Histiocytic sarcoma combined with acute monocytic leukemia: a case report

Zhao, Jiangning; Niu, Xiamu; Wang, Zhao; Lu, Hua-Dong; Lin, Xinhua; Lu, Quanyi

doi:10.1186/s13000-015-0350-9

Cited by 17 publications

(16 citation statements)

References 23 publications

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“…HS, which frequently occurs as a secondary event following these hematolymphoid malignancies, has been demonstrated to harbor the same molecular or cytogenetic abnormalities as the primary malignancy. There have been reported cases of HS as a secondary event following the diagnosis of follicular lymphoma , acute monocytic leukemia (AMoL) , hairy cell leukemia , mantle cell lymphoma , MALT type lymphoma , diffuse large B‐cell lymphoma , acute lymphoblastic lymphoma , chronic lymphocytic leukemia , chronic myelomonocytic leukemia , mediastinal germ cell tumors , idiopathic myelofibrosis , and in our case a diagnosis of HS associated with CML. Some of the commonly associated cases compiled from the literature along with their clinical characteristics are summarized in Table .…”

Section: Definition and Epidemiologymentioning

confidence: 73%

Histiocytic sarcoma as a secondary malignancy: pathobiology, diagnosis, and treatment

Ansari

Naqash

Munker

et al. 2016

European J of Haematology

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Histiocytic sarcoma (HS) is an extremely rare non-Langerhans cell disorder with an aggressive course and limited treatment options. Recent advances in molecular/genetic sequencing have suggested a common clonal origin between various hematolymphoid disorders and cases of secondary HS. Deriving conclusions from previously reported cases of HS arising secondarily to certain hematolymphoid disorders, here we have tried to provide insight into the mechanisms influencing this evolution. We also discuss a clinical case of a 72-year-old man with a diagnosis of chronic myeloid leukemia (CML), presenting subsequently with a heterogeneous liver mass positive with a diagnosis of HS. The liver mass showed a retained BCR-ABL1 translocation suggesting clonality between the CML and HS. As seen in our case and other reported cases of HS derived secondarily, the concurrent expression of immunoglobulin heavy (IGH)-/lightchain rearrangements or cytogenetic markers common to the primary malignancy suggests an evolutionary mechanism involving lineage switching that could potentially be influenced by genetic or epigenetic cues which may occur at the level of a progenitor or the malignant cell itself. Clinical caseA 72-year-old male was brought to the emergency room with a one-month history of progressively worsening bilateral lower extremity swelling, more than 10 lbs. of weight loss, lack of appetite, and rapidly declining performance status. His past medical history was notable for CML, which was diagnosed 30 months prior to presentation (Fig. 1). The patient was treated on a protocol with imatinib (400 mg daily) and demonstrated a complete molecular response to tyrosine kinase inhibitor (TKI) therapy. Focused physical examination demonstrated an emaciated male in mild distress from abdominal pain, right upper quadrant tenderness on deep palpation, and abdominal distension without any signs of an acute abdomen.His peripheral blood smear revealed normochromic, normocytic anemia with hemoglobin of 7.6 g/dL (normal range, 12.5-16.3 g/dL), a white blood count of 7 730/lL (normal range, 3 600-11 200/lL), a red blood cell count of 2.78 M/lL (normal range 4.06-5.63 M/lL), and a platelet count of 114 000/lL (normal range, 159 000-386 000/lL). Serum iron was low (21 lg/dL) with a low TIBC (216 lg/dL), which was attributed to anemia of chronic disease. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed the absence of the BCR/ABL transcript in the peripheral blood.Computed tomography scan of the chest and abdomen revealed a large, complex, heterogeneous, hypodense mass involving nearly all of the caudate and left lobes of the liver. These lesions were not present in the previous examination carried out 1 year before.Biopsy of the liver mass revealed diffuse infiltration of large and irregular pleomorphic cells with lobulated nuclei with some binucleated and trinucleated cells containing

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Section: Definition and Epidemiologymentioning

confidence: 73%

Histiocytic sarcoma as a secondary malignancy: pathobiology, diagnosis, and treatment

