Role of transforming growth factor-β in chronic lymphocytic leukemia

Israels, L. G.; Israels, Sara J.; Begleiter, Asher; Verburg, Linda; Schwartz, Lauren E.; Mowat, Michael; Johnston, James B.

doi:10.1016/0145-2126(93)90144-a

Cited by 11 publications

(4 citation statements)

References 23 publications

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“…Moreover, the level of TGF-b inhibition is lower than that observed on normal CD5 þ B lymphocytes (data not shown). These observations are in agreement with the data reported by Israels et al (1993) who demonstrated that the inhibition of spontaneous DNA synthesis by TGF-b was significantly less marked in CLL cells than in normal polyvalent B lymphocytes. The lower sensitivity of leukaemic cells to TGF-b inhibition seems therefore in relation with the malignant state of these cells and not an inherent property of the CD5 þ B-cell lineage.…”

Section: Discussionsupporting

confidence: 93%

Heterogenous response of B lymphocytes to transforming growth factor‐beta in B‐cell chronic lymphocytic leukaemia: correlation with the expression of TGF‐β receptors

et al. 1997

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Summary.We investigated the potential role of transforming growth factor-beta (TGF-b) on spontaneous and cytokineinduced proliferation of B-cell chronic lymphocytic leukaemia (B-CLL) cells in vitro. Purified B lymphocytes from 21 B-CLL patients were cultured for 5 d in the presence of medium alone, IL-2 and/or IL-10, in the presence or absence of TGF-b, and proliferation was measured by 3 H-thymidine incorporation. TGF-b inhibited B-cell proliferation in the majority of patients (15/21) but no inhibition was detected in 6/21 patients whatever the type of stimulant used. Addition of neutralizing antibodies to TGF-b increased spontaneous and cytokine-induced proliferation; this effect was dose dependent and specific because addition of an irrelevant chicken IgG had no effect on B-CLL proliferation. In resistant patients, neutralizing antibodies to TGF-b did not increase the proliferation. The expression of TGF-b receptors on B-CLL cells was significantly lower than the one observed on normal CD5 þ B lymphocytes for which the sensitivity to TGF-b inhibition was more marked than in CLL. In addition, we found a strong correlation between the response of leukaemic B cells to TGF-b inhibitory action and the expression of TGF-b receptors on these cells. In summary, TGF-b appears to function in CLL as a negative regulator of B lymphocytes but loss of responsiveness to this factor accompanied by a decrease of TGF-b receptor expression, might provide a selective advantage to B-CLL lymphocytes.

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Section: Discussionsupporting

confidence: 93%

Heterogenous response of B lymphocytes to transforming growth factor‐beta in B‐cell chronic lymphocytic leukaemia: correlation with the expression of TGF‐β receptors

et al. 1997

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“…To date, no evidence suggests a similar role for betaglycan, but betaglycan has been implicated in presentation of TGF-,B to TGF3RII, forming a ternary complex that increases receptor binding affinity and cell responsiveness to TGF-03 (15). Recent studies have suggested that lack of responsiveness to TGF-f3 inhibition may play a role in the progression of certain neoplasms and is characteristic of some neoplastic B-and T-cell lines (16)(17)(18).…”

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confidence: 99%

Reduced surface expression of transforming growth factor beta receptor type II in mitogen-activated T cells from Sézary patients.

Capocasale

Lamb

Vonderheid

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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“…9 However, TGF-b has been shown to produce marked inhibition of DNA synthesis in normal B lymphocytes and a decreased ability to inhibit DNA synthesis of CD34 TGF-b1 TGF-b2 TGF-bRI TGF-bRII bFGF FGF-R1 FGF-R2 FGF-R3 FGF-R4 VEGF VEGF-R1 VEGF- Loss of this negative growth control might permit the development of lymphoid malignancies.…”

Section: Discussionmentioning

confidence: 99%

B-Cell Chronic Lymphocytic Leukemia

Phyliky²,

Li³

2006

Applied Immunohistochemistry &Amp; Molecular Morphology

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B-cell chronic lymphocytic leukemia (B-CLL) is characterized by the accumulation of non-cycling B cells in lymphatic and extralymphatic tissues. Earlier studies had validated that angiogenesis was increased in B-CLL. Increased serum concentrations of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) connote a poor prognosis in early-stage B-CLL. Early progression is also related to transforming growth factor-beta (TGF-beta), which inhibits B-cell proliferation and immunoglobulin production. The authors investigated the expression of CD34, VEGF, bFGF, and TGF-beta and their receptors in different stages of B-CLL by analyzing bone marrow samples from 23 patients (11 with Rai stages 0-II; 12 with stages III or IV). TGF-beta2 was expressed more strongly in stages 0 to II than in stages III or IV (P=0.03). There was no significant difference in the intensity of CD34, TGF-beta1, VEGF, and bFGF and their receptors between stages 0 to II and stages III or IV. Staining showed bFGF expression to be stronger than VEGF expression (P=0.001). Results did not confirm an association between the intensity of angiogenesis and B-CLL stage. The expression of TGF-beta2 was stronger in early-stage disease and may help slow disease progression.

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Role of transforming growth factor-β in chronic lymphocytic leukemia

Cited by 11 publications

References 23 publications

Heterogenous response of B lymphocytes to transforming growth factor‐beta in B‐cell chronic lymphocytic leukaemia: correlation with the expression of TGF‐β receptors

Heterogenous response of B lymphocytes to transforming growth factor‐beta in B‐cell chronic lymphocytic leukaemia: correlation with the expression of TGF‐β receptors

Reduced surface expression of transforming growth factor beta receptor type II in mitogen-activated T cells from Sézary patients.

B-Cell Chronic Lymphocytic Leukemia

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