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1.
Nutrients ; 15(18)2023 Sep 07.
Article in English | MEDLINE | ID: mdl-37764684

ABSTRACT

Although the incidence of invasive breast cancer (BC) among women in Asian is generally lower than that in Western countries, the incidence of BC has been on the rise in the past three decades in Asian countries. This hospital-based case-control study aimed to explore the relationship between dietary and metabolic factors and BC risk in pre- and post-menopausal women. We enrolled 285 patients with newly diagnosed BC at the National Taiwan University Hospital and 297 controls from the local community and hospital staff. Before receiving anticancer therapy, all patients with BC and control participants completed a 57-question semi-quantitative Food Frequency Questionnaire. For pre-menopausal women, plant-based factor scores rich in seeds and nuts, soy, fruits, and seaweeds correlated significantly with reduced BC risks, whereas menarche occurring at <12 years of age, reduced physical activity, and high-density lipoprotein <40 mg/dL were associated with increased BC risks. For post-menopausal women, plant-based dietary factor scores were also associated with reduced risks, whereas increased body mass index and energy intake levels correlated with increased BC risks. Diets rich in plant-based dietary patterns are protective against BC risk, regardless of menopausal status. Habitual physical activity is protective against BC risk among pre-menopausal Taiwanese women. Maintaining optimal weight and caloric intake is beneficial for reducing post-menopausal BC risk.


Subject(s)
Breast Neoplasms , Humans , Female , Case-Control Studies , Risk Factors , Taiwan/epidemiology , Breast Neoplasms/epidemiology , Breast Neoplasms/prevention & control , Breast Neoplasms/etiology , Premenopause , Life Style , Energy Intake
2.
Oral Oncol ; 81: 16-21, 2018 06.
Article in English | MEDLINE | ID: mdl-29884409

ABSTRACT

Because of the anatomical location, patients with head and neck cancer (HNC) frequently experience dysphagia and malnutrition at the time of diagnosis and these conditions are often exacerbated after chemoradiotherapy. There is an emerging medical need to establish a consensus on nutritional intervention for these patients. A panel of 30 senior physicians and experts from multidisciplinary teams drafted clinical recommendations to improve the management of nutritional interventions in Taiwan and to provide updated treatment strategy recommendations in hope of improving the nutritional status of patients with HNC. This clinical review describes the resulting consensus document, including the impact of malnutrition on clinical outcomes, the role of prophylactic tube feeding, the choice of tube feeding, and the benefit of oral nutritional supplements in patients with HNC undergoing chemoradiotherapy. The outcomes of this review will support clinicians in their efforts to improve the nutritional status of patients with HNC.


Subject(s)
Chemoradiotherapy , Consensus , Head and Neck Neoplasms/diet therapy , Head and Neck Neoplasms/therapy , Enteral Nutrition , Humans , Taiwan
3.
Int J Cancer ; 141(12): 2537-2550, 2017 12 15.
Article in English | MEDLINE | ID: mdl-28833104

ABSTRACT

The mechanistic role of colonic low folate metabolic stress (LFMS) in colorectal cancer (CRC) malignancy development remains unknown. Folate analysis on the 99 paired human CRC tissues localized LFMS to the deep invasive T3/T4 staged tumours with hypo-methylated sonic hedgehog (Shh) promoter region and amplified expressions of Shh ligand and Gli1 effector, which coincided with deregulated expressions of the epithelial-mesenchymal transition (EMT) mediators. Colonic folate levels of CRC were inversely correlated with pluripotent expressions of the SOX2, NANOG and OCT4 markers (p < 0.05). Exposure of human colon adenocarcinoma cells to LFMS microenvironment significantly hypomethylated Shh promoter region, activated Shh signaling, induced transcript and protein expressions of the pluripotent markers, promoted trans-differentiation as EMT by deregulation of Snail mediator and epithelial marker E-cadherin, increased MMP2/MMP9 enzymatic digestion on matrix protein for invasion, and promoted self-renewal capability of anchorage-independent tumor-spheroid formation. LFMS-induced cancer stem cell (CSC) signature and CRC invasion is synergized with inhibition of DNA methylation by 5-Aza-2-deoxycytidine (5AZA) in rewiring EMT genotypes, which can be blockade by the Shh inhibitor (cyclopamine). The in vivo and in vitro data corroboratively identify CSC-like molecular targets specific to the LFMS-predisposed invasive CRC through reprogramming DNA methylation-activated Shh signaling. The study highlights CSC targets specific to LFMS-predisposed invasive CRC in optimizing folate co-chemotherapy to minimize tumour metastasis potential of CRC patients.


