Bone marrow histopathologic patterns and immunologic findings in B-chronic lymphocytic leukemia

Montserrat, Emilio; Marques-Pereira, João Pedro; Gallart, Magdalena; Rozmán, C

doi:10.1002/1097-0142(19840801)54:3<447::aid-cncr2820540312>3.0.co;2-z

Cited by 17 publications

(7 citation statements)

References 32 publications

(3 reference statements)

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“…The marrow of CLL patients is invariably infiltrated with CLL cells, following a pattern that can be diffuse and extensive, interstitial, nodular, or a mixture of interstitial and nodular (4)(5)(6). A diffuse infiltration refers to a uniform replacement of normal hematopoietic tissues by CLL cells, while in nodular and interstitial infiltrations, there is gross preservation of areas of normal marrow architecture (5).…”

Section: Disruption Of Lymphoid Architecture In Cllmentioning

confidence: 60%

Structure and function of the hematopoietic cancer niche focus on chronic lymphocytic leukemia

Kipps¹

2012

Front Biosci

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Chronic Lymphocytic Leukemia (CLL) is a B cell malignancy characterized by the accumulation of mature monoclonal CD5-positive B cells in the blood, secondary lymphoid tissues, and marrow. The infiltration of CLL cells in lymphoid tissues is a key element of disease pathogenesis. It is in such tissues that are found the microenvironments that provide CLL cells protection from spontaneous and/or drug-induced apoptosis. CLL cells actively shape their microenvironment by producing cytokines and chemokines, and by subverting normal accessory cells to promote leukemia-cell survival, proliferation, and escape from immune detection. In this review, we discuss how CLL cells disrupt the niches required for normal hematopoiesis or immune function and subvert normal cells in the microenvironment to support neoplastic cell growth and survival.

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Section: Disruption Of Lymphoid Architecture In Cllmentioning

confidence: 60%

Structure and function of the hematopoietic cancer niche focus on chronic lymphocytic leukemia

Kipps¹

2012

Front Biosci

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“…The turnover of CLL cells has been hypothesized to occur primarily in lymph nodes and in bone marrow (43), but the assumed influence of microenvironmental stimuli on the maintenance of the leukemic clone within these compartments is largely based on in vitro studies (16,18,19,(44)(45)(46). Recently, examination of lymph node CLL cells provided additional support to this hypothesis as these cells were shown to have an antiapoptotic expression profile with up-regulation of Mcl-1, Bcl-XL, and survivin and concomitant down-regulation of Noxa when compared with CLL cells in blood (17).…”

Section: Discussionmentioning

confidence: 99%

In vivo Dynamics of Stable Chronic Lymphocytic Leukemia Inversely Correlate with Somatic Hypermutation Levels and Suggest No Major Leukemic Turnover in Bone Marrow

et al. 2008

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Although accumulating evidence indicates that chronic lymphocytic leukemia (CLL) is a disease with appreciable cell dynamics, it remains uncertain whether this also applies to patients with stable disease. In this study, 2 H 2 O was administered to a clinically homogeneous cohort of nine stable, untreated CLL patients. CLL dynamics in blood and bone marrow were determined and compared with normal B-cell dynamics in blood from five healthy individuals who underwent a similar 2 H 2 O labeling protocol. Average CLL turnover rates (0.08-0.35% of the clone per day) were f2-fold lower than average B-cell turnover rates from healthy individuals (0.34-0.89%), whereas the rate at which labeled CLL cells in blood disappeared (0.00-0.39% of B cells per day) was f10-fold lower compared with labeled B cells from healthy individuals (1.57-4.24% per day). Leukemic cell turnover variables inversely correlated with the level of somatic hypermutation of the CLL clone (IgVH mutations). Although CLL cells in bone marrow had a higher level of label enrichment than CLL cells in blood, no difference between proliferation rates and proapoptotic and antiapoptotic profiles of CLL cells from these compartments was observed. These data suggest that, in stable disease, there is a biological relationship between the degree of somatic hypermutation of the CLL clone and its dynamics in vivo. Furthermore, in contrast to lymph nodes, the bone marrow does not seem to be a major CLL proliferation site. [Cancer Res 2008;68(24):10137-44]

