UNIPROT:Q86TM3 - FACTA Search

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Query: UNIPROT:Q86TM3 (cage)
29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two hundred and thirty-six cases of multiple primary cancer associated with hematological malignancies, collected from 35 medical institutions in Japan, are reported. Based on the time interval between the first cancer and the second cancer, they were divided into three groups: synchronous cancer (94 cases), metachronous cancer subsequent to hematological malignancy (61 cases) and metachronous hematological malignancy subsequent to carcinoma (76 cases). The most common initial cancers were acute leukemia (including atypical leukemia and erythroleukemia), non-Hodgkin's lymphoma, multiple myeloma and chronic myelogenous leukemia of the hematological malignancies, and gastric cancer of the carcinomas. Patients with cancer of the uterus and breast in the metachronous cancer group metachronously developed hematological malignancies more frequently than those in the synchronous cancer group. Multiple primary cancer was observed more frequently in men than in women both in the synchronous cancer group and in the group with metachronous cancer subsequent to hematological malignancies. Acute leukemia was the most frequent disease type in incidence among the metachronous hematological malignancies. This secondary acute leukemia was characterized by a mostly granulocytic nature, poor response to chemotherapy and poor prognosis.
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PMID:Multiple primary cancers associated with hematological malignancies. 400 83

Overgrowth syndromes are rare genetic conditions which present as global or segmental hyperplasia and are sometimes associated with increased risk of malignancy. Trisomy of the terminal portion of 15q which includes the IGFR1 gene, produces a rare overgrowth phenotype that has been termed 15q overgrowth syndrome (15q OGS). Upregulation of IGF1R has long been implicated in oncogenesis of multiple cancer types, including acute leukemias, and has been shown to render cells more susceptible to other transforming events. To date, too few cases of 15q OGS have been reported to identify any cancer predisposition. We present a case of a 34-year-old female with intellectual disability, macrocephaly, and subtle dysmorphic features who was diagnosed with mixed phenotype acute leukemia (lymphoid and myeloid). Prior to initiation of therapy she was referred to medical genetics for further evaluation and was identified as having a chromosomal translocation resulting in a partial trisomy of chromosome 15q, consistent with 15q OGS. A review of the literature for cases of malignancy in individuals with increased copy number of 15q revealed only one other reported patient. Given the small number of reported individuals, we cannot rule out an increased risk of cancer associated with this chromosomal overgrowth syndrome. Although concerns have been raised regarding treatment feasibility in the setting of chromosomal disorders, the reported patient underwent successful treatment with allogeneic hematopoietic stem-cell transplant.
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PMID:Acute leukemia in a patient with 15q overgrowth syndrome. 3086 14

Trimethylated histone H3 lysine 27 (H3K27me3) regulates gene repression, cell-fate determination and differentiation. We report that a conserved bromo-adjacent homology (BAH) module of BAHCC1 (BAHCC1^BAH) 'recognizes' H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and integrated chromatin immunoprecipitation-sequencing-based analyses demonstrate that direct readout of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-L-lysine-binding 'cage' formed by BAHCC1^BAH, mediating colocalization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is highly expressed in human acute leukemia and interacts with transcriptional corepressors. In leukemia, depletion of BAHCC1, or disruption of the BAHCC1^BAH-H3K27me3 interaction, causes derepression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to suppression of oncogenesis. In mice, introduction of a germline mutation at Bahcc1 to disrupt its H3K27me3 engagement causes partial postnatal lethality, supporting a role in development. This study identifies an H3K27me3-directed transduction pathway in mammals that relies on a conserved BAH 'reader'.
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PMID:BAHCC1 binds H3K27me3 via a conserved BAH module to mediate gene silencing and oncogenesis. 3313 53