The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Shu Nakamoto - One of the best experts on this subject based on the ideXlab platform.
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High viral load of Merkel Cell polyomavirus DNA sequences in Langerhans Cell Sarcoma tissues
Infectious Agents and Cancer, 2014Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu NakamotoAbstract:Background Langerhans Cell (LC) Sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel Cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. Findings We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328–0.772 copies/Cell (Merkel Cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). Conclusions Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/Cell) than low load of LCH (0.003, median of 12 cases) ( P
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high viral load of merkel Cell polyomavirus dna sequences in Langerhans Cell Sarcoma tissues
Infectious Agents and Cancer, 2014Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu NakamotoAbstract:BACKGROUND: Langerhans Cell (LC) Sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel Cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. FINDINGS: We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328-0.772 copies/Cell (Merkel Cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). CONCLUSIONS: Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/Cell) than low load of LCH (0.003, median of 12 cases) (P < 0.01) may suggest a virally induced tumorigenic process in some LCS. Although the absence of LT antigen expression may indicate a different role for MCPyV in this pathology, some subtypes of LCS may develop in the background of MCPyV-infected LC. To the best of our knowledge, this is the first report on the relationship between MCPyV and LCS. The recent discovery of MCPyV opened new therapeutic avenues for MCC. These data open novel possibilities for therapeutic interventions against LCS.
Ichiro Murakami - One of the best experts on this subject based on the ideXlab platform.
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Merkel Cell polyomavirus and Langerhans Cell neoplasm
Cell Communication and Signaling, 2018Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Noriko Wada, Junko Nakashima, Mitsuko Iguchi, Yumiko Hashida, Tomonori Higuchi, Masanori Daibata, Satoshi KuwamotoAbstract:Background The relationship between various external agents such as pollen, food, and infectious agents and human sensitivity exists and is variable depending upon individual’s health conditions. For example, we believe that the pathogenetic potential of the Merkel Cell polyomavirus (MCPyV), the resident virus in skin, is variable and depends from the degree of individual’s reactivity. MCPyV as well as Epstein-Barr virus, which are normally connected with humans under the form of subclinical infection, are thought to be involved at various degrees in several neoplastic and inflammatory diseases. In this review, we cover two types of Langerhans Cell neoplasms, the Langerhans Cell Sarcoma (LCS) and Langerhans Cell histiocytosis (LCH), represented as either neoplastic or inflammatory diseases caused by MCPyV. Methods We meta-analyzed both our previous analyses, composed of quantitative PCR for MCPyV-DNA, proteomics, immunohistochemistry which construct IL-17 endocrine model and interleukin-1 (IL-1) activation loop model, and other groups’ data. Results We have shown that there were subgroups associated with the MCPyV as a causal agent in these two different neoplasms. Comparatively, LCS, distinct from the LCH, is a neoplastic lesion (or Sarcoma) without presence of inflammatory granuloma frequently observed in the elderly. LCH is a proliferative disease of Langerhans-like abnormal Cells which carry mutations of genes involved in the RAS / MAPK signaling pathway. We found that MCPyV may be involved in the development of LCH. Conclusion We hypothesized that a subgroup of LCS developed according the same mechanism involved in Merkel Cell carcinoma pathogenesis. We proposed LCH developed from an inflammatory process that was sustained due to gene mutations. We hypothesized that MCPyV infection triggered an IL-1 activation loop that lies beneath the pathogenesis of LCH and propose a new triple-factor model.
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High viral load of Merkel Cell polyomavirus DNA sequences in Langerhans Cell Sarcoma tissues
Infectious Agents and Cancer, 2014Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu NakamotoAbstract:Background Langerhans Cell (LC) Sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel Cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. Findings We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328–0.772 copies/Cell (Merkel Cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). Conclusions Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/Cell) than low load of LCH (0.003, median of 12 cases) ( P
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high viral load of merkel Cell polyomavirus dna sequences in Langerhans Cell Sarcoma tissues
Infectious Agents and Cancer, 2014Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu NakamotoAbstract:BACKGROUND: Langerhans Cell (LC) Sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel Cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. FINDINGS: We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328-0.772 copies/Cell (Merkel Cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). CONCLUSIONS: Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/Cell) than low load of LCH (0.003, median of 12 cases) (P < 0.01) may suggest a virally induced tumorigenic process in some LCS. Although the absence of LT antigen expression may indicate a different role for MCPyV in this pathology, some subtypes of LCS may develop in the background of MCPyV-infected LC. To the best of our knowledge, this is the first report on the relationship between MCPyV and LCS. The recent discovery of MCPyV opened new therapeutic avenues for MCC. These data open novel possibilities for therapeutic interventions against LCS.
