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  1. Article ; Online: Targeting lineage plasticity overcomes chemoresistance.

    Ogawa, Seishi

    Cancer cell

    2022  Volume 40, Issue 9, Page(s) 905–907

    Abstract: In this issue of Cancer Cell, Wang et al. reveal that chemoresistant muscle-invasive bladder cancer is associated with partial squamous differentiation. Targeting of Cathepsin H overcomes this chemotherapy-induced semi-squamatization and promotes ... ...

    Abstract In this issue of Cancer Cell, Wang et al. reveal that chemoresistant muscle-invasive bladder cancer is associated with partial squamous differentiation. Targeting of Cathepsin H overcomes this chemotherapy-induced semi-squamatization and promotes terminal squamous differentiation and tumor suppression.
    MeSH term(s) Carcinoma, Squamous Cell ; Drug Resistance, Neoplasm ; Humans ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/pathology
    Language English
    Publishing date 2022-08-25
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2022.08.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5650: Show issues Location:
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  2. Article ; Online: A growing genetic tree in the soil of prostate.

    Ogawa, Seishi

    Cell stem cell

    2021  Volume 28, Issue 7, Page(s) 1185–1187

    Abstract: In this issue of Cell Stem Cell, Grossmann et al. (2021) reconstructed the developmental history of the prostate gland in a 59-year-old male by 3D tracking of somatic mutations across 319 micro-dissected specimens. It provides a genetic picture of how ... ...

    Abstract In this issue of Cell Stem Cell, Grossmann et al. (2021) reconstructed the developmental history of the prostate gland in a 59-year-old male by 3D tracking of somatic mutations across 319 micro-dissected specimens. It provides a genetic picture of how the human prostate gland is shaped during embryogenesis, puberty, and adult life.
    MeSH term(s) Adult ; Embryonic Development ; Humans ; Male ; Middle Aged ; Prostate ; Soil ; Trees
    Chemical Substances Soil
    Language English
    Publishing date 2021-07-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2021.06.002
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    Zs.A 6589: Show issues Location:
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  3. Article ; Online: Deciphering the Clonal Origin of Relapsed Acute Lymphoblastic Leukemia in Children.

    Ogawa, Seishi

    Blood cancer discovery

    2020  Volume 1, Issue 1, Page(s) 21–22

    Abstract: In this issue ... ...

    Abstract In this issue of
    MeSH term(s) Child ; Clonal Evolution/genetics ; Clone Cells/pathology ; Genomics ; Humans ; Mutation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/diagnosis
    Language English
    Publishing date 2020-06-22
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3028898-8
    ISSN 2643-3249 ; 2643-3230
    ISSN (online) 2643-3249
    ISSN 2643-3230
    DOI 10.1158/2643-3249.BCD-20-0056
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  4. Article ; Online: Adult Low-Hypodiploid Acute Lymphoblastic Leukemia Evolves from TP53-Mutated Clonal Hematopoiesis.

    Saiki, Ryunosuke / Ogawa, Seishi

    Blood cancer discovery

    2023  Volume 4, Issue 2, Page(s) 102–105

    Abstract: Summary: Low-hypodiploid acute lymphoblastic leukemia (LH-ALL) in both children and adults is characterized by biallelic TP53 alterations in virtually all cases. However, in contrast to a common germline origin of the TP53 mutations in pediatric cases, ... ...

    Abstract Summary: Low-hypodiploid acute lymphoblastic leukemia (LH-ALL) in both children and adults is characterized by biallelic TP53 alterations in virtually all cases. However, in contrast to a common germline origin of the TP53 mutations in pediatric cases, those in adult cases are mostly somatic and are derived from age-related clonal hematopoiesis (ARCH), highlighting the role of TP53-mutant ARCH in the development not only of myeloid leukemogenesis but also of LH-ALL in aged populations. See related article by Kim et al., p. 134 (4).
    MeSH term(s) Adult ; Humans ; Child ; Aged ; Clonal Hematopoiesis/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Mutation ; Aneuploidy ; Acute Disease ; Tumor Suppressor Protein p53/genetics
    Chemical Substances TP53 protein, human ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2023-07-07
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3028898-8
    ISSN 2643-3249 ; 2643-3230
    ISSN (online) 2643-3249
    ISSN 2643-3230
    DOI 10.1158/2643-3230.BCD-23-0006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Genetic basis of myelodysplastic syndromes.