Subject(s)
Colorectal Neoplasms/metabolism , DNA Methylation , Folic Acid/metabolism , Hedgehog Proteins/genetics , Neoplastic Stem Cells/metabolism , Cell Line, Tumor , Colorectal Neoplasms/genetics , Colorectal Neoplasms/pathology , Epithelial-Mesenchymal Transition , Female , Gene Expression Regulation, Neoplastic , Humans , Male , Promoter Regions, Genetic , Signal Transduction , Stress, Physiological , Zinc Finger Protein GLI1/genetics
4.
Carcinogenesis ; 33(6): 1158-68, 2012 Jun.
Article in English | MEDLINE | ID: mdl-22461522

ABSTRACT

Low folate status is well recognized as one of the metabolic stressors for colorectal cancer carcinogenesis, but its role in colon cancer invasion remains unknown. Activation of the Sonic hedgehog (Shh) signal in interaction with the transcription nuclear factor-kappa B (NF-κB) pathway is crucial for cancer aggressiveness. The aims of this study were to investigate whether and how folate deprivation promotes invasion by colon cancer cells in relation to Shh signaling and NF-κB pathway activation. Cultivation of epithelial colon carcinoma-derived cells (HCT116) in folate-deficient (FD) medium enhanced cellular migration and invasion, in correlation with epithelial-mesenchymal transition (EMT) associated with Snail expression and E-cadherin suppression, increased production of ß1 integrin and increased proteolysis by matrix metalloproteinase 2. Blockade of Shh signaling by cyclopamine (CYC) or of NF-κB activation by BAY abolished FD-enhanced EMT and invasion by HCT116 cells. FD cells had 50-80% less intracellular folate, associated with aberrant hypomethylation of the Shh promoter, than control cells, and increased binding of nuclear NF-κB subunit p65 to the Shh promoter region, which coincided with increased Shh expression and protein production of Shh ligand; in addition, the FD-induced Shh signaling targeted Gli1 transcription activator as well as Ptch receptor. The FD-induced Shh induction and activated signaling were blocked by NF-κB inhibitor BAY. Blockade of Shh signaling abrogated FD-promoted NF-κB activation measured by IκBα degradation and by target gene TNFα expression. Taken together, these findings demonstrate that folate deprivation enhanced invasiveness of colon cancer cells mediated by activation of Shh signaling through promoter hypomethylation and cross actions with the NF-κB pathway.


Subject(s)
Colonic Neoplasms/pathology , DNA Methylation , Folic Acid Deficiency , Hedgehog Proteins/genetics , Hedgehog Proteins/metabolism , NF-kappa B/metabolism , Promoter Regions, Genetic , Cadherins/antagonists & inhibitors , Cadherins/biosynthesis , Cell Line, Tumor , Cell Movement , Colonic Neoplasms/genetics , Colonic Neoplasms/metabolism , DNA/metabolism , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Hedgehog Proteins/antagonists & inhibitors , Humans , I-kappa B Kinase/metabolism , Integrin beta1/biosynthesis , Matrix Metalloproteinase 2/metabolism , NF-kappa B/antagonists & inhibitors , NF-kappa B/genetics , Neoplasm Invasiveness , Nitriles/pharmacology , Patched Receptors , Patched-1 Receptor , Receptors, Cell Surface/metabolism , Signal Transduction/genetics , Snail Family Transcription Factors , Sulfones/pharmacology , Transcription Factor RelA/metabolism , Transcription Factors/biosynthesis , Tumor Necrosis Factor-alpha/biosynthesis , Veratrum Alkaloids/pharmacology , Zinc Finger Protein GLI1
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