Elaine S Jaffe - One of the best experts on this subject based on the ideXlab platform.
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Clonally related histiocytic/dendritic Cell Sarcoma and chronic lymphocytic leukemia/small lymphocytic lymphoma: a study of seven cases
Modern Pathology, 2011Co-Authors: Haipeng Shao, Rhett P. Ketterling, Liqiang Xi, Mark Raffeld, Andrew L Feldman, Ryan Knudson, Jaime Rodriguez-canales, Jeffrey Hanson, Stefania Pittaluga, Elaine S JaffeAbstract:Histiocytic and interdigitating dendritic Cell Sarcomas are rare tumors originating from bone marrow-derived myeloid stem Cells. Recent studies have shown evidence of cross-lineage transdifferentiation of B Cells in follicular lymphoma to histiocytic and dendritic Cell Sarcomas. In this study, we report the morphologic, molecular and cytogenetic analysis of seven cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) associated with histiocytic and dendritic Cell Sarcomas. All seven patients were elderly males (median age 71 years). The B-Cell neoplasms preceded the development of the histiocytic and dendritic Cell Sarcomas in six of seven patients, and one patient had both tumors diagnosed at the same time. The tumors included four interdigitating dendritic Cell Sarcomas: one Langerhans Cell Sarcoma, one histiocytic Sarcoma and one immature neoplasm with evidence of histiocytic origin. Laser-capture microdissection and PCR analysis showed identical clonal immunoglobulin gene rearrangements in the two phenotypically distinct components in all cases. There was a preferential usage of IGHV4-39 by the V–D–J gene rearrangement. By fluorescence in situ hybridization (FISH) analysis, two cases showed deletion 17p in both components, whereas four cases had normal cytogenetic findings by FISH in the CLL/SLL Cells, but acquired cytogenetic abnormalities in the corresponding histiocytic and dendritic tumors. Chromosome 17p abnormalities were the most common cytogenetic abnormality detected in the Sarcomas, seen in five of six cases studied. Compared with the CLL/SLL Cells, the histiocytic/dendritic Cells were largely negative for PAX5, but showed strong expression of PU.1 and variable and weak expression of CEBP β . Our study provides evidence for transdifferentiation of CLL/SLL B Cells to tumors of dendritic and less often histiocytic lineage, and suggests that secondary genetic events may play a role in this phenomenon.
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Clonally related histiocytic/dendritic Cell Sarcoma and chronic lymphocytic leukemia/small lymphocytic lymphoma: a study of seven cases.
Modern Pathology, 2011Co-Authors: Haipeng Shao, Rhett P. Ketterling, Liqiang Xi, Mark Raffeld, Andrew L Feldman, Ryan Knudson, Jaime Rodriguez-canales, Stefania Pittaluga, Jeffrey C. Hanson, Elaine S JaffeAbstract:Histiocytic and interdigitating dendritic Cell Sarcomas are rare tumors originating from bone marrow derived myeloid stem Cells. Recent studies have shown evidence of cross-lineage transdifferentiation of B-Cells in follicular lymphoma to histiocytic and dendritic Cell Sarcomas. In this study, we report the morphologic, molecular and cytogenetic analysis of 7 cases of chronic lymphocytic leukemia/small lymphocytic lymphoma associated with histiocytic and dendritic Cell Sarcomas. All seven patients were elderly males (median age, 71 years). The B-Cell neoplasms preceded the development of the histiocytic and dendritic Cell Sarcomas in 6 of 7 patients, and one patient had both tumors diagnosed at the same time. The tumors included 4 interdigitating dendritic Cell Sarcomas; 1 Langerhans Cell Sarcoma, 1 histiocytic Sarcoma, and 1 immature neoplasm with evidence of histiocytic origin. Laser-capture microdissection and PCR analysis showed identical clonal immunoglobulin gene rearrangements in the two phenotypically distinct components in all cases. There was a preferential usage of IGHV4-39 by the V-D-J gene rearrangement. By FISH analysis two cases showed deletion 17p in both components, while 4 cases had normal cytogenetic findings by FISH in the CLL/SLL Cells, but acquired cytogenetic abnormalities in the corresponding histiocytic and dendritic tumors. Chromosome 17p abnormalities were the most common cytogenetic abnormality detected in the Sarcomas, seen in 5 of 6 cases studied. Compared with the CLL/SLL Cells, the histiocytic/dendritic Cells were largely negative for PAX5, but showed strong expression of PU.1 and variable and weak expression of CEBPβ. Our study provides evidence for transdifferentiation of CLL/SLL B-Cells to tumors of dendritic and less often histiocytic lineage, and suggests that secondary genetic events may play a role in this phenomenon.
