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Christy E Cauley - One of the best experts on this subject based on the ideXlab platform.

  • infiltrating tumor border configuration is a poor prognostic factor in stage ii and iii Colon Adenocarcinoma
    Annals of Surgical Oncology, 2021
    Co-Authors: Yasmeen Z Qwaider, Naomi M Sell, Caitlin Stafford, Hiroko Kunitake, James C Cusack, Rocco Ricciardi, Liliana Bordeianou, Vikram Deshpande, Robert N Goldstone, Christy E Cauley
    Abstract:

    Tumor border configuration (TBC) is a prognostic factor in colorectal Adenocarcinoma; however, the significance of TBC is not well-documented in Colon Adenocarcinoma alone. Our aim was to study the effect of TBC on overall and disease-free survival in stage II and III Colon Adenocarcinoma. We included patients with stage II and III Colon Adenocarcinoma who were surgically treated at a tertiary medical center between 2004 and 2015, to ensure long-term follow-up. Patients were stratified into four groups based on stage and TBC. A Cox regression was used to model the relationship of groups while accounting for relevant confounders. The cohort consisted of 700 patients (371 stage II and 329 stage III). Infiltrating TBC was statistically significantly associated with stage (p < 0.001) and extramural vascular invasion (p < 0.001), but not histologic grade (p = 0.7). Compared with pushing TBC, infiltrating TBC increased the hazard of death by a factor of 1.8 [95% confidence interval (CI) 1.4–2.4; p < 0.001] and 1.7 (95% CI 1.3–2.2; p < 0.001). The hazard of death in patients with stage II disease (infiltrating TBC) or stage III disease (pushing TBC) was not significantly different (adjusted hazard ratio 1.1, 95% CI 0.7–1.7; p = 0.8). Infiltrating TBC is a high-risk feature in patients with stage II and III Colon Adenocarcinoma. Stage II disease patients with infiltrating TBC and who are node-negative should be considered for adjuvant chemotherapy.

  • infiltrating tumor border configuration is a poor prognostic factor in stage ii and iii Colon Adenocarcinoma
    Annals of Surgical Oncology, 2020
    Co-Authors: Yasmeen Z Qwaider, Naomi M Sell, Caitlin Stafford, Hiroko Kunitake, James C Cusack, Rocco Ricciardi, Liliana Bordeianou, Vikram Deshpande, Robert N Goldstone, Christy E Cauley
    Abstract:

    INTRODUCTION Tumor border configuration (TBC) is a prognostic factor in colorectal Adenocarcinoma; however, the significance of TBC is not well-documented in Colon Adenocarcinoma alone. OBJECTIVE Our aim was to study the effect of TBC on overall and disease-free survival in stage II and III Colon Adenocarcinoma. METHODS We included patients with stage II and III Colon Adenocarcinoma who were surgically treated at a tertiary medical center between 2004 and 2015, to ensure long-term follow-up. Patients were stratified into four groups based on stage and TBC. A Cox regression was used to model the relationship of groups while accounting for relevant confounders. RESULTS The cohort consisted of 700 patients (371 stage II and 329 stage III). Infiltrating TBC was statistically significantly associated with stage (p < 0.001) and extramural vascular invasion (p < 0.001), but not histologic grade (p = 0.7). Compared with pushing TBC, infiltrating TBC increased the hazard of death by a factor of 1.8 [95% confidence interval (CI) 1.4-2.4; p < 0.001] and 1.7 (95% CI 1.3-2.2; p < 0.001). The hazard of death in patients with stage II disease (infiltrating TBC) or stage III disease (pushing TBC) was not significantly different (adjusted hazard ratio 1.1, 95% CI 0.7-1.7; p = 0.8). CONCLUSION Infiltrating TBC is a high-risk feature in patients with stage II and III Colon Adenocarcinoma. Stage II disease patients with infiltrating TBC and who are node-negative should be considered for adjuvant chemotherapy.

Yun-hee Shon - One of the best experts on this subject based on the ideXlab platform.

  • Chemopreventive effects of polysaccharides extract from Asterina pectinifera on HT-29 human Colon Adenocarcinoma cells.
    BMB reports, 2009
    Co-Authors: Kyung-soo Nam, Yun-hee Shon
    Abstract:

    We examined the effects of polysaccharides extracted from Asterina pectinifera on the activities of quinone reductase (QR), glutathione S-transferase (GST), ornithine decarboxylase (ODC), cyclooxygenase (COX)-2 and glutathione (GSH) levels in HT-29 human Colon Adenocarcinoma cells. We found that the polysaccharides extract induced QR activity in a dose-dependent manner over a concentration range of 20 approximately 60 microg/ml and increased GST activity as much as 1.4-fold over controls. GSH levels were increased 1.3- and 1.5-fold with the extract at 40 and 60 microg/ml, respectively. The activity and protein expression of ODC in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Colon cancer cells was inhibited by the extract. The polysaccharides suppressed TPA-induced prostaglandin (PG) production. These data indicate that polysaccharides from A. pectinifera increase phase II detoxification enzyme activity and inhibit ODC and COX-2 activities in HT-29 human Colon Adenocarcinoma cells. Consequently, this effect may contribute to the protective effect of polysaccharides from A. pectinifera against Colon cancer.

