Prognostic Value of Translocation t(11;18) in Tumoral Response of Low-Grade Gastric Lymphoma of Mucosa-Associated Lymphoid Tissue Type to Oral Chemotherapy

Lévy, Michaël; Copie‐Bergman, Christiane; Gameiro, Christine; Chaumette, Marie-Thérèse; Delfau‐Larue, Marie‐Hélène; Haı̈oun, Corinne; Charachon, Antoine; Hémery, François; Gaulard, Philippe; Leroy, Karen; Delchier, Jean‐Charles

doi:10.1200/jco.2005.05.660

Cited by 108 publications

(58 citation statements)

References 33 publications

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“…Five patients (21%) relapsed 1-8 years after chemotherapy was discontinued. Of note, the presence of the t(11;18) translocation was associated with alkylator resistance in this cohort [90]. A Japanese group has found no difference in outcome between oral monochemotherapy and radiation as second-line therapy in patients who do not respond to eradication therapy [91].…”

Section: Chemoimmunotherapymentioning

confidence: 62%

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Non-Hodgkin's Lymphoma of Mucosa-Associated Lymphoid Tissue

et al. 2006

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Section: Chemoimmunotherapymentioning

confidence: 62%

“…Witzig and coworkers treated four patients with stage IV MALT lymphomas of various primary sites with Zevalin ® (Biogen Inc, Cambridge, MA) (the anti-CD20 antibody ibritumomab conjugated to 90 Y). Zevalin demonstrated significant activity in these patients, who were previously treated with both chemotherapy and radiation therapy.…”

Section: Thementioning

confidence: 99%

Non-Hodgkin's Lymphoma of Mucosa-Associated Lymphoid Tissue

et al. 2006

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“…Also, although antigen stimulation may be important for the growth of indolent B-cell malignancies, it might no longer be required by the subsequent aggressive malignancy. 9 With respect to RS, antigen stimulation contributes to CLL predisposition to DLBCL, 6 but it is unclear whether antigen retains any role once that transformation has occurred.…”

Section: 6mentioning

confidence: 99%

Molecular history of Richter syndrome: origin from a cell already present at the time of chronic lymphocytic leukemia diagnosis

Rossi¹,

Spina²,

Forconi³

et al. 2011

Intl Journal of Cancer

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Richter syndrome (RS) represents the transformation of chronic lymphocytic leukemia to aggressive lymphoma. We explored intraclonal diversification (ID) of immunoglobulin genes in order to (i) follow the evolutionary history of the RS clone (ii) compare the role of ID in clonally related RS vs. clonally unrelated cases. Most (10/11, 90.9%) clonally related RS stem from the predominant clone observed at CLL diagnosis. One single RS had a transformation pattern compatible with sequential evolution from a secondary CLL subclone. Once RS transformation had occurred, all secondary CLL subclones disappeared and were substituted by the dominant RS clone with its own descendants. These observations suggest that genetic lesions associated with RS transformation are acquired by a cell belonging to the original CLL clone, rather than being progressively accumulated by later CLL subclones. Accordingly, most (9/11, 81.1%) clonally related RS harbored a genetic lesion disrupting TP53 that was already present, though at subclonal levels, in 5/11 (45.5%) samples of the paired CLL phase. A fraction of clonally related RS switched off ID (4/11, 36.4%) or reduced the levels of ID (5/11, 45.4%) at transformation. Conversely, all clonally unrelated RS harbored ID and were characterized by a significantly higher mutation frequency compared to clonally related RS (median: 1.18 3 10 23 vs. 0.13 3 10 -3 ; p 50.002). These data indicate that (i) clonally related RS stems from a cell that is already present within the initial CLL clone and (ii) clonally unrelated and clonally related RS are biologically distinct disorders also in terms of antigen affinity maturation.The definition of Richter syndrome (RS) encompasses two biologically different conditions: (i) transformation of chronic lymphocytic leukemia (CLL) to clonally related diffuse large B-cell lymphoma (DLBCL) and (ii) development of a DLBCL unrelated to the CLL clone. [1][2][3][4] The role of antigen in promoting CLL transformation to RS is supported by the recent observation of a high prevalence of stereotyped B-cell receptors in CLL transforming to RS, and by the documentation of biased usage of immunoglobulin heavy variable (IGHV) genes, including IGHV4-39. 5,6A common assumption in the context of transformation from indolent to aggressive B-cell malignancy holds that transformation reflects the final stage of evolution of the indolent B-cell clone.7 An alternative scenario, however, might be the divergent evolution of both the indolent and the aggressive phase from a common precursor cell. 7,8 In RS, the precise timing of onset of the RS clone during CLL history is unknown. Also, although antigen stimulation may be important for the growth of indolent B-cell malignancies, it might no longer be required by the subsequent aggressive malignancy.9 With respect to RS, antigen stimulation contributes to CLL predisposition to DLBCL, 6 but it is unclear whether antigen retains any role once that transformation has occurred.

