Hidetaka Katabuchi

ORCID: 0000-0002-2403-6134
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About
Contact & Profiles
Research Areas
  • Ovarian cancer diagnosis and treatment
  • Endometrial and Cervical Cancer Treatments
  • Endometriosis Research and Treatment
  • Uterine Myomas and Treatments
  • Cancer Genomics and Diagnostics
  • Reproductive System and Pregnancy
  • Cancer Research and Treatments
  • Cervical Cancer and HPV Research
  • Gestational Trophoblastic Disease Studies
  • Reproductive Biology and Fertility
  • Pregnancy and preeclampsia studies
  • Virus-based gene therapy research
  • Estrogen and related hormone effects
  • Monoclonal and Polyclonal Antibodies Research
  • Intraperitoneal and Appendiceal Malignancies
  • Cancer Cells and Metastasis
  • Ectopic Pregnancy Diagnosis and Management
  • Maternal and fetal healthcare
  • Cancer Risks and Factors
  • Genetic Syndromes and Imprinting
  • Cancer Mechanisms and Therapy
  • Prenatal Screening and Diagnostics
  • Sarcoma Diagnosis and Treatment
  • Immune Cell Function and Interaction
  • Cancer-related molecular mechanisms research

Kumamoto University
2015-2024

Honda (Japan)
2019

Kumamoto Medical Center
2018

Johns Hopkins University
1995-2014

Ministry of National Defence and Sport
2013

Jichi Medical University
2012

Niigata University
2012

Yokohama City University
2012

Yokohama City University Hospital
2012

Kagoshima City Hospital
2012

Tumor‐associated macrophages (TAM) are known to possess the immunosuppressive M2 macrophage phenotype. They contribute tumor growth, invasion, and metastasis by producing various mediators. Macrophages, especially polarized macrophages, preferentially express CD163 CD204, but few studies have investigated phenotypes in human ovarian tumors. The purpose of present study was therefore results on differentiation serous mucinous epithelial method focused immunostaining paraffin‐embedded samples....

10.1111/j.1440-1827.2009.02369.x article EN Pathology International 2009-04-21

High-grade serous ovarian cancers are heterogeneous not only in terms of clinical outcome but also at the molecular level. Our aim was to establish a novel risk classification system based on gene expression signature for predicting overall survival, leading suggesting therapeutic strategies high-risk patients.In this large-scale cross-platform study six microarray data sets consisting 1,054 cancer patients, we developed survival by applying elastic net and 10-fold cross-validation Japanese...

10.1158/1078-0432.ccr-11-2725 article EN Clinical Cancer Research 2012-01-13

Ascites macrophages in advanced epithelial ovarian cancer (AdEOC) are involved metastasis and progression by modifying the tumor microenvironment. However, precise mechanisms of cell‐to‐cell interaction between cells still unclear. This study focused on activation signal transducer activator transcription 3 (Stat3) which is a critical transduction molecule at point convergence for numerous oncogenic signaling pathways as well controlling M2‐poralization macrophages. AdEOC ascites, high...

10.1111/j.1349-7006.2010.01652.x article EN Cancer Science 2010-06-23

Advanced-stage ovarian cancer patients are generally treated with platinum/taxane-based chemotherapy after primary debulking surgery. However, there is a wide range of outcomes for individual patients. Therefore, the clinicopathological factors alone insufficient predicting prognosis. Our aim to identify progression-free survival (PFS)-related molecular profile advanced-stage serous cancer.Advanced-stage tissues from 110 Japanese who underwent surgery and were profiled using oligonucleotide...

10.1371/journal.pone.0009615 article EN cc-by PLoS ONE 2010-03-11

The Fourth Edition of the Guidelines for Treatment Uterine Body Neoplasm was published in 2018. These guidelines include 9 chapters: 1. Overview guidelines, 2. Initial treatment endometrial cancer, 3. Postoperative adjuvant therapy 4. Post-treatment surveillance 5. advanced or recurrent 6. Fertility-sparing therapy, 7. uterine carcinosarcoma and sarcoma, 8. trophoblastic disease, 9. Document collection; nine algorithms: 1-3. carcinosarcoma, choriocarcinoma. Each chapter includes overviews...

