise Chapiro ◽  
Nabila Belhouachi ◽  
Hong-Anh Cung ◽  
Boris Keren ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Lymphocytic Leukemia ◽  
Small Lymphocytic Lymphoma ◽  
Trisomy 12

Comparison of Small Lymphocytic Lymphoma with Chronic Lymphocytic Leukemia The M.D Anderson Cancer Center Experience.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 921-921
Author(s):  
Apostolia-Maria Tsimberidou ◽  
Michael J. Keating ◽  
Peter McLaughlin ◽  
Susan O’Brien ◽  
William Wierda ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Univariate Analysis ◽  
Absolute Lymphocyte Count ◽  
Lymphocytic Leukemia ◽  
World Health ◽  
Cancer Center ◽  
Small Lymphocytic Lymphoma ◽  
Β2 Microglobulin ◽  
Cell Counts ◽  
Trisomy 12

Abstract Introduction: Small lymphocytic lymphoma (SLL) and chronic lymphocytic leukemia (CLL) are viewed as similar entities by the World Health Organization. Patients with SLL are usually treated on protocols for indolent lymphomas, although the biology of SLL differs from that of follicular lymphomas. The purpose of this study was to assess differences, if any, in presenting characteristics, cytogenetics, treatment outcomes, and factors predicting survival between patients with CLL and those with absolute lymphocyte counts <5,000 (SLL). Methods: An electronic database search of patients with CLL/SLL who presented at The University of Texas M.D. Anderson Cancer Center Department of Leukemia between 1985 and 2005 was performed. Results: Among 2,051 patients with untreated CLL/SLL, 199 patients had SLL and 1852 patients had CLL. Patients with SLL were referred for node enlargement (33%), coincidental abnormal white blood cell counts (27%), fatigue (11%), B-symptoms (10%), bruising/low platelets (8%), surgical specimens (8%), and other reasons (8%). In univariate analysis, patients with SLL had higher hemoglobin levels (p<0.001), lower IgA and IgM immunoglobulin levels (p=0.03 and p=0.01, respectively), and lower rates of bone marrow lymphocytic infiltration (p<0.001) than those with CLL. Age, sex, Binet stage, and β2-microglobulin levels were similar between the two groups. Fluorescence in situ hybridization (FISH) abnormalities were more frequent in tested patients with CLL compared with SLL patients (70% and 45%, respectively). Among 40 SLL patients with FISH abnormalities, 18% had 11q-, 25% had trisomy 12, 33% had 13q-, and 5% had 17p- abnormalities. Among 314 CLL patients with FISH abnormalities, 14% had 11q-, 16% had trisomy 12, 51% had 13q-, and 5% had 17p- abnormalities. Forty percent of patients with SLL and 49% of CLL patients required therapy after a median follow-up of 5.8 and 3.0 years, respectively (p<0.001). Among evaluable patients (SLL, 32; CLL, 710), the overall response rates to various therapies were 78% (CR, 41%) and 88% (CR, 48%), respectively. Responses were more frequent among SLL patients treated with fludarabine, mitoxantrone, and dexamethasone (FND), FND with rituximab (R-FND) or fludarabine, cyclophosphamide, and rituximab (FCR) and among patients with CLL treated with FCR. In multivariate analysis of all 2,051 SLL/CLL patients, factors predicting longer survival were younger age (p<0.0001), lower β2-microglobulin levels (p<0.0001), lower alkaline phosphatase levels (p<0.0001), higher hemoglobin levels (p<0.0001), smaller number of nodal sites (p<0.001), and lower lactate dehydrogenase levels (p=0.01); the absolute lymphocyte count was not a significant factor in survival (p=0.30). Conclusions: The presentation, cytogenetic abnormalities, and clinical outcome of SLL are similar but not identical to those of CLL. Our results suggest that SLL and CLL can be treated similarly. Regimens that include rituximab and a nucleoside analog, such as FCR or R-FND, are highly effective. Further characterization of SLL by genetic analysis is needed. Common response criteria should be standardized for both CLL and SLL, including the disappearance of radiologic and hematologic evidence of disease.

Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma With Trisomy 12 and Focal Cyclin D1 Expression: A Potential Diagnostic Pitfall

2005 ◽  
Vol 129 (1) ◽  
pp. 92-95
Author(s):  
Dennis P. O'Malley ◽  
Gail H. Vance ◽  
Attilio Orazi
Keyword(s):  
Lymph Node ◽  
Chronic Lymphocytic Leukemia ◽  
Cyclin D1 ◽  
Mantle Cell Lymphoma ◽  
Cell Lymphoma ◽  
Lymphocytic Leukemia ◽  
Small Lymphocytic Lymphoma ◽  
Diagnostic Pitfall ◽  
Mantle Cell ◽  
Trisomy 12

