Histiocytic Sarcoma Arising From Clonally Related Mantle Cell Lymphoma

Hure, Michelle C.; Elco, Christopher P.; Ward, David; Hutchinson, Lloyd; Meng, Xiuling; Dorfman, David M.; Yu, Hongbo

doi:10.1200/jco.2011.38.8553

Cited by 37 publications

(28 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Some cases of HS occur subsequent to or concurrent with B-or T-lymphoblastic lymphoma/leukemia or mature B-cell neoplasms such as follicular lymphoma, chronic lymphocytic leukemia, mantle cell lymphoma, extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue, splenic marginal zone lymphoma and diffuse large B-cell lymphoma. 11,12,[21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] Most associated mature B-cell lymphomas are low-grade B-cell lymphomas. The interval between the occurrence of lymphoma and that of HS is between 2 months and 17 years.…”

Section: Definitionmentioning

confidence: 99%

Histiocytic Sarcoma : An Updated Literature Review Based on the 2008 WHO Classification

Takahashi

Nakamura

2013

J Clin Exp Hematopathol

175

259

View full text Add to dashboard Cite

Section: Definitionmentioning

confidence: 99%

Histiocytic Sarcoma : An Updated Literature Review Based on the 2008 WHO Classification

Takahashi

Nakamura

2013

J Clin Exp Hematopathol

175

259

View full text Add to dashboard Cite

“…12 In contrast, other studies have reported some human HS cases to be associated with follicular lymphoma, diffuse large Bcell lymphoma or mantle cell lymphoma. 4,[13][14][15] Similarly, previous reports described that several HS cases coexist with B-cell lymphoma, which might have a common clonal origin of the HS in mice, 16,17 thus indicating that HS may originate from clonal hematopoietic progenitor cells of lymphoma. Our study showed that germ cell tumors and lymphoma components do not coexist in murine hepatic HS cells using immunohistochemical analysis, thus suggesting that HS occurrence may stem from an independent origin in the liver rather than from the transformation of other tumors.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Detection of Possible Cellular Origin of Hepatic Histiocytic Sarcoma in Mice

Ohnishi

Tanaka

Oghiso

et al. 2012

J Clin Exp Hematopathol

View full text Add to dashboard Cite

Histiocytic sarcoma (HS) spontaneously arises in the liver in mice ; however, the cellular origins of hepatic HS have not been fully clarified. In this study, we immunohistochemically analyzed 18 cases of hepatic HS from the archives of our previous experiments. In all cases, the tumor cells showed positive reactions for the macrophage-specific markers F4/80 and CD68. The cells were negative for mesenchymal cell and lymphoid cell markers, suggesting that germ cell tumor or lymphoma components do not coexist in the neoplasm. We detected scattered Ly6C + F4/80 -macrophage precursors in the extramedullary hematopoietic foci and liver tissue around the HS lesions. We also showed that certain populations of HS cells express the Ly-6C antigen. These findings suggest that Ly-6C + macrophage progenitor cells are a possible cellular origin of murine hepatic HS. Our study identified a novel phenotype of murine HS in two of 18 cases. These cases showed the nodular accumulations of tumor cells with cohesive cytoplasm mimicking the features of epithelioid granuloma. In agreement with the expression of CD204 in epithelioid cells in granulomatous diseases, these HS cells hardly expressed CD204, although the common type HS cells were strongly positive for this antigen. These data suggest that hepatic HS may stem from Ly-6C + macrophage precursors. Furthermore, a subset of hepatic HS cases can possibly differentiate into epithelioid cell-like phenotypes. 〔J Clin Exp Hematopathol 52(3) : 171-177, 2012〕

show abstract

Section: Mutations Of Epigenetic Modifier Genes In Cells With Multilimentioning

confidence: 99%

“…The finding that TET2 and DNMT3A are recurrently mutated within CD34 ϩ cells is also consistent with the previously described notion that epigenetic dysregulation within precursor cells creates a premalignant state conducive to the acquisition of transforming alterations. 51,52 Mutations associated with follicular lymphoma within HSCsTo explore lymphoma ontogeny, we used a donor-recipient pair who both developed FL 7 years after allogeneic bone marrow transplantation and donor lymphocyte infusions (DLIs; Figure 4A). 53 Both FLs harbored the same BCL2-IGH and IGH V-DJ rearrangements, 53 indicating that they derived from the same …”

