Cell death regulation during multistep lymphomagenesis

Hsu, Brenda; Marin, Maria C; McDonnell, Timothy J.

doi:10.1016/0304-3835(95)03836-l

Cited by 11 publications

(5 citation statements)

References 35 publications

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“…This could of course be due to the low percentage of p53 positive cases, indicating that p53 mutations are not of major importance in primary gastric lymphomas. Our study underscores the importance of apoptosis in relation to proliferation in gastric lymphomas, and probably in oncogenesis in general 37 . New directions of therapy therefore should focus more on influencing this process.…”

Section: Discussionsupporting

confidence: 61%

Proliferation and apoptosis in primary gastric B‐cell non‐Hodgkin's lymphoma

Gisbertz¹,

Schouten²,

Bot³

et al. 1997

Histopathology

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To elucidate the role of cell turnover in primary gastric B-cell non-Hodgkin's lymphomas we studied tissue samples of 72 patients-26 small cell (25 MALT lymphomas) and 46 large cell (31 MALT lymphomas). Proliferation indices and apoptotic indices were measured by Mib-1 expression and terminal deoxynucleotidyltransferase (TdT)-mediated nick end labelling, respectively. Furthermore, expression of the apoptosis related gene-products bcl-2 and p53 was studied. Large cell lymphomas showed significantly higher proliferation indices (59.1% vs. 15.4%) and apoptotic indices (3.2% vs.0.7%) than small cell lymphomas. Proliferation and apoptotic indices were positively correlated (r = 0.371, P = 0.03). Expression of the bcl-2 protein was significantly higher in the small cell lymphomas. Furthermore, cases with a high bcl-2 expression showed both a significantly decreased proliferation (P < 0.0001) and apoptotic index (P = 0.0096) compared to bcl-2 negative cases. Expression of the mutant p53 protein was present in 8.0% of small cell and in 18.2% of large cell lymphomas. p53 positive cases showed significantly higher proliferation indices, but showed no correlation with apoptotic index. These data suggest that impaired apoptosis by bcl-2 may be more prominent than proliferation in the genesis of small cell lymphomas, whereas a high cell turnover characterizes large cell primary gastric lymphomas.

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Section: Discussionsupporting

confidence: 61%

Proliferation and apoptosis in primary gastric B‐cell non‐Hodgkin's lymphoma

Gisbertz¹,

Schouten²,

Bot³

et al. 1997

Histopathology

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“…29 and 30). While such mutations are frequent in EMyc-induced lymphomas, they are rare in tumors from EBcl-2͞E-Myc double transgenic mice (31), suggesting that the biological effects of Bcl-2 overexpression and of p53 mutations may overlap. Since our results suggest that the overexpression of Gfi-1 and Bcl-2 may be equivalent, we conclude that the biological outcomes of Gfi-1 overexpression and of p53 mutations may also overlap.…”

Section: Discussionmentioning

confidence: 99%

The Gfi-1 protooncoprotein represses Bax expression and inhibits T-cell death

Grimes

Gilks²,

Chan³

et al. 1996

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

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The Gfi-1 protooncogene encodes a nuclear zinc-finger protein that carries a novel repressor domain, SNAG, and functions as a position-and orientationindependent active transcriptional repressor. The Gfi-1 repressor allows interleukin 2 (IL-2)-dependent T cells to escape G 1 arrest induced by IL-2 withdrawal in culture and collaborates with c-myc and pim-1 for the induction of retrovirusinduced lymphomas in animals. Here we show that overexpression of Gfi-1 also inhibits cell death induced by cultivation of IL-2-dependent T-cell lines in IL-2-deficient media. Similarly, induction of Gfi-1 in primary thymocytes from mice carrying a metal-inducible Gfi-1 transgene inhibits cell death induced by cultivation in vitro. The protein and mRNA levels of the proapoptotic regulator Bax are down-regulated by Gfi-1 in both immortalized T-cell lines and primary transgenic thymocytes. The repression is direct and depends on several Gfi-1-binding sites in the p53-inducible Bax promoter. In addition to Bax, Gfi-1 also represses Bak, another apoptosispromoting member of the Bcl-2 gene family. Therefore, Gfi-1 may inhibit apoptosis by means of its repression of multiple proapoptotic regulators. The antiapoptotic properties of Gfi-1 provide a potential explanation for its strong collaboration with c-myc during oncogenesis.

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“…on May 10, 2018. by guest www.bloodjournal.org From lymphomagenesis. 14,15 By analogy, DLBCL with the same translocation may be related to follicular lymphoma and the t(14;18) may also be important in its pathogenesis. In this study, we looked for the presence of the t(14;18) in a series of DLBCL using 2 techniques, FISH and PCR.…”

Section: Discussionmentioning

confidence: 99%