  • pectinifera on HT-29 human Colon Adenocarcinoma cells
    2008
    Co-Authors: Kyung-soo Nam, Yun-hee Shon
    Abstract:

    We examined the effects of polysaccharides extracted from Asterina pectinifera on the activities of quinone reductase (QR), glutathione S-transferase (GST), ornithine decarboxylase (ODC), cyclooxygenase (COX)-2 and glutathione (GSH) levels in HT-29 human Colon Adenocarcinoma cells. We found that the poly-saccharides extract induced QR activity in a dose-dependent manner over a concentration range of 20∼60 μg/ml and in-creased GST activity as much as 1.4-fold over controls. GSH lev-els were increased 1.3- and 1.5-fold with the extract at 40 and 60 μg/ml, respectively. The activity and protein expression of ODC in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Colon cancer cells was inhibited by the extract. The polysaccharides suppressed TPA-induced prostaglandin (PG) production. These data indicate that polysaccharides from A. pectinifera increase phase II detoxification enzyme activity and inhibit ODC and COX-2 activities in HT-29 human Colon Adenocarcinoma cells. Consequently, this effect may contribute to the protective effect of polysaccharides from A. pectinifera against Colon cancer. [BMB reports 2009; 42(5): 277-280

  • chemopreventive effect of protein extract of asterina pectinifera in ht 29 human Colon Adenocarcinoma cells
    Archives of Pharmacal Research, 2006
    Co-Authors: Yun-hee Shon, Kyung-soo Nam
    Abstract:

    We investigated the effect of protein extract ofAsterina pectinifera on the activity of 4 enzymes that may play a role in Adenocarcinoma of the Colon: quinone reductase (QR), glutathioneS-transferase (GST), ornithine decarboxylase (ODC), and cyclooxygenase (COX)-2. QR and GST activity increased in HT-29 human Colon Adenocarcinoma cells increased that had been exposed to 4 concentrations of the protein extract (80, 160, 200 and 240 μg/mL). Additionally, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ODC activity decreased significantly in cells exposed to the extract in concentrations of 160 μg/mL (p<0.05), 200 μg/mL (p<0.005), and 240 μg/mL (p<0.005). TPA-induced COX-2 activity also decreased in cells exposed to extract concentrations of 10, 20, 40, and 60 μg/mL. COX-2 expression was also inhibited in cells exposed to this extract. These results suggest that this protein extract ofA pectinifera has chemopreventive activity in HT-29 human Colon Adenocarcinoma cells, and therefore, may have the potential to function as a chemopreventive agent in human colorectal cancer.

Kyung-soo Nam - One of the best experts on this subject based on the ideXlab platform.

  • Chemopreventive effects of polysaccharides extract from Asterina pectinifera on HT-29 human Colon Adenocarcinoma cells.
    BMB reports, 2009
    Co-Authors: Kyung-soo Nam, Yun-hee Shon
    Abstract:

    We examined the effects of polysaccharides extracted from Asterina pectinifera on the activities of quinone reductase (QR), glutathione S-transferase (GST), ornithine decarboxylase (ODC), cyclooxygenase (COX)-2 and glutathione (GSH) levels in HT-29 human Colon Adenocarcinoma cells. We found that the polysaccharides extract induced QR activity in a dose-dependent manner over a concentration range of 20 approximately 60 microg/ml and increased GST activity as much as 1.4-fold over controls. GSH levels were increased 1.3- and 1.5-fold with the extract at 40 and 60 microg/ml, respectively. The activity and protein expression of ODC in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Colon cancer cells was inhibited by the extract. The polysaccharides suppressed TPA-induced prostaglandin (PG) production. These data indicate that polysaccharides from A. pectinifera increase phase II detoxification enzyme activity and inhibit ODC and COX-2 activities in HT-29 human Colon Adenocarcinoma cells. Consequently, this effect may contribute to the protective effect of polysaccharides from A. pectinifera against Colon cancer.

