Samuel Chi‐ho Mok
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA;, firstname.lastname@example.org, (W.H.);, ...
KOL Resume for Samuel Chi‐ho Mok
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA;, (W.H.);, (L.Z.);, (S.F.-B.);, (H.T.C.);, (T.-L.Y.);, (P.T.S.);, (K.H.L.);, (S.C.M.)
The University of Texas MD Anderson Cancer Center, Houston, TX, United States
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA;, (S.Y.K.);, (K.K.W.);, (P.T.S.);, (K.H.L.)
The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at Houston, 77030, Houston, TX, USA
The University of Texas MD Anderson Cancer Center, Houston, TX
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA;, (T.-L.Y.);, (C.C.T.);, (C.S.L.);, (C.-L.A.Y.);, (M.S.T.);, (K.H.L.);, (R.S.F.);, (K.-K.W.)
The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA.
Department of Gynecologic Oncology, and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.
The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas, USA.
Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA;, (T.L.Y.);, (C.S.L.)
The University of Texas MD Anderson Cancer Center, Houston, TX, USA
The University of Texas MD Anderson Cancer Center Department of Gynecologic Oncology and Reproductive Medicine Houston Texas
Cancer Biology Program, The University of Texas at Houston Graduate School of Biomedical Sciences, Houston, TX 77030, USA
Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America
Department of Gynecologic Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, United States of America
Brigham and Women's Hospital, Harvard School of Public Health, Boston, Massachusetts, United States of America
Authors' Affiliations: Departments of Gynecologic Oncology and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas
Authors' Affiliations: Division of Gynecologic Oncology, Department of Obstetrics, Gynecology and Reproductive Biology and Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Department of Pathology, Brigham and Women's Hospital and Dana-Farber Harvard Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts; and Department of Gynecologic Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas
Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
Department of Gynecologic Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX
Department of Obstetrics, Gynecology and Reproductive Biology, Division of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Boston University School of Medicine (M.E.L.) and Brigham and Women's Hospital (S.M.) — both in Boston
Department of Obstetrics, Gynecology, and Reproductive Biology, Laboratory of Gynecologic Oncology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Gillette Center for Women's Cancer, Dana-Farber Harvard Cancer Center, Boston, MA
From the Cell and Cancer Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD
Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA
Laboratory of Gynecology Oncology, Brigham and Women's Hospital, Harvard Medical School, USA
Departments of Obstetrics, Gynecology and Reproductive Biology and
Osaka City Gen Hosp, Osaka, Japan; Univ of Tokyo, Tokyo, Japan; Tohoku Univ Graduate Sch of Medicine, Sendai, Japan; National Cancer Institute, Rockville, MD; Brigham & Women’s Hosp, Boston, MA
Samuel Chi‐ho Mok: Influence Statistics
|investigation mir155hg expression||#1|
|skov3 monolayer su11274||#1|
|brca2 primary cultures||#1|
|exon ispecific rtpcr||#1|
|knockdown xdab2 expression||#1|
|s100a7 protein plasma||#1|
|somites myogenic markers||#1|
|dab2 protein mouse||#1|
|188 unbalanced translocations||#1|
|new technologies identification||#1|
|invasion real time||#1|
|highly metastatic skov3||#1|
|identified multiple lncrnas||#1|
|highly dysregulated mirnas||#1|
|recurrent interstitial deletion||#1|
|proteomic screening study||#1|
|strongest dab2 expression||#1|
|underlying adherent cells||#1|
|impedance 4 khz||#1|
|skov3 cell mutation||#1|
|sporadic ovarian tumors||#1|
|exon piicontaining transcripts||#1|
|investigation primary tumors||#1|
|xenopus embryos vivo||#1|
|serous electrophoresis gel||#1|
|myogenic markers somites||#1|
|hdab2 tumor suppressor||#1|
|outstanding candidate review||#1|
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Prominent publications by Samuel Chi‐ho Mok
BACKGROUND: When ovarian carcinoma is diagnosed in stage I, up to 90% of patients can be cured with surgery and currently available chemotherapy. At present, less than 25% of cases are diagnosed at this stage. To increase the fraction of ovarian cancers detected at an early stage, screening strategies have been devised that utilize a rising serum CA125 level to trigger the performance of transvaginal sonography. One limitation of CA125 as an initial step in such a screening strategy is ...
