The Experts below are selected from a list of 120 Experts worldwide ranked by ideXlab platform
Daniel C Chung - One of the best experts on this subject based on the ideXlab platform.
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surveillance endoscopy in the management of hereditary diffuse gastric cancer syndrome
Clinical Gastroenterology and Hepatology, 2021Co-Authors: Madeline Friedman, Tomer Adar, Devanshi Patel, Gregory Y Lauwers, Sam S Yoon, John T Mullen, Daniel C ChungAbstract:Hereditary diffuse gastric cancer (HDGC) syndrome results from a germline CDH1 mutation, and microscopic foci of Signet-Ring Carcinoma cells (SRCC) are present in nearly all gastrectomy specimens.1 The lifetime risk of invasive gastric cancer (GC) has been thought to be 70%,2 but recent data have suggested a lower risk of 37%.3 Prophylactic total gastrectomy is considered the standard of care, but many patients choose surveillance endoscopy instead. We sought to define the outcomes in CDH1-positive individuals who pursued endoscopic surveillance.
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hereditary diffuse gastric cancer updated consensus guidelines for clinical management and directions for future research
Journal of Medical Genetics, 2010Co-Authors: Rebecca C Fitzgerald, Daniel C Chung, Richard H Hardwick, David G Huntsman, Fatima Carneiro, Parry Guilford, Vanessa Blair, Jeffrey A Norton, Krishnadath Ragunath, Han J Van KriekenAbstract:25-30% of families fulfilling the criteria for hereditary diffuse gastric cancer have germline mutations of the CDH1 (E-cadherin) gene. In light of new data and advancement of technologies, a multidisciplinary workshop was convened to discuss genetic testing, surgery, endoscopy and pathology reporting. The updated recommendations include broadening of CDH1 testing criteria such that: histological confirmation of diffuse gastric criteria is only required for one family member; inclusion of individuals with diffuse gastric cancer before the age of 40 years without a family history; and inclusion of individuals and families with diagnoses of both diffuse gastric cancer (including one before the age of 50 years) and lobular breast cancer. Testing is considered appropriate from the age of consent following counselling and discussion with a multidisciplinary team. In addition to direct sequencing, large genomic rearrangements should be sought. Annual mammography and breast MRI from the age of 35 years is recommended for women due to the increased risk for lobular breast cancer. In mutation positive individuals prophylactic total gastrectomy at a centre of excellence should be strongly considered. Protocolised endoscopic surveillance in centres with endoscopists and pathologists experienced with these patients is recommended for: those opting not to have gastrectomy, those with mutations of undetermined significance, and in those families for whom no germline mutation is yet identified. The systematic histological study of prophylactic gastrectomies almost universally shows pre-invasive lesions including in situ Signet Ring Carcinoma with pagetoid spread of Signet Ring cells. Expert histopathological confirmation of these early lesions is recommended.
Farabi Hussain - One of the best experts on this subject based on the ideXlab platform.
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a rare case of concurrent Signet Ring Carcinoma of breast and microangiopathic hemolytic anemia
Journal of Surgical Case Reports, 2016Co-Authors: Kelly Lara, Esther Bae, Hanna Park, Farabi HussainAbstract:Microangiopathic hemolytic anemia (MAHA) can be an uncommon presentation of an underlying malignancy, most often due to Signet-Ring cell Carcinoma (SRCC). Additionally, pure SRCC in a breast primary-tumor comprises <2% of all breast cancers (Shin SY, Park H, Chae SW, Woo HY. Microangiopathic hemolytic anemia as the first manifestation of metastatic Signet-Ring cell Carcinoma of unknown origin: a case report and review of literature. Kor J Lab Med 2011;31:157–61). To the best of our knowledge, the combination of these two entities, pure breast primary SRCC along with MAHA, has not been reported. Here, we present such a rare case. We also evaluate the current literature regarding this and similar disease processes, of which evidence is scarce and further research is needed.