    Ogawa, Seishi

    Proceedings of the Japan Academy. Series B, Physical and biological sciences

    2020  Volume 96, Issue 3, Page(s) 107–121

    Abstract: During the past decade, substantial progress has been made in the field of the genetics of myelodysplastic syndromes (MDS). These comprise a group of chronic myeloid neoplasms with abnormal cell morphology and progression to acute myeloid leukemia (AML), ...

    Abstract During the past decade, substantial progress has been made in the field of the genetics of myelodysplastic syndromes (MDS). These comprise a group of chronic myeloid neoplasms with abnormal cell morphology and progression to acute myeloid leukemia (AML), where revolutionary sequencing technologies have played a major role. Through extensive sequencing of a large number of MDS genomes, a comprehensive registry of driver mutations involved in the pathogenesis of MDS has been revealed, along with their impacts on clinical phenotype and prognosis. The most frequently affected molecules are involved in DNA methylations, chromatin modification, RNA splicing, transcription, signal transduction, cohesin regulation, and DNA repair. These mutations show strong positive and negative correlations with each other, suggesting the presence of functional interactions between mutations, which dictate disease progression. Because these mutations are associated with disease phenotype, drug response, and clinical outcomes, it is essential to be familiar with MDS genetics not only for better understanding of MDS pathogenesis but also for management of patients.
    MeSH term(s) Cell Cycle Proteins/genetics ; Chromosomal Proteins, Non-Histone/genetics ; DNA Methylation ; DNA Repair ; DNA, Neoplasm/genetics ; DNA, Neoplasm/metabolism ; Disease Progression ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Chronic-Phase/genetics ; Mutation ; Myelodysplastic Syndromes/classification ; Myelodysplastic Syndromes/genetics ; Phenotype ; Prognosis ; RNA Splicing ; Sequence Analysis, DNA ; Signal Transduction ; Cohesins
    Chemical Substances Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; DNA, Neoplasm
    Language English
    Publishing date 2020-03-05
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 161781-3
    ISSN 1349-2896 ; 0386-2208
    ISSN (online) 1349-2896
    ISSN 0386-2208
    DOI 10.2183/pjab.96.009
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  6. Article ; Online: Genetics of MDS.

    Ogawa, Seishi

    Blood

    2019  Volume 133, Issue 10, Page(s) 1049–1059

    Abstract: Our knowledge about the genetics of myelodysplastic syndromes (MDS) and related myeloid disorders has been dramatically improved during the past decade, in which revolutionized sequencing technologies have played a major role. Through intensive efforts ... ...

    Abstract Our knowledge about the genetics of myelodysplastic syndromes (MDS) and related myeloid disorders has been dramatically improved during the past decade, in which revolutionized sequencing technologies have played a major role. Through intensive efforts of sequencing of a large number of MDS genomes, a comprehensive registry of driver mutations recurrently found in a recognizable fraction of MDS patients has been revealed, and ongoing efforts are being made to clarify their impacts on clinical phenotype and prognosis, as well as their role in the pathogenesis of MDS. Among major mutational targets in MDS are the molecules involved in DNA methylations, chromatin modification, RNA splicing, transcription, signal transduction, cohesin regulation, and DNA repair. Showing substantial overlaps with driver mutations seen in acute myeloid leukemia (AML), as well as age-related clonal hematopoiesis in healthy individuals, these mutations are presumed to have a common clonal origin. Mutations are thought to be acquired and positively selected in a well-organized manner to allow for expansion of the initiating clone to compromise normal hematopoiesis, ultimately giving rise to MDS and subsequent transformation to AML in many patients. Significant correlations between mutations suggest the presence of functional interactions between mutations, which dictate disease progression. Mutations are frequently associated with specific disease phenotype, drug response, and clinical outcomes, and thus, it is essential to be familiar with MDS genetics for better management of patients. This review aims to provide a brief overview of the recent progresses in MDS genetics.
    MeSH term(s) Chromosome Aberrations ; DNA Methylation ; DNA Repair ; Disease Progression ; Gene Dosage ; Genetic Association Studies ; Genetic Predisposition to Disease ; Hematology/trends ; Hematopoiesis/genetics ; Humans ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Myelodysplastic Syndromes/diagnosis ; Myelodysplastic Syndromes/genetics ; Prognosis ; RNA Splicing
    Language English
    Publishing date 2019-01-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-10-844621
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.140: Show issues Location:
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  7. Article: Novel mechanism of immune evasion in cancer via structural variations of the PD-L1 gene.