Satoshi Kuwamoto - One of the best experts on this subject based on the ideXlab platform.
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Merkel Cell polyomavirus and Langerhans Cell neoplasm
Cell Communication and Signaling, 2018Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Noriko Wada, Junko Nakashima, Mitsuko Iguchi, Yumiko Hashida, Tomonori Higuchi, Masanori Daibata, Satoshi KuwamotoAbstract:Background The relationship between various external agents such as pollen, food, and infectious agents and human sensitivity exists and is variable depending upon individual’s health conditions. For example, we believe that the pathogenetic potential of the Merkel Cell polyomavirus (MCPyV), the resident virus in skin, is variable and depends from the degree of individual’s reactivity. MCPyV as well as Epstein-Barr virus, which are normally connected with humans under the form of subclinical infection, are thought to be involved at various degrees in several neoplastic and inflammatory diseases. In this review, we cover two types of Langerhans Cell neoplasms, the Langerhans Cell Sarcoma (LCS) and Langerhans Cell histiocytosis (LCH), represented as either neoplastic or inflammatory diseases caused by MCPyV. Methods We meta-analyzed both our previous analyses, composed of quantitative PCR for MCPyV-DNA, proteomics, immunohistochemistry which construct IL-17 endocrine model and interleukin-1 (IL-1) activation loop model, and other groups’ data. Results We have shown that there were subgroups associated with the MCPyV as a causal agent in these two different neoplasms. Comparatively, LCS, distinct from the LCH, is a neoplastic lesion (or Sarcoma) without presence of inflammatory granuloma frequently observed in the elderly. LCH is a proliferative disease of Langerhans-like abnormal Cells which carry mutations of genes involved in the RAS / MAPK signaling pathway. We found that MCPyV may be involved in the development of LCH. Conclusion We hypothesized that a subgroup of LCS developed according the same mechanism involved in Merkel Cell carcinoma pathogenesis. We proposed LCH developed from an inflammatory process that was sustained due to gene mutations. We hypothesized that MCPyV infection triggered an IL-1 activation loop that lies beneath the pathogenesis of LCH and propose a new triple-factor model.
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High viral load of Merkel Cell polyomavirus DNA sequences in Langerhans Cell Sarcoma tissues
Infectious Agents and Cancer, 2014Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu NakamotoAbstract:Background Langerhans Cell (LC) Sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel Cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. Findings We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328–0.772 copies/Cell (Merkel Cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). Conclusions Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/Cell) than low load of LCH (0.003, median of 12 cases) ( P
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high viral load of merkel Cell polyomavirus dna sequences in Langerhans Cell Sarcoma tissues
Infectious Agents and Cancer, 2014Co-Authors: Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu NakamotoAbstract:BACKGROUND: Langerhans Cell (LC) Sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel Cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent. FINDINGS: We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328-0.772 copies/Cell (Merkel Cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7). CONCLUSIONS: Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/Cell) than low load of LCH (0.003, median of 12 cases) (P < 0.01) may suggest a virally induced tumorigenic process in some LCS. Although the absence of LT antigen expression may indicate a different role for MCPyV in this pathology, some subtypes of LCS may develop in the background of MCPyV-infected LC. To the best of our knowledge, this is the first report on the relationship between MCPyV and LCS. The recent discovery of MCPyV opened new therapeutic avenues for MCC. These data open novel possibilities for therapeutic interventions against LCS.