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“…16,27 Influence of systemic dissemination on survival is controversial, being significantly associated with poorer prognosis in some studies. 17,28 Interestingly the t(11;18)(q21;q21), a translocation specific of MALT-type lymphoma and detected in 18% to 24% of patients with gastric MALT lymphoma, has been correlated to a resistance to H pylori eradication therapy 29 and to alkylating agents 30 and but not to rituximab.…”

Section: Outcome and Prognostic Factorsmentioning

confidence: 99%

Clinical Presentation and Management of Marginal Zone Lymphomas

Thiéblemont¹

2005

Hematology

109

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Marginal-zone lymphoma (MZL) includes three subtypes depending on the site of lymphoma involvement: extranodal marginal zone B-cell lymphoma of mucosaassociated lymphoid tissue (MALT-lymphoma); splenic MZL; and nodal MZL. Beside a common cell-of-origin and similarities concerning a possible chronic antigenic stimulation by microbial pathogens and/or autoantigens, the clinical presentation is very different with symptoms related to lymphoma location. MALT and splenic MZL present with an indolent disease with good performance status, no B symptoms, and no adverse prognostic factors and are associated with long survival. Patients with nodal MZL present with a more aggressive disease and have a shorter failurefree survival. Clinical and biological prognostic factors identified in reported series are heterogeneous. The optimal treatment has yet to be defined for the three subtypes, and current strategies will be described in this review.Marginal zone B-cell lymphomas (MZL) represent a group of lymphomas whose cells originate from B lymphocytes normally present in a distinct anatomical location, the socalled "marginal zone" (MZ) of the secondary lymphoid follicles.1 These cells are anatomically localized in the lymphoid organs (spleen and lymph nodes) and in the nonlymphoid organs (mucosa-associated lymphoid tissue [MALT] or non-mucosal tissue such as skin, orbit and dura). Depending on the site of involvement, the International Lymphoma Study Group individualized three distinct subtypes of MZL: (1) extranodal MZL of MALT type, (2) splenic MZL (with or without villous lymphocytes), and (3) nodal MZL (with or without monocytoid B cells).2,3 Despite this classification, the relative rarity of these lymphomas and difficulties in distinguishing them from other low-grade lymphoma subtypes are obstacles to conducting epidemiological surveys and to describing clinical features and outcomes. Moreover, no prospective studies on large series have been published to date, making therapeutic decisions difficult. Data regarding clinical and biological prognostic markers are limited, and it is therefore difficult to predict those in whom the disease will be more aggressive. This review will present recent data describing the epidemiology, clinical features, staging, and therapy of these lymphomas. EpidemiologyMZL account for between 5% and 17% of all non-Hodgkin lymphomas (NHL) in adults depending on the series. MALT lymphoma is the most frequent of the MZL subtypes, representing 50% to 70% of MZL and 7% to 8% of NHL. The splenic and the nodal MZL represent 20% and 10% of MZL, respectively, and account for less than 1% of NHL. Most of the cases occur in adults, with a median age of approximately 60 years, except for splenic MZL with villous lymphocytes (SLVL), occurring in adults at a median age of around 70 years. [4][5][6][7][8]

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Prognostic Value of Translocation t(11;18) in Tumoral Response of Low-Grade Gastric Lymphoma of Mucosa-Associated Lymphoid Tissue Type to Oral Chemotherapy

Abstract: Presence of t(11;18) in GML is predictive of resistance to oral alkylating agents, with less than 10% of durable remission at long-term follow-up.

Cited by 108 publications

References 33 publications

Non-Hodgkin's Lymphoma of Mucosa-Associated Lymphoid Tissue

Non-Hodgkin's Lymphoma of Mucosa-Associated Lymphoid Tissue

Molecular history of Richter syndrome: origin from a cell already present at the time of chronic lymphocytic leukemia diagnosis

Clinical Presentation and Management of Marginal Zone Lymphomas

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