    Ogawa, Seishi

    Rinsho ketsueki] The Japanese journal of clinical hematology

    2017  Volume 58, Issue 8, Page(s) 957–965

    Abstract: Cancer cells are thought to circumvent immune surveillance through PD-1/PD-L1 signaling. However, the genetic basis for PD-L1-PD-L1-mediated immune escape has not been completely understood, with the exception of elevated PD-L1 expression by gene ... ...

    Abstract Cancer cells are thought to circumvent immune surveillance through PD-1/PD-L1 signaling. However, the genetic basis for PD-L1-PD-L1-mediated immune escape has not been completely understood, with the exception of elevated PD-L1 expression by gene amplification and the utilization of an ectopic promoter by translocation. Recently, we demonstrated a unique genetic mechanism of immune escape caused by structural variations (SVs) commonly disrupting the 3' part of the PD-L1 gene. These SVs invariably cause a marked elevation of aberrant PD-L1 transcripts that are stabilized by truncation of the 3'-untranslated region (UTR), and thereby widely affect multiple common cancer types, including adult T-cell leukemia/lymphoma (27%), diffuse large B-cell lymphoma (8%), and adenocarcinoma of the stomach (2%). All SVs invariably result in a prominent increase of aberrant PD-L1 transcripts commonly lacking an intact 3'-UTR, which most typically generate gene fusions with ectopic sequences including integrated viral genomes. In this review, the critical role of 3'-UTR disruption is briefly summarized.
    Language Japanese
    Publishing date 2017
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 390900-1
    ISSN 0485-1439
    ISSN 0485-1439
    DOI 10.11406/rinketsu.58.957
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    Zs.MO 535: Show issues

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  8. Article: Chromatin-Spliceosome Mutations in Acute Myeloid Leukemia.

    Ochi, Yotaro / Ogawa, Seishi

    Cancers

    2021  Volume 13, Issue 6

    Abstract: Recent genetic studies on large patient cohorts with acute myeloid leukemia (AML) have cataloged a comprehensive list of driver mutations, resulting in the classification of AML into distinct genomic subgroups. Among these subgroups, chromatin- ... ...

    Abstract Recent genetic studies on large patient cohorts with acute myeloid leukemia (AML) have cataloged a comprehensive list of driver mutations, resulting in the classification of AML into distinct genomic subgroups. Among these subgroups, chromatin-spliceosome (CS)-AML is characterized by mutations in the spliceosome, cohesin complex, transcription factors, and chromatin modifiers. Class-defining mutations of CS-AML are also frequently identified in myelodysplastic syndrome (MDS) and secondary AML, indicating the molecular similarity among these diseases. CS-AML is associated with myelodysplasia-related changes in hematopoietic cells and poor prognosis, and, thus, can be treated using novel therapeutic strategies and allogeneic stem cell transplantation. Functional studies of CS-mutations in mice have revealed that CS-mutations typically cause MDS-like phenotypes by altering the epigenetic regulation of target genes. Moreover, multiple CS-mutations often synergistically induce more severe phenotypes, such as the development of lethal MDS/AML, suggesting that the accumulation of many CS-mutations plays a crucial role in the progression of MDS/AML. Indeed, the presence of multiple CS-mutations is a stronger indicator of CS-AML than a single mutation. This review summarizes the current understanding of the genetic and clinical features of CS-AML and the functional roles of driver mutations characterizing this unique category of AML.
    Language English
    Publishing date 2021-03-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13061232
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  9. Article ; Online: Clonal expansion in non-cancer tissues.