|Known for Ovarian Cancers | Ca125 Expression | Neoplasm Biomarkers | Serum Markers | Early Stage|
Altered expression of BRCA1, BRCA2, and a newly identified BRCA2 exon 12 deletion variant in malignant human ovarian, prostate, and breast cancer cell lines
[ PUBLICATION ]
Germline mutations of BRCA1 and BRCA2 predispose to hereditary breast, ovarian, and possibly prostate cancer, yet structural mutations in these genes are infrequent in sporadic cancer cases. To better define the involvement of these genes in sporadic cancers, we characterized expression levels of BRCA1 and BRCA2 transcripts in cancer cell lines derived from neoplasms of the ovary, prostate, and breast and compared them with those expressed in primary cultures of normal epithelial cells ...
|Known for Breast Cancer | Brca1 Brca2 | Neoplastic Genes | Altered Expression | Exon 12|
Dicer, Drosha, and Outcomes in Patients with Ovarian Cancer
[ PUBLICATION ]
BACKGROUND: We studied Dicer and Drosha, components of the RNA-interference machinery, in ovarian cancer.
METHODS: We measured messenger RNA (mRNA) levels of Dicer and Drosha in specimens of invasive epithelial ovarian cancer from 111 patients, using a quantitative reverse-transcriptase-polymerase-chain-reaction assay, and compared the results with clinical outcomes. Validation was performed with the use of published microarray data from cohorts of patients with ovarian, breast, and lung ...
|Known for Ovarian Cancer | Dicer Drosha | Messenger Rna | Hazard Ratio | Neoplastic Humans|
Bcl-2 and p53 Protein Expression, Apoptosis, and p53 Mutation in Human Epithelial Ovarian Cancers
[ PUBLICATION ]
Bcl-2 and p53 gene products have been both linked to cell death by apoptosis. In the present study, we examined the relationship of Bcl-2 and p53 protein expression, p53 mutation and apoptosis in normal human ovaries and different types of human ovarian epithelial tumors by immunohistochemical localization, in situ terminal transferase-mediated dUTP nick end labeling and polymerase chain reaction-single strand conformation polymorphism. It was found that Bcl-2 expressed strongly in the ...
|Known for Protein Expression | Epithelial Ovarian | P53 Mutation | Malignant Tumors | Normal Ovaries|
Expression of human estrogen receptor-α and -β, progesterone receptor, and androgen receptor mRNA in normal and malignant ovarian epithelial cells
[ PUBLICATION ]
Our understanding of the roles played by sex hormones in ovarian carcinogenesis has been limited by a lack of data concerning the mode of sex hormone action in human ovarian surface epithelial (HOSE) cells, the tissue of origin of >90% of ovarian cancers. We have compared the relative abundance of estrogen receptor (ER)alpha, ERbeta, progesterone receptor (PR), and androgen receptor (AR) mRNA in four primary cultures of HOSE cells obtained from postmenopausal women to those found in late ...
|Known for Estrogen Receptor | Epithelial Cells | Eralpha Erbeta | Malignant Ovarian | Neoplastic Humans|
TGF-β Modulates Ovarian Cancer Invasion by Upregulating CAF-Derived Versican in the Tumor Microenvironment
[ PUBLICATION ]
TGF-β has limited effects on ovarian cancer cells, but its contributions to ovarian tumor growth might be mediated through elements of the tumor microenvironment. In the present study, we tested the hypothesis that TGF modulates ovarian cancer progression by modulating the contribution of cancer-associated fibroblasts (CAF) that are present in the microenvironment. Transcriptome profiling of microdissected stromal and epithelial components of high-grade serous ovarian tumors and ...
|Known for Tumor Microenvironment | Ovarian Cancer | Transforming Growth Factor | Tgf Β | Vcan Expression|
Prostasin, a Potential Serum Marker for Ovarian Cancer: Identification Through Microarray Technology
[ PUBLICATION ]
BACKGROUND: Screening biomarkers for ovarian cancer are needed because of its late stage at diagnosis and poor survival. We used microarray technology to identify overexpressed genes for secretory proteins as potential serum biomarkers and selected prostasin, a serine protease normally secreted by the prostate gland, for further study.