Han J Van Krieken - One of the best experts on this subject based on the ideXlab platform.
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hereditary diffuse gastric cancer updated consensus guidelines for clinical management and directions for future research
Journal of Medical Genetics, 2010Co-Authors: Rebecca C Fitzgerald, Daniel C Chung, Richard H Hardwick, David G Huntsman, Fatima Carneiro, Parry Guilford, Vanessa Blair, Jeffrey A Norton, Krishnadath Ragunath, Han J Van KriekenAbstract:25-30% of families fulfilling the criteria for hereditary diffuse gastric cancer have germline mutations of the CDH1 (E-cadherin) gene. In light of new data and advancement of technologies, a multidisciplinary workshop was convened to discuss genetic testing, surgery, endoscopy and pathology reporting. The updated recommendations include broadening of CDH1 testing criteria such that: histological confirmation of diffuse gastric criteria is only required for one family member; inclusion of individuals with diffuse gastric cancer before the age of 40 years without a family history; and inclusion of individuals and families with diagnoses of both diffuse gastric cancer (including one before the age of 50 years) and lobular breast cancer. Testing is considered appropriate from the age of consent following counselling and discussion with a multidisciplinary team. In addition to direct sequencing, large genomic rearrangements should be sought. Annual mammography and breast MRI from the age of 35 years is recommended for women due to the increased risk for lobular breast cancer. In mutation positive individuals prophylactic total gastrectomy at a centre of excellence should be strongly considered. Protocolised endoscopic surveillance in centres with endoscopists and pathologists experienced with these patients is recommended for: those opting not to have gastrectomy, those with mutations of undetermined significance, and in those families for whom no germline mutation is yet identified. The systematic histological study of prophylactic gastrectomies almost universally shows pre-invasive lesions including in situ Signet Ring Carcinoma with pagetoid spread of Signet Ring cells. Expert histopathological confirmation of these early lesions is recommended.
Toshio Bessho - One of the best experts on this subject based on the ideXlab platform.
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human gastric Signet Ring Carcinoma kato iii cell apoptosis induced by vitex agnus castus fruit extract through intracellular oxidative stress
The International Journal of Biochemistry & Cell Biology, 2005Co-Authors: Kunio Ohyama, Takenori Akaike, Masahiko Imai, Hiroo Toyoda, Chieko Hirobe, Toshio BesshoAbstract:We have previously reported that an ethanol extract of the dried ripe fruit of Vitex agnus-castus (Vitex) displays cytotoxic activity against certain kinds of human cancer cell line resulting in the induction of apoptosis. In this paper, we investigate the molecular mechanism of apoptosis induced by Vitex using a human gastric Signet Ring Carcinoma cell line, KATO-III. DNA fragmentation was observed in Vitex-treated KATO-III cells in a time- and dose-dependent manner. DNA fragmentation was accompanied by the following phenomena: elevation in the level of hemeoxygenase-1 protein and thioredoxin reductase mRNA; repression of Mn-superoxide dismutase and catalase mRNAs; release of cytochrome c from mitochondria into the cytosol; activation of caspases-8, -9 and -3; decrease in the level of Bcl-2, Bcl-XL and Bid protein; increase in the level of Bad protein. The intracellular oxidized state, measured using 2',7'-dichlorofluorescin diacetate, increased after Vitex treatment. While the amount of intracellular GSH decreased significantly after treatment with Vitex, the level of GSSG was unaffected. Furthermore, no significant perturbation in the amount of proteins/mRNAs related to glutathione metabolism could be detected. These apoptotic alterations induced by exposure to Vitex were blocked by the presence of an anti-oxidative reagent, N-acetyl-l-cysteine, or the addition of exogenous GSH. Our results demonstrate that intracellular oxidative stress and mitochondrial membrane damage is responsible for Vitex-induced apoptosis, which may be mediated by a diminution of reduced type glutathione within the cell.
