The splenic form of mantle cell lymphoma

Angelopoulou, Maria K.; Siakantariz, Marina P.; Vassilakopoulos, Theodoros P.; Kontopidou, Flora N.; Rassidakis, George Z.; Dimopoulou, Maria; Kittas, Christos; Pangalis, Gerassimos A.

doi:10.1034/j.1600-0609.2002.00551.x

Cited by 43 publications

(21 citation statements)

References 51 publications

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“…On the other hand, it is well known that cellular adhesion molecules (CAM) are involved in the pattern of growth and dissemination of lymphoproliferative disorders [26][27][28][29][30]. MCL is characterized by low levels or absence of L-selectin and CD11c, low expression of CD11a/CD18 (Leukocyte function antigen (LFA)-1), and high levels of CD44, CD54 (Intracellular adhesion molecule-1), and VLA-5 [31,32]. In this regard, the lack of expression of LFA-1 has been related to lymphoma dissemination and aggressive behavior [30,33].…”

Section: Discussionmentioning

confidence: 99%

Central nervous system involvement in mantle cell lymphoma

Ferrer¹,

Bosch²,

Villamor³

et al. 2008

Annals of Oncology

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Background: Extranodal involvement, including central nervous system (CNS), is a frequent event in patients with mantle cell lymphoma (MCL). However, the incidence, risk factors, and impact on outcome remain controversial. Patients and methods:Main clinical, biological, and evolutive features of 82 patients (60 males/22 females; median age: 61 years) diagnosed with MCL (blastoid, 26%) in a single institution were analyzed for risk of CNS involvement and prognosis. Results: Most patients had advanced stage and intermediate or high-risk International Prognostic Index (IPI). Elevenpatients eventually developed CNS involvement with an actuarial 5-year risk of 26% (95% confidence interval 10% to 42%). In one asymptomatic patient, cerebrospinal fluid infiltration was detected at staging maneuvers (1/62; 1.6%). The remaining 10 patients developed neurological symptoms during the course of the disease (median time from diagnosis, 25 months). Initial variables predicting CNS involvement were blastoid histology, high proliferative index measured by Ki-67 staining, high lactate dehydrogenase (LDH) and intermediate-or high-risk IPI. Histological subtype and serum LDH maintained significance in multivariate analysis. Treatment of CNS infiltration consisted of intrathecal chemotherapy (two cases), and intrathecal chemotherapy plus systemic treatment (seven cases). Median survival after CNS involvement was 4.8 months, patients with this complication having shorter survival than those with no CNS disease.Conclusion: This study confirms the high incidence of CNS involvement in MCL patients. Treatments aimed at preventing this complication are warranted.

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Section: Discussionmentioning

confidence: 99%

Central nervous system involvement in mantle cell lymphoma

Ferrer¹,

Bosch²,

Villamor³

et al. 2008

Annals of Oncology

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“…Given the asymptomatic nature of the leukemic phase, some patients may only be diagnosed at the end of this process, when the extensive nodal disease develops. We recently proposed the term "nonnodal type of MCL" for this subtype of MCL (64) because it reflects the main, although not entirely specific clinical feature and because it gives credit to the initial clinical observations of this subgroup of tumors (62,69).…”

Section: Are All Mcls Created Equal? An Alternative Pathogenetic Pathmentioning

confidence: 99%

Molecular pathogenesis of mantle cell lymphoma

Jares

Colomer²,

Campo³

2012

J. Clin. Invest.

328

302

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Mantle cell lymphoma is a B cell malignancy in which constitutive dysregulation of cyclin D1 and the cell cycle, disruption of DNA damage response pathways, and activation of cell survival mechanisms contribute to oncogenesis. A small number of tumors lack cyclin D1 overexpression, suggesting that its dysregulation is always not required for tumor initiation. Some cases have hypermutated IGHV and stable karyotypes, a predominant nonnodal disease, and an indolent clinical evolution, which suggests that they may correspond to distinct subtypes of the disease. In this review, we discuss the molecular pathways that contribute to pathogenesis, and how improved understanding of these molecular mechanisms offers new perspectives for the treatment of patients. IntroductionMantle cell lymphoma (MCL) is a B cell malignancy with a broad spectrum of clinical, pathological, and biological features. The identification of the translocation event t(11;14)(q13;q32) and the resulting cyclin D1 overexpression were of paramount importance in recognizing the clinical and biological diversity of this tumor. In addition to this constitutive dysregulation of the cell cycle, other mechanisms such as DNA damage response alterations and activation of cell survival pathways are integrated to drive MCL pathogenesis (1, 2). New observations are expanding our views on the ontogeny and pathogenesis of this lymphoma. Furthermore, these new insights into MCL oncogenesis are promoting the development of new therapeutic strategies, intended to target the molecular mechanism of the disease, and opening up new clinical perspectives for optimal diagnosis and management of the patients.

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“…[13][14][15][16][17][18][19][20][21][22][23][24] Nevertheless, we consistently complement physical examination with the ultrasonographic assessment of superficial lymphatic stations and abdomen to highlight any lymphadenomegaly that could be eventually considered for subsequent histologic analysis. 25 Similar to clinical presentations, baseline laboratory findings of patients with SLs may be rather overlapping and thus poorly informative for diagnostic purposes.…”

Section: Clinical Evidencementioning

confidence: 99%

How I diagnose and treat splenic lymphomas

Iannitto

Tripodo

2011

Blood

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The incidental finding of an isolated splenomegaly during clinical assessment of patients evaluated for unrelated causes has become increasingly frequent because of the widespread use of imaging. Therefore, the challenging approach to the differential diagnosis of spleen disorders has emerged as a rather common issue of clinical practice. A true diagnostic dilemma hides in distinguishing pathologic conditions primarily involving the spleen from those in which splenomegaly presents as an epiphenomenon of hepatic or systemic diseases. Among the causes of isolated splenomegaly, lymphoid malignancies account for a relevant, yet probably underestimated, number of cases. Splenic lymphomas constitute a wide and heterogeneous array of diseases, whose clinical behavior spans from indolent to highly aggressive. Such a clinical heterogeneity is paralleled by the high degree of biologic variation in the lymphoid populations from which they originate. Nevertheless, the presenting clinical, laboratory, and pathologic features of these diseases often display significant overlaps. In this manuscript, we present our approach to the diagnosis and treatment of these rare lymphomas, whose complexity has been so far determined by the lack of prospectively validated prognostic systems, treatment strategies, and response criteria. (Blood. 2011;117(9):2585-2595)

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The splenic form of mantle cell lymphoma

Abstract: We conclude that this presentation represents a separate form of MCL which requires splenectomy. It remains to be seen whether it carries a better prognosis than classical MCL.

Cited by 43 publications

References 51 publications

Central nervous system involvement in mantle cell lymphoma

Central nervous system involvement in mantle cell lymphoma

Molecular pathogenesis of mantle cell lymphoma

How I diagnose and treat splenic lymphomas

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