Weiwei Chen - One of the best experts on this subject based on the ideXlab platform.
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Langerhans Cell Sarcoma arising from small lymphocytic lymphoma lineage analysis and braf v600e mutation study
American Journal of Clinical Pathology, 2013Co-Authors: Weiwei Chen, Ronald Jaffe, Anne Marie W Block, Sheila N J Sait, Buer SongAbstract:Langerhans Cell neoplasm and B-Cell lymphoma/leukemia are generally thought to be two different types of neoplasms derived from the dendritic/histiocytic and the lymphoid hematopoietic lineages, respectively. However, recent studies have shown that dendritic/histiocytic neoplasms can be transdifferentiated from lymphoproliferative disorders. Nonetheless, …
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Langerhans Cell Sarcoma arising from chronic lymphocytic lymphoma small lymphocytic leukemia lineage analysis and braf v600e mutation study
North American Journal of Medical Sciences, 2013Co-Authors: Weiwei Chen, Ronald Jaffe, Linsheng Zhang, Charlie Hill, Anne Marie W Block, Sheila N J Sait, Boer SongAbstract:Background: The phenomenon that histiocytic/dendritic Cell Sarcomas may be transformed from lymphoproliferative diseases is dubbed 'transdifferentiation'. Langerhans Cell Sarcoma (LCS) transdifferentiated from chronic lymphocytic leukemia/small Cell lymphoma (CLL/SLL) is extremely rare. The underlying mechanisms of LCS tumorogenesis and its transdifferentiation from CLL/SLL are largely unknown. Aims: the authors strive to further characterize LCS, to understand the potential molecular changes in LCS and the underlying mechanisms of CLL/SLL transformation to LCS. Materials and Methods: a progressively enlarging right inguinal lymph node from a 68-year-old female patient with a history of CLL was biopsied and submitted for flow cytometry analysis, routine hematoxylin, and eosin (H and E) stain and immunohistochemical study. Furthermore, clonality study (fluorescent in situ hybridization (FISH) analysis with a CLL panel probes) and BRAF V600E mutation study (pyrosequencing and immunostain) were performed. Results: two different neoplasms, LCS and CLL/SLL, were discovered to occur simultaneously in the same lymph node. These two entities were shown to be clonally related. More importantly, for the first time, BRAF V600E mutation was detected in LCS. Conclusions: LCS can be transdifferentiated from CLL/SLL and BRAF V600E mutation may provide the foundation for alternative therapy of LCS.
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Langerhans Cell Sarcoma Arising from Chronic Lymphocytic Lymphoma/Small Lymphocytic Leukemia: Lineage Analysis and BRAF V600E Mutation Study.
North American Journal of Medical Sciences, 2013Co-Authors: Weiwei Chen, Ronald Jaffe, Linsheng Zhang, Charlie Hill, Anne Marie W Block, Sheila N J Sait, Boer SongAbstract:Background: The phenomenon that histiocytic/dendritic Cell Sarcomas may be transformed from lymphoproliferative diseases is dubbed 'transdifferentiation'. Langerhans Cell Sarcoma (LCS) transdifferentiated from chronic lymphocytic leukemia/small Cell lymphoma (CLL/SLL) is extremely rare. The underlying mechanisms of LCS tumorogenesis and its transdifferentiation from CLL/SLL are largely unknown. Aims: the authors strive to further characterize LCS, to understand the potential molecular changes in LCS and the underlying mechanisms of CLL/SLL transformation to LCS. Materials and Methods: a progressively enlarging right inguinal lymph node from a 68-year-old female patient with a history of CLL was biopsied and submitted for flow cytometry analysis, routine hematoxylin, and eosin (H and E) stain and immunohistochemical study. Furthermore, clonality study (fluorescent in situ hybridization (FISH) analysis with a CLL panel probes) and BRAF V600E mutation study (pyrosequencing and immunostain) were performed. Results: two different neoplasms, LCS and CLL/SLL, were discovered to occur simultaneously in the same lymph node. These two entities were shown to be clonally related. More importantly, for the first time, BRAF V600E mutation was detected in LCS. Conclusions: LCS can be transdifferentiated from CLL/SLL and BRAF V600E mutation may provide the foundation for alternative therapy of LCS.