10.3802/jgo.2020.31.e18 article EN cc-by-nc Journal of Gynecologic Oncology 2019-10-25

Surgical pathologists often encounter hydropic villi in products of conception at the first trimester and must determine whether represent complete hydatidiform mole (CM), partial (PM), or abortion (HA). The distinction between these is important for determining appropriate treatment patients. This study assessed interobserver intraobserver variability histologic diagnosis among 5 placental pathologists. To evaluate variability, one representative slide from each 50 mixed cases PM, CM, HA...

10.1097/01.pas.0000157996.23059.c1 article EN The American Journal of Surgical Pathology 2005-06-14

Ovarian surface epithelium (OSE) is considered to give rise epithelial ovarian carcinomas (EOCs). To elucidate early processes contributing the development of EOCs from OSE, two batches primary human OSE cells were transduced with non-viral genes (mutant Cdk4 , cyclinD1 and hTERT ) so as efficiently establish normal diploid without chromosomal instability. Then defined genetic alterations frequently observed in into cells. A combination p53 inactivation oncogenic K ras transduction did not...

10.1093/carcin/bgp007 article EN Carcinogenesis 2009-01-06

Epithelial ovarian cancer is a highly lethal malignancy; moreover, overcoming chemoresistance the major challenging in treating patients. The stem cell (CSC) hypothesis considers CSCs to be main culprits driving tumor initiation, metastasis, and resistance conventional therapy. Although growing evidence suggest that are responsible for chemoresistance, contribution of CSC marker EpCAM chemotherapy remains unresolved.Here we have demonstrated cancers containing high levels significantly much...

10.18632/oncotarget.17871 article EN Oncotarget 2017-05-15

Cancer stem cells ( CSC s) drive tumor initiation and metastasis in several types of human cancer. However, the contribution ovarian s to peritoneal remains unresolved. The cell adhesion molecule CD 44 has been identified as a major marker for solid tumors, including epithelial exists standard form 44s) also numerous variant isoforms 44v) generated by alternative mRNA splicing. Here we show that disseminated tumors pelvic peritoneum contain highly enriched 44v6‐positive cancer cells, which...

10.1111/cas.12765 article EN cc-by-nc-nd Cancer Science 2015-08-06

Lymph node ( LN ) macrophages play critical roles in anti‐tumor immunity, which develops via the activation of cytotoxic T cells CTL and NK cells. The present study aims to determine prognostic significance CD 169 + patients with endometrial carcinoma EC ). number or ‐to‐ 68 macrophage ratio regional RLN ), 8 57 tumor tissues were investigated by immunohistochemistry paraffin‐embedded tissue samples from 79 . A high density was correlated an early clinical stage no metastasis. a...

10.1111/cas.12929 article EN cc-by-nc-nd Cancer Science 2016-03-19

Ultrastructure studies of pelvic peritoneal tissue from women undergoing laparotomy suggest that before endometriosis has become established in the peritoneum, there might be a metaplastic change by mesothelial cells into endometrial glandular cells. A new vitro experimental model using human ovarian surface epithelium shown evidence endometriotic lesions can arise process metaplasia epithelium. In this model, when both and stromal were cocultured with 17β estradiol three-dimensional...

10.1159/000052855 article EN Gynecologic and Obstetric Investigation 1999-01-01

Ovarian serous carcinoma (OSC) is the most common and lethal histologic type of ovarian epithelial malignancy. Mutations TP53 dysfunction Brca1 and/or Brca2 tumor-suppressor proteins have been implicated in molecular pathogenesis a large fraction OSCs, but frequent somatic mutations other well-established genes not identified. Using genome-wide screen DNA copy number alterations 36 primary we identified two tumors with apparent homozygous deletions NF1 gene. Subsequently, 18...

10.1593/neo.08784 article EN cc-by-nc-nd Neoplasia 2008-12-01
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