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“…Reliable prognostic factors are important because they can be useful in counselling patients regarding treatment, assessing the likelihood of response to treatment and provide insight into the biology or pathophysiology of the disease. Prognostic factors have been identified in CLL, namely that poor prognosis is associated with advanced stage (Skinnider et al , 1982); increased serum beta‐2 microglobulin (β2‐M) (Spati et al , 1980; Molica et al , 1999a), soluble CD23 (Sarfati et al , 1996; Molica et al , 1999a), soluble CD27 (van Oers et al , 1993; Molica et al , 1998), lactate dehydrogenase (LDH) level (Lee et al , 1987); cytogenetic abnormalities (Dohner et al , 1997; Cordone et al , 1998); leukaemia cell expression of CD38 (Damle et al , 1999; Del Poeta et al, 2001) and non‐mutated IgV gene (Damle et al , 1999; Hamblin et al , 1999); and diffuse pattern of bone marrow involvement (Montserrat et al , 1984).…”

mentioning

confidence: 99%

Plasma interleukin 8 level predicts for survival in chronic lymphocytic leukaemia

et al. 2003

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Summary. The malignant B cells of patients with chronic lymphocytic leukaemia (CLL) constitutively express interleukin 8 (IL-8) and IL-8 receptors. Ex vivo culture with exogenous IL-8 enhances IL-8 expression and prolongs leukaemia cell survival, partly through increased bcl-2 expression. IL-8 may function as an autocrine growth and apoptosis resistance factor in CLL. Therefore, we evaluated the prognostic relevance of plasma IL-8 levels in 151 CLL patients [median age 61 years (range, 32-84 years), median plasma IL-8 level 18AE9 pg/ml (9AE1-89AE1 pg/ml)]. All Rai stages were represented; advanced stage was associated with significantly higher plasma IL-8 levels (P < 0AE0001, Kruskal-Wallis). Also, plasma IL-8 level was correlated with serum b2-microglobulin (b2-M) (R ¼ 0AE24, P ¼ 0AE0081), haemoglobin (R ¼ )0AE39, P < 0AE0001) and platelet count (R ¼ )0AE23, P ¼ 0AE0049) by Spearman's rank correlation.Univariate analysis using Cox proportional hazards models identified elevated IL-8 and b2-M as significant prognostic factors with relative risks of 7AE43 (P ¼ 9AE1 · 10 )9 ) and 16AE40 (P ¼ 5AE9 · 10 )10 ) respectively. High levels of IL-8 were associated with shorter survival independent of b2-M level. Using recursive-partitioning procedures, an IL-8 cutoff point of 26AE2 pg/ml segregated a group of CLL patients with significantly shorter survival (median 9AE3 months) (P < 0AE0001). In conclusion, plasma IL-8 level in CLL patients correlates with other prognostic factors, such as Rai stage and b2-M, and is associated with increased risk of death in CLL patients. The role of IL-8 inhibitors in the treatment of patients with CLL should be explored.

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Bone marrow histopathologic patterns and immunologic findings in B-chronic lymphocytic leukemia

Cited by 17 publications

References 32 publications

Structure and function of the hematopoietic cancer niche focus on chronic lymphocytic leukemia

Structure and function of the hematopoietic cancer niche focus on chronic lymphocytic leukemia

In vivo Dynamics of Stable Chronic Lymphocytic Leukemia Inversely Correlate with Somatic Hypermutation Levels and Suggest No Major Leukemic Turnover in Bone Marrow

Plasma interleukin 8 level predicts for survival in chronic lymphocytic leukaemia

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