Ansari

Naqash

Munker

et al. 2016

European J of Haematology

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“…HS is an invasive tumor that responds poorly to treatment and for which there is yet no widely accepted effective therapy (9). Due to the fact that the vast majority of patients are at an advanced stage when they seek medical advice, the survival time is usually <2 years due to the poor response to chemotherapy (10). In recent years, it has been demonstrated that the use of radiotherapy and chemotherapy combined with autologous hematopoietic stem cell transplantation may improve treatment efficacy.…”

Section: Discussionmentioning

confidence: 99%

Histiocytic sarcoma of the neck: A case report

et al. 2018

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Histiocytic sarcoma (HS) is a term used to describe malignant hyperplasia of cells exhibiting morphological and immunophenotypical characteristics similar to those of mature cells, with expression of one or more tissue cell markers, excluding acute monocytic leukemia and primitive monocytic sarcoma. We herein describe a case of histiocytic sarcoma of the neck supported by histopathological and immunohistological evidence. A 53-year-old female patient of Chinese descent presented with a rapidly enlarging right neck mass. Imaging studies revealed multiple right cervical lymphadenectases with right jugular vein involvement. The tumor was composed of diffusely distributed large non-cohesive tumor cells, round or oval and focally spindle-shaped. The tumor cells were immunopositive for macrophage-associated antigen CD68 and lysosomes, mostly consistent with a diagnosis of HS. HS is very prone to systemic metastasis; therefore, early diagnosis and timely treatment are crucial.

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“…Hematopoiesis, once viewed as a unidirectional maturation of pluripotent hematopoietic stem cells into specific lineages (such as lymphoid and myeloid), shows considerable plasticity in both normal and malignant hematopoietic cells. Lineage switching has been described in histiocytic sarcoma (HS), Langerhans cell sarcoma or dendritic cell tumor that occur secondary to or synchronous with mediastinal germ cell tumors [ 14 ], lymphoid [ 12 , 13 , 15 – 22 ], and myeloid malignancies [ 23 , 24 ]. Histiocytic sarcoma cells are derived from bone marrow monocyte precursors [ 25 ], expresses monocyte-macrophage antigens (CD163, CD68, and lysozyme) and lack expression of myeloid antigens such as CD33, CD13 and MPO [ 11 , 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

Myeloid transformation of plasma cell myeloma: molecular evidence of clonal evolution revealed by next generation sequencing

Gralewski¹,

Post²,

Rhee³

et al. 2018

Diagn Pathol

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Background: Plasma cell myeloma (PCM) is a neoplasm of terminally differentiated B lymphocytes with molecular heterogeneity. Although therapy-related myeloid neoplasms are common in plasma cell myeloma patients after chemotherapy, transdifferentiation of plasma cell myeloma into myeloid neoplasms has not been reported in literature. Here we report a very rare case of myeloid neoplasm transformed from plasma cell myeloma. Case presentation: A 60-year-old man with a history of plasma cell myeloma with IGH-MAF gene rearrangement and RAS/RAF mutations developed multiple soft tissue lesions one year following melphalan-based chemotherapy and autologous stem cell transplant. Morphological and immunohistochemical characterization of the extramedullary disease demonstrated that the tumor cells were derived from the monocyte-macrophage lineage. Next generation sequencing (NGS) studies detected similar clonal aberrations in the diagnostic plasma cell population and post-therapy neoplastic cells, including IGH-MAF rearrangement, multiple genetic mutations in RAS signaling pathway proteins, and loss of tumor suppressor genes. Molecular genetic analysis also revealed unique genomic alterations in the transformed tumor cells, including gain of NF1 and loss of TRAF3. Conclusion: To our knowledge, this is the first case of myeloid sarcoma transdifferentiated from plasma cell neoplasm. Our findings in this unique case suggest clonal evolution of plasma cell myeloma to myeloma neoplasm and the potential roles of abnormal RAS/RAF signaling pathway in lineage switch or transdifferentiation.

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Histiocytic sarcoma combined with acute monocytic leukemia: a case report

Cited by 17 publications

References 23 publications

Histiocytic sarcoma as a secondary malignancy: pathobiology, diagnosis, and treatment

Histiocytic sarcoma as a secondary malignancy: pathobiology, diagnosis, and treatment

Histiocytic sarcoma of the neck: A case report

Myeloid transformation of plasma cell myeloma: molecular evidence of clonal evolution revealed by next generation sequencing

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