  • pectinifera on HT-29 human Colon Adenocarcinoma cells
    2008
    Co-Authors: Kyung-soo Nam, Yun-hee Shon
    Abstract:

    We examined the effects of polysaccharides extracted from Asterina pectinifera on the activities of quinone reductase (QR), glutathione S-transferase (GST), ornithine decarboxylase (ODC), cyclooxygenase (COX)-2 and glutathione (GSH) levels in HT-29 human Colon Adenocarcinoma cells. We found that the poly-saccharides extract induced QR activity in a dose-dependent manner over a concentration range of 20∼60 μg/ml and in-creased GST activity as much as 1.4-fold over controls. GSH lev-els were increased 1.3- and 1.5-fold with the extract at 40 and 60 μg/ml, respectively. The activity and protein expression of ODC in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Colon cancer cells was inhibited by the extract. The polysaccharides suppressed TPA-induced prostaglandin (PG) production. These data indicate that polysaccharides from A. pectinifera increase phase II detoxification enzyme activity and inhibit ODC and COX-2 activities in HT-29 human Colon Adenocarcinoma cells. Consequently, this effect may contribute to the protective effect of polysaccharides from A. pectinifera against Colon cancer. [BMB reports 2009; 42(5): 277-280

  • chemopreventive effect of protein extract of asterina pectinifera in ht 29 human Colon Adenocarcinoma cells
    Archives of Pharmacal Research, 2006
    Co-Authors: Yun-hee Shon, Kyung-soo Nam
    Abstract:

    We investigated the effect of protein extract ofAsterina pectinifera on the activity of 4 enzymes that may play a role in Adenocarcinoma of the Colon: quinone reductase (QR), glutathioneS-transferase (GST), ornithine decarboxylase (ODC), and cyclooxygenase (COX)-2. QR and GST activity increased in HT-29 human Colon Adenocarcinoma cells increased that had been exposed to 4 concentrations of the protein extract (80, 160, 200 and 240 μg/mL). Additionally, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ODC activity decreased significantly in cells exposed to the extract in concentrations of 160 μg/mL (p<0.05), 200 μg/mL (p<0.005), and 240 μg/mL (p<0.005). TPA-induced COX-2 activity also decreased in cells exposed to extract concentrations of 10, 20, 40, and 60 μg/mL. COX-2 expression was also inhibited in cells exposed to this extract. These results suggest that this protein extract ofA pectinifera has chemopreventive activity in HT-29 human Colon Adenocarcinoma cells, and therefore, may have the potential to function as a chemopreventive agent in human colorectal cancer.

Hiroshige Hibasami - One of the best experts on this subject based on the ideXlab platform.

  • induction of apoptosis by gallic acid in human stomach cancer kato iii and Colon Adenocarcinoma colo 205 cell lines
    Oncology Reports, 2000
    Co-Authors: Kazumi Yoshioka, Tomoko Kataoka, Tomoko Hayashi, M Hasegawa, Yaeko Ishi, Hiroshige Hibasami
    Abstract:

    Antitumor effects of gallic acid on human stomach cancer KATO III cells and human Colon Adenocarcinoma COLO 205 cells were investigated. The exposures of KATO III and COLO 205 cells to gallic acid led to both growth inhibition and induction of apoptosis. Morphological changes showing apoptotic bodies were observed in both the cell lines treated with gallic acid. The fragmentations by gallic acid of DNA to oligonucleosomal-sized fragments, that are characteristics of apoptosis, were observed to be concentration- and time-dependent. These findings suggest that growth inhibitions by gallic acid of KATO III cells and COLO 205 cells result from the apoptosis induced by gallic acid. Thus, gallic acid might be a candidate drug for digestive gut cancer treatment to overcome the resistance to chemotherapeutic drugs.

Basil Rigas - One of the best experts on this subject based on the ideXlab platform.

  • effect of aspirin on induction of apoptosis in ht 29 human Colon Adenocarcinoma cells
    Biochemical Pharmacology, 1998
    Co-Authors: Liang Qiao, Rashid Hanif, Eleana Sphicas, Steven J Shiff, Basil Rigas
    Abstract:

    Abstract Aspirin (ASA) and other nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit colorectal tumorigenesis. Apoptosis is a critical determinant of tissue mass homeostasis and may play a role in carcinogenesis. We studied the effect of ASA on the survival of a human Colon cancer cell line using more sensitive methods than we had applied previously. ASA induced apoptosis in HT-29 Colon Adenocarcinoma cells at concentrations ≥1 mM as established by: (a) morphological changes consistent with apoptosis in cells examined by fluorescence microscopy and semi-thin cell sections, and (b) DNA strand breaks: 45% of the cells were TdT-mediated dUTP nick end labeling (TUNEL) positive at 3 mM at 72 hr, and 70% were positive by the comet assay. Electron microscopy also confirmed the induction of apoptosis by ASA. ASA-induced apoptosis was not associated with: (a) a ladder pattern on genomic DNA electrophoresis, or (b) a subdiploid peak on flow cytometry. Apoptotic bodies were virtually absent on standard morphological assessments and only a few were detected on semi-thin sections. For the above reasons, this apoptosis induced by ASA is “atypical,” and the unusual features of ASA-induced apoptosis, besides their taxonomic value, may offer clues to the mechanisms that control the process of apoptosis or perhaps the cancer chemopreventive properties of this compound. These findings demonstrate that ASA induces apoptosis in human Colon cancer cells, bolstering the hypothesis that apoptosis may be a mechanism by which NSAIDs inhibit Colon carcinogenesis. These findings should be examined in animal and/or clinical research studies in vivo .