mentioning

confidence: 99%

“…For example, FL, CLL, and MCL can all precede or simultaneously present with histiocytic/dendritic cell neoplasms that share the same BCL2-IGH and/or immunoglobulin rearrangements. 51,69,70 Thus, the histiocytic/dendritic cells derive from a cell that underwent V(D)J recombination and then switched to the myeloid lineage. Similar to the murine models outlined in this section, the histiocytic/dendritic cell neoplasms lack expression of PAX5 but express the myeloid transcription factors C/EBP␣ and PU.1.…”

mentioning

confidence: 99%

See 1 more Smart Citation

The evolving contribution of hematopoietic progenitor cells to lymphomagenesis

Weigert

Weinstock

2012

Blood

View full text Add to dashboard Cite

Recent genomic studies have outlined a landscape of recurrent alterations within some subtypes of lymphoid cancer. Yet, the timing and cellular contexts during which these alterations occur (ie, the molecular ontogeny) remain poorly understood. Lymphoid malignancies offer an exceptional opportunity to delineate the ontogeny of somatic alterations, as lymphocyte differentiation absolutely requires the introduction of indelible genetic rearrangements at antigen receptor loci during specific stages of maturation. We review competing models of lymphomagenesis and highlight evolving evidence that somatic alterations in uncommitted hematopoietic progenitors contribute to some mature lymphoid neoplasms. These progenitors could serve as reservoirs for further clonal evolution and thereby contribute to therapeutic resistance, tumor relapse, and the development of second hematologic malignancies. Defining the pathways that are dysregulated within early progenitors and the ontogeny of subsequent alterations that contribute to lymphoid transformation could establish novel therapeutic targets across a variety of hematologic malignancies and even guide avenues for future preventive strategies. (Blood. 2012; 120(13):2553-2561) Introduction B-cell and T-cell lymphomas compose Ͼ 90% of lymphoid malignancies worldwide and 4% of new cancers each year. 1 Recent studies have catalogued hundreds of genetic and transcriptional alterations across large panels of lymphomas, with extensive representation of the 2 most common subtypes, follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL). [2][3][4][5][6][7][8][9][10][11] Within a short period, the large majority of lymphoma-associated alterations will probably be known, leaving 2 great challenges. The first is to clarify which alterations functionally contribute to the lymphoma phenotype. The second challenge is to define the clonal architecture of individual lymphomas, including the cellular contexts in which each alteration develops (ie, the molecular ontogeny).New insights from both hematologic and epithelial tumors indicate that malignancies can harbor extensive clonal heterogeneity across multiple stages of differentiation. [12][13][14][15][16][17] However, the investigation of ontogeny in nonlymphoid cancers requires the use of surrogates for differentiation stage, such as immunophenotype, which are inherently variable (eg, through epigenetic plasticity). In contrast, lymphocyte differentiation absolutely requires the introduction of indelible genetic alterations at antigen receptor loci. Like all hematopoietic cells, lymphocytes derive from hematopoietic stem cells (HSCs) through a process of lineage-specific differentiation that is orchestrated by master regulators, including transcription factors and microRNA. Both the RAG recombinase and activation-induced deaminase (AID) introduce characteristic rearrangements at antigen receptor loci, as well as off-target damage at oncogenes and tumor suppressor genes that contribute to lymphoid transformation. 18,19 Thus, lymph...

show abstract

Histiocytic Sarcoma Arising From Clonally Related Mantle Cell Lymphoma

Cited by 37 publications

References 9 publications

Histiocytic Sarcoma : An Updated Literature Review Based on the 2008 WHO Classification

Histiocytic Sarcoma : An Updated Literature Review Based on the 2008 WHO Classification

Immunohistochemical Detection of Possible Cellular Origin of Hepatic Histiocytic Sarcoma in Mice

The evolving contribution of hematopoietic progenitor cells to lymphomagenesis

Contact Info

Product

Resources

About