METHODS: RNA was isolated and pooled from three ovarian cancer cell lines and from three normal human ovarian surface epithelial (HOSE) cell lines. ...
|Known for Ovarian Cancer | Microarray Technology | Serum Marker | Neoplasm Sensitivity | Messenger Rna|
A Population-Based Study of BRCA1 and BRCA2 Mutations in Jewish Women With Epithelial Ovarian Cancer
[ PUBLICATION ]
OBJECTIVE: To determine the frequency of BRCA1 mutations 185delAG and 5382insC and BRCA2 mutation 6174delT in Jewish women with ovarian cancer and in matched controls in a population-based study.
METHODS: Forty-eight Jewish women with epithelial ovarian cancer (32 invasive and 16 borderline) and 33 Jewish control subjects were obtained from a population-based, case-control study of ovarian cancer in eastern Massachusetts and New Hampshire. Mutational analysis on exons 2 and 20 of BRCA1 ...
|Known for Brca2 Mutations | Jewish Women | Ovarian Cancer | Female Genes | Mutational Analysis|
Matrix Metalloproteinases and Their Inhibitors in Gestational Trophoblastic Diseases and Normal Placenta
[ PUBLICATION ]
OBJECTIVE: Our purpose was to investigate the expression of matrix metalloproteinases (MMPs) in gestational trophoblastic diseases and normal first-trimester placenta.
METHODS: Paraffin sections of 16 partial moles, 25 complete moles, 10 gestational choriocarcinomas, and 11 normal first-trimester placentas were studied immunohistochemically for expression of MMP-1, MMP-2, MMP-3, MMP-9, MMP-13, and tissue inhibitor of metalloproteinase-1 (TIMP-1).
RESULTS: Nine (90.0%) of the ...
|Known for Normal Placenta | Matrix Metalloproteinases | Extravillous Trophoblast | Choriocarcinoma Expression | Tissue Inhibitor|
SPARC (Secreted Protein Acidic and Rich in Cysteine) Induces Apoptosis in Ovarian Cancer Cells
[ PUBLICATION ]
Secreted protein acidic and rich in cysteine (SPARC) is an extracellular Ca(2+)-binding matricellular glycoprotein that associates with cell populations undergoing migration, morphogenesis, and differentiation. Studies on endothelial cells have established that its principal functions in vitro are counteradhesion and antiproliferation. The mechanism(s) underlying these antitumor effects is unknown. In this study, we showed that SPARC expression in ovarian cancer cells is inversely ...
|Known for Cancer Cells | Secreted Protein | Cysteine Sparc | Neoplastic Humans | Expression Regulation|
PAX2 Expression in Low Malignant Potential Ovarian Tumors and Low-Grade Ovarian Serous Carcinomas
[ PUBLICATION ]
Ovarian tumors of low malignant potential and low-grade ovarian serous carcinomas are thought to represent different stages on a tumorigenic continuum and to develop along pathways distinct from high-grade ovarian serous carcinoma. We performed gene expression profiling on three normal human ovarian surface epithelia samples, and 10 low-grade and 10 high-grade ovarian serous carcinomas. Analysis of gene expression profiles of these samples has identified 80 genes upregulated and 232 ...
|Known for Pax2 Expression | Ovarian Serous | Low Grade | Malignant Potential | Upregulated Genes|
OBJECTIVES: We have previously described that bioactive lysophospholipids-lysophosphatidic acid (LPA), sphingosine 1-phosphate (S1P), and sphingosylphosphorylcholine (SPC)-are present in ascitic fluids from patients with ovarian cancer. To understand the role of these lipids in ovarian cancer, we investigated the effects of these lipids on interleukin-8 (IL-8) production in ovarian cancer cells. IL-8 is a proinflammatory and proangiogenic factor, which is potentially involved in ovarian ...
|Known for Ovarian Cancer Cells | Lpa S1p | Neoplastic Humans | Lysophospholipids Increase | Mrna Levels|
Key People For Ovarian Cancer
Samuel Chi‐ho Mok:Expert Impact
Concepts for whichSamuel Chi‐ho Mokhas direct influence:Ovarian cancer, Normal placenta, Complete mole, Cancer cells, Ovarian cancer cells, Papillary serous carcinoma, Epithelial ovarian, Ovarian tumors.
Samuel Chi‐ho Mok:KOL impact
Concepts related to the work of other authors for whichfor which Samuel Chi‐ho Mok has influence:Ovarian cancer, Gene expression, Tumor microenvironment, Cell proliferation, Neoplastic humans.
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