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1.
Clin Epidemiol ; 13: 1095-1108, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34876856

RESUMO

PURPOSE: Ductal carcinoma in situ with microinvasion (DCISM) can be challenging to balance the risks of overtreatment versus undertreatment. We aim to identify prognostic factors in patients with DCISM and construct a nomogram to predict breast cancer-specific survival (BCSS). MATERIALS AND METHODS: A retrospective cohort study of women diagnosed with DCISM from 1988 to 2015 who were identified in the Surveillance, Epidemiology and End Results database. Clinical variables and tumor characteristics were evaluated, and Cox proportional-hazards regression was performed. A nomogram was constructed from the multivariate logistic regression to combine all the prognostic factors to predict the prognosis of DCISM patients at 5 years, 10 years, and 15 years. RESULTS: We identified 5438 total eligible breast cancer patients with a median and max survival time of 78 and 227 months, respectively. Here, patients with poorer survival outcomes were those diagnosed between 1988 and 2001, African-American race, under 40 years of age, higher tumor N stage, progesterone receptor-negative tumor, and received no surgery. The nomogram was constructed by the seven variables and passed the calibration and validation steps. The area under the receiver operating characteristic (ROC) curve (AUC) of both the training set and the validating set (5-year AUC: 0.77 and 0.88, 10-year AUC: 0.75 and 0.73, 15-year AUC: 0.72 and 0.65). Receiving chemotherapy was associated with a better BCSS (hazard ratio, HR=0.45, 95% confidence interval, 95% CI = 0.23-0.89), especially in patients with estrogen receptor (ER) negative, progesterone receptor (PR) negative (HR = 0.35, 95% CI = 0.13-0.97) and ER+PR-/ER-PR+ DCISM (HR = 0.07, 95% CI = 0.01-0.59). CONCLUSION: Our current study is the first to construct nomograms of patients with DCISM which could help physicians identify breast cancer patients that more likely to benefit from more intensive treatment and follow-up. Chemotherapy might benefit patients with ER-PR- and ER+PR-/ER-PR+ DCISM.

2.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 27(11): 1227-30, 2011 Nov.
Artigo em Zh | MEDLINE | ID: mdl-22078453

RESUMO

AIM: discuss the biological function and regulation mechanism of curcumin in promoting human gastric carcinoma BGC-823 apoptosis. METHODS: Conventional in virto culture in logarithmic phase gastric carcinoma BGC-823 cells; cells are divided into four groups: control group, low treatment group, middle treatment group and high treatment group, with curcumin concentration being 0 mg/L, 5 mg/L, 10 mg/L, and 20 mg/L, respectively. 24 hours after curcumin is treated, cell proliferation level and apoptosis rate are measured with MTT colorimetry and flow cytometry, Bax, Bcl-2 protein expression is measured with immunohistochemistry; mRNA of Caspase-3 is tested by means of PCR. RESULTS: MTT test indicates that curcumin can inhibit human gastric carcinoma BGC-823 cell proliferation, showing concentration dependency; flow cytometry shows that curcumin can effectively induce apoptosis, showing concentration dependency, where the apoptosis rate is 48.3% 24 hours after 20 mg/L curcumin is treated; immunohistochemistry test shows that curcumin treatment enables Bax expression level in human gastric carcinoma BGC-823 cells to go up, meanwhile, the Bcl-2 protein expression level to go down, besides, the mRNA expression level of Caspase-3 in cells increases through induction of curcumin. CONCLUSION: Curcumin has obvious inhibitory effect on human gastric carcinoma BGC-823 cell proliferation, showing concentration dependency to promote apoptosis. Such biological effect may be associated with activating Caspase-3 signal channel by activating Bax protein expression and inhibiting Bcl-2 protein. This study lays an important foundation for further discussing the mechanism of curcumin in inducing human gastric carcinoma BGC-823 apoptosis.


Assuntos
Apoptose/efeitos dos fármacos , Caspase 3/metabolismo , Curcumina/farmacologia , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Proteína X Associada a bcl-2/metabolismo , Caspase 3/efeitos dos fármacos , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Humanos , Proteínas Proto-Oncogênicas c-bcl-2/efeitos dos fármacos , Neoplasias Gástricas/prevenção & controle , Proteína X Associada a bcl-2/efeitos dos fármacos
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