    Kakiuchi, Nobuyuki / Ogawa, Seishi

    Nature reviews. Cancer

    2021  Volume 21, Issue 4, Page(s) 239–256

    Abstract: Cancer is a clonal disorder derived from a single ancestor cell and its progenies that are positively selected by acquisition of 'driver mutations'. However, the evolution of positively selected clones does not necessarily imply the presence of cancer. ... ...

    Abstract Cancer is a clonal disorder derived from a single ancestor cell and its progenies that are positively selected by acquisition of 'driver mutations'. However, the evolution of positively selected clones does not necessarily imply the presence of cancer. On the contrary, it has become clear that expansion of these clones in phenotypically normal or non-cancer tissues is commonly seen in association with ageing and/or in response to environmental insults and chronic inflammation. Recent studies have reported expansion of clones harbouring mutations in cancer driver genes in the blood, skin, oesophagus, bronchus, liver, endometrium and bladder, where the expansion could be so extensive that tissues undergo remodelling of an almost entire tissue. The presence of common cancer driver mutations in normal tissues suggests a strong link to cancer development, providing an opportunity to understand early carcinogenic processes. Nevertheless, some driver mutations are unique to normal tissues or have a mutation frequency that is much higher in normal tissue than in cancer, indicating that the respective clones may not necessarily be destined for evolution to cancer but even negatively selected for carcinogenesis depending on the mutated gene. Moreover, tissues that are remodelled by genetically altered clones might define functionalities of aged tissues or modified inflammatory processes. In this Review, we provide an overview of major findings on clonal expansion in phenotypically normal or non-cancer tissues and discuss their biological significance not only in cancer development but also in ageing and inflammatory diseases.
    MeSH term(s) Aging/genetics ; Aging/pathology ; Anemia, Aplastic/genetics ; Anemia, Aplastic/pathology ; Barrett Esophagus/genetics ; Barrett Esophagus/pathology ; Bronchi/cytology ; Bronchi/metabolism ; Carcinogenesis ; Cell Proliferation/genetics ; Clonal Evolution ; Clonal Hematopoiesis/genetics ; Clone Cells/cytology ; Colitis, Ulcerative/genetics ; Colitis, Ulcerative/pathology ; Colon/cytology ; Colon/metabolism ; Endometrium/cytology ; Endometrium/metabolism ; Esophagus/cytology ; Esophagus/metabolism ; Female ; Gastric Mucosa/metabolism ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Liver/cytology ; Liver/metabolism ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Male ; Metaplasia ; Mutation ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes/genetics ; Skin/cytology ; Skin/metabolism ; Stomach/pathology ; Urothelium/cytology ; Urothelium/metabolism
    Language English
    Publishing date 2021-02-24
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/s41568-021-00335-3
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    Zs.A 5563: Show issues Location:
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  10. Article ; Online: Cutaneous Adnexal Adenocarcinoma: Genomic Analysis and Successful HER2-targeted Therapy of Metastatic Disease.

    Hirano-Lotman, Yui / Ishida, Yoshihiro / Endo, Yuichiro / Ogawa, Seishi / Kabashima, Kenji

    Acta dermato-venereologica

    2023  Volume 103, Page(s) adv9399

    MeSH term(s) Humans ; Skin/pathology ; Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Genomics ; Receptor, ErbB-2/genetics
    Chemical Substances Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2023-08-16
    Publishing country Sweden
    Document type Journal Article
    ZDB-ID 80007-7
    ISSN 1651-2057 ; 0001-5555
    ISSN (online) 1651-2057
    ISSN 0001-5555
    DOI 10.2340/actadv.v103.9399
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