Kunio Ohyama - One of the best experts on this subject based on the ideXlab platform.
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human gastric Signet Ring Carcinoma kato iii cell apoptosis induced by vitex agnus castus fruit extract through intracellular oxidative stress
The International Journal of Biochemistry & Cell Biology, 2005Co-Authors: Kunio Ohyama, Takenori Akaike, Masahiko Imai, Hiroo Toyoda, Chieko Hirobe, Toshio BesshoAbstract:We have previously reported that an ethanol extract of the dried ripe fruit of Vitex agnus-castus (Vitex) displays cytotoxic activity against certain kinds of human cancer cell line resulting in the induction of apoptosis. In this paper, we investigate the molecular mechanism of apoptosis induced by Vitex using a human gastric Signet Ring Carcinoma cell line, KATO-III. DNA fragmentation was observed in Vitex-treated KATO-III cells in a time- and dose-dependent manner. DNA fragmentation was accompanied by the following phenomena: elevation in the level of hemeoxygenase-1 protein and thioredoxin reductase mRNA; repression of Mn-superoxide dismutase and catalase mRNAs; release of cytochrome c from mitochondria into the cytosol; activation of caspases-8, -9 and -3; decrease in the level of Bcl-2, Bcl-XL and Bid protein; increase in the level of Bad protein. The intracellular oxidized state, measured using 2',7'-dichlorofluorescin diacetate, increased after Vitex treatment. While the amount of intracellular GSH decreased significantly after treatment with Vitex, the level of GSSG was unaffected. Furthermore, no significant perturbation in the amount of proteins/mRNAs related to glutathione metabolism could be detected. These apoptotic alterations induced by exposure to Vitex were blocked by the presence of an anti-oxidative reagent, N-acetyl-l-cysteine, or the addition of exogenous GSH. Our results demonstrate that intracellular oxidative stress and mitochondrial membrane damage is responsible for Vitex-induced apoptosis, which may be mediated by a diminution of reduced type glutathione within the cell.
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cytotoxicity and apoptotic inducibility of vitex agnus castus fruit extract in cultured human normal and cancer cells and effect on growth
Biological & Pharmaceutical Bulletin, 2003Co-Authors: Kunio Ohyama, Takenori Akaike, Chieko Hirobe, Toshio YamakawaAbstract:A crude extract was prepared with ethanol from dried ripened Vitex agnus-castus fruits growing in Israel (Vitex extract). Cytotoxicity of the extract against human uterine cervical canal fibroblast (HCF), human embryo fibroblast (HE-21), ovarian cancer (MCF-7), cervical Carcinoma (SKG-3a), breast Carcinoma (SKOV-3), gastric Signet Ring Carcinoma (KATO-III), colon Carcinoma (COLO 201), and small cell lung Carcinoma (Lu-134-A-H) cells was examined. After culture for 24 h (logarithmic growth phase) or 72 h (stationary growth phase), the cells were treated with various concentrations of Vitex extract. In both growth phases, higher growth activity of cells and more cytotoxic activity of Vitex extract were seen. The cytotoxic activity against stationary growth-phase cells was less than that against logarithmic growth-phase cells. DNA fragmentation of Vitex extract-treated cells was seen in SKOV-3, KATO-III, COLO 201, and Lu-134-A-H cells. The DNA fragmentation in Vitex extract-treated KATO-III cells was inhibited by the presence of the antioxidative reagent pyrrolidine dithiocarbamate or N-acetyl-L-cysteine (NAC). Western blotting analysis showed that in Vitex extract-treated KATO-III cells, the presence of NAC also inhibited the expression of heme oxygenase-1 and the active forms of caspases-3, -8 and -9. It is concluded that the cytotoxic activity of Vitex extract may be attributed to the effect on cell growth, that cell death occurs through apoptosis, and that this apoptotic cell death may be attributed to increased intracellular oxidation by Vitex extract treatment.