Abstract Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and mantle cell lymphoma usually are distinctly different in regard to clinical presentation, morphology, immunophenotype, and molecular/genetic findings. In spite of this, select cases may show overlapping characteristics and represent a diagnostic challenge. Cyclin D1 immunohistochemical staining is usually envisioned as a definitive method for resolving this differential diagnosis, with positivity supporting a diagnosis of mantle cell lymphoma. We report a case involving a 58-year-old man with a diagnosis of CLL/SLL for several years. A lymph node excision was performed after increased adenopathy was noted in the cervical region. The excised lymph node showed typical morphologic findings of CLL/SLL, including the presence of characteristic proliferation centers. Cyclin D1 staining, using 3 different antibodies, was present in scattered prolymphocytes and paraimmunoblasts, mostly within proliferation centers. Fluorescence in situ hybridization and conventional cytogenetics demonstrated trisomy 12 and an absence of t(11;14) in lymph node tissue. Focal cyclin D1 expression by immunohistochemistry in nodal CLL/SLL is quite unusual and is discussed as a potential diagnostic pitfall.

THE ROLE OF THE GENETIC ABNORMALITIES, EPIGENETIC AND microRNA IN THE PROGNOSIS OF CHRONIC LYMPHOCYTIC LEUKEMIA

2018 ◽  
Vol 40 (4) ◽  
pp. 261-267 ◽  
Author(s):  
K Tari ◽  
Z Shamsi ◽  
H Reza Ghafari ◽  
A Atashi ◽  
M Shahjahani ◽  
...  
Keyword(s):  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
Kinase Inhibitors ◽  
Bone Marrow Involvement ◽  
P53 Mutation ◽  
Lymphocytic Leukemia ◽  
Gene Promoters ◽  
Epigenetic Changes ◽  
Genetic Changes ◽  
Trisomy 12

Chronic lymphocytic leukemia (CLL) is increased proliferation of B-cells with peripheral blood and bone marrow involvement, which is usually observed in older people. Genetic mutations, epigenetic changes and miRs play a role in CLL pathogenesis. Del 11q, del l17q, del 6q, trisomy 12, p53 and IgVH mutations are the most important genetic changes in CLL. Deletion of miR-15a and miR-16a can increase bcl2 gene expression, miR-29 and miR-181 deletions decrease the expression of TCL1, and miR-146a deletion prevents tumor metastasis. Epigenetic changes such as hypo- and hypermethylation, ubiquitination, hypo- and hyperacetylation of gene promoters involved in CLL pathogenesis can also play a role in CLL. Expression of CD38 and ZAP70, presence or absence of mutation in IgVH and P53 mutation are among the factors involved in CLL prognosis. Use of monoclonal antibodies against surface markers of B-cells like anti-CD20 as well as tyrosine kinase inhibitors are the most important therapeutic approaches for CLL.

scholarly journals The pathological features of leukemic cells infiltrating the renal interstitium in chronic lymphocytic leukemia/small lymphocytic lymphoma from a large single Chinese center

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Hui Wang ◽  
Xiaojuan Yu ◽  
Xu Zhang ◽  
Suxia Wang ◽  
Minghui Zhao
Keyword(s):  
Electron Microscopy ◽  
Chronic Lymphocytic Leukemia ◽  
Renal Injury ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Cell Infiltration ◽  
Small Lymphocytic Lymphoma ◽  
Tubulointerstitial Injury ◽  
Renal Interstitium ◽  
Monoclonal Immunoglobulins

Abstract Background Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is rare in Asians, and patients with CLL/SLL seldomly undergo kidney biopsy. The histopathological features and clinical relevance of tubulointerstitial injury in CLL/SLL have not been extensively characterized. Hence, we attempted to describe the clinical characteristics, renal pathology and clinical outcome of a well-characterized population of CLL/SLL patients with CLL cell infiltration in the renal interstitium from a large single center in China. Methods Between January 1st, 2010 and September 31st, 2020, 31946renal biopsies were performed at Peking University First Hospital, and 10 CLL/SLL patients with CLL cell infiltration in the renal interstitium were included. Complete clinical data were collected from these 10 patients, and renal specimens were examined by routine light microscopy, immunofluorescence and electron microscopy. Results The extent of the infiltrating CLL cells in patients with CLL/SLL varied among different patients and ranged from 10 to 90% of kidney parenchyma. Six (60%) of 10 patients presented with an extent of infiltrating CLL cells ≥50%. Interestingly, we found that three patients (3/10, 30%) expressed monoclonal immunoglobulins in the infiltrating CLL cells, and special cytoplasmic crystalline structures were found in two of the three patients by electron microscopy for the first time. Severe renal insufficiency (Scr ≥200 μmol/L) was associated with ≥50% interstitial infiltration of CLL cells in the renal interstitium. Conclusions The current study confirmed that CLL cells infiltrating the renal interstitium can directly secrete monoclonal immunoglobulins, indicating that the interstitial infiltrating CLL cells possibly cause renal injury directly by secreting monoclonal immunoglobulins in situ. This finding may prove a new clue to elucidate the pathogenetic mechanism of renal injury involved with CLL/SLL.

Sign in / Sign up

Export Citation Format

Share Document