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Do genetic polymorphisms of the vitamin D receptor contribute to breast/ovarian cancer? A systematic review and network meta-analysis.
Li, J, Li, B, Jiang, Q, Zhang, Y, Liu, A, Wang, H, Zhang, J, Qin, Q, Hong, Z, Li, BA
Gene. 2018;:211-227
Abstract
BACKGROUND To identify the most suitable genetic model for detecting the risk of breast cancer (BC)/ovarian cancer (OC) in specific populations. METHODS Databases were searched for related studies published up to October 2017. First, VDR genetic polymorphisms were compared in patients with and without cancer. Second, a network meta-analysis was used to reveal the relation between VDR genetic polymorphisms with disease outcomes. Subgroup analyses and a meta-regression were performed according to cancer types, ethnicity and genotypic method. The study is registered in PROSPERO with an ID: CRD42017075505. RESULTS Forty-five studies were eligible, which included 65,754 patients and 55 clinical analyses. Of genetic models, results suggested that the recessive model with the CDX2 polymorphism predicted the risk of BC in all cases. The recessive polymorphism model with the rs2228570 (FokI) polymorphism seemed to the best predictor of BC in Caucasian patients, whereas the homozygote model with the CDX2 polymorphism appeared to best predict BC in African-American patients. The homozygote model with the rs2228570 (FokI) polymorphism model appeared to detect the risk of OC in all cases, whereas the heterozygote model with the rs1544410 (BsmI) polymorphism seemed to detect the risk of OC in Caucasian patients. CONCLUSIONS By detecting the risk of BC, the recessive model with the rs2228570 (FokI) polymorphism is likely the best genetic model in Caucasian patients, and the homozygote model with the CDX2 polymorphism appears to be best genetic model in African-American patients. Moreover, for detecting clinical risk of OC, heterozygote models with the rs1544410 (BsmI) polymorphism is likely the best genetic model for detecting the risk of OC in Caucasian patients.
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Bronchobiliary fistula following radiofrequency ablation for liver metastases from breast cancer: A case report and literature review.
Xi, XJ, Zhang, Y, Yin, YH, Li, H, Ma, DD, Qu, YQ
Medicine. 2018;(43):e12760
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Abstract
RATIONALE Bronchobiliary fistula (BBF) is a rare clinical condition which is characterized by a channel between biliary tract and bronchial tree. BBF can present with fever, dyspnea, and cough. However, it can be easily misdiagnosed as biliary vomiting, dyspnea, or even severe pneumonia. PATIENT CONCERNS A 53-year-old woman was diagnosed with breast cancer in April 2011 and underwent radical mastectomy and lymph node dissection, chemotherapy, and radiotherapy. Unfortunately, the patient suffered from bone metastasis during the 1st year and liver metastasis during the 2nd year after radical mastectomy. In 2013, the patient underwent transcatheter arterial chemoembolization therapy twice for liver metastasis. The patient was then treated with radiofrequency ablation (RFA) in 2016. Unfortunately, the patient developed a cough with bitter-tasting yellow sputum and chest tightness 2 weeks after the RFA treatment. Approximately 6 months later, the patient still complained of a cough with yellow sputum and persistent chest tightness. The patient was then admitted to our department. DIAGNOSES The presence of bile in the sputum supported a diagnosis of BBF. Bronchoscopy was performed, and the presence of bile in the lavage fluid confirmed the diagnosis of BBF. INTERVENTIONS The patient was treated with antibiotics including sulbactam, cefoperazone, levofloxacin and meropenem, was well as hepatoprotectants, nutritional support and other supportive treatments in our department. OUTCOMES The patient died because of liver failure. LESSONS This case demonstrates that we should consider the possibility of BBF when patients experience a recurrent cough with discolored sputum after RFA. In particular, a diagnosis of BBF should be considered in patients who do not respond to antibiotic treatment.
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Integrated bioinformatics, computational and experimental methods to discover novel Raf/extracellular-signal regulated kinase (ERK) dual inhibitors against breast cancer cells.
Chen, Y, Zheng, Y, Jiang, Q, Qin, F, Zhang, Y, Fu, L, He, G
European journal of medicinal chemistry. 2017;:997-1011
Abstract
Beginning with our previously reported ERK inhibitor BL-EI001, we found Raf1 to be an important regulator in the ERK interactive network, and then we designed and synthesized a novel series of Raf1/ERK dual inhibitors against human breast cancers through integrative computational, synthetic and biological screening methods. Moreover, we found that compound 9d suppressed the proliferation of breast cancer cell lines and induced cellular apoptosis via a mitochondrial pathway with only partial dependence on Raf1 and ERK. Our results suggest that an integrative method including in silico design, chemical synthesis, biological screening and bioinformatics analysis could be an attractive strategy for the discovery of multi-target inhibitors against breast cancer.
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Risk of second primary breast cancer after radioactive iodine treatment in thyroid cancer: a systematic review and meta-analysis.
Zhang, Y, Liang, J, Li, H, Cong, H, Lin, Y
Nuclear medicine communications. 2016;(2):110-5
Abstract
The aim of this study was to determine whether the risk of second primary breast cancer (SPBC) is increased in thyroid cancer patients treated with radioactive iodine (RAI). We searched the MEDLINE, EMBASE, and the Cochrane Library and Chinese database for studies that reported the risk of SPBC in thyroid cancer patients treated with RAI and patients not treated with RAI. Two independent reviewers screened citations and reviewed full-text papers. A meta-analysis was carried out using the Review Manager software. Six cohort studies (three from Europe, one from America, and two from east Asia) with 17,914 patients were included in this review. The relative risk of SPBC in thyroid cancer survivors treated with RAI was 0.61 (95% confidence interval 0.47-0.79) relative to thyroid cancer survivors not treated with RAI. The risk of SPBC in thyroid cancer survivors treated with RAI is not increased compared with thyroid cancer survivors not treated with RAI.
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Curcumin Suppresses Proliferation and Migration of MDA-MB-231 Breast Cancer Cells through Autophagy-Dependent Akt Degradation.
Guan, F, Ding, Y, Zhang, Y, Zhou, Y, Li, M, Wang, C
PloS one. 2016;(1):e0146553
Abstract
Previous studies have evidenced that the anticancer potential of curcumin (diferuloylmethane), a main yellow bioactive compound from plant turmeric was mediated by interfering with PI3K/Akt signaling. However, the underlying molecular mechanism is still poorly understood. This study experimentally revealed that curcumin treatment reduced Akt protein expression in a dose- and time-dependent manner in MDA-MB-231 breast cancer cells, along with an activation of autophagy and suppression of ubiquitin-proteasome system (UPS) function. The curcumin-reduced Akt expression, cell proliferation, and migration were prevented by genetic and pharmacological inhibition of autophagy but not by UPS inhibition. Additionally, inactivation of AMPK by its specific inhibitor compound C or by target shRNA-mediated silencing attenuated curcumin-activated autophagy. Thus, these results indicate that curcumin-stimulated AMPK activity induces activation of the autophagy-lysosomal protein degradation pathway leading to Akt degradation and the subsequent suppression of proliferation and migration in breast cancer cell.
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AIB1 polymorphisms with breast cancer susceptibility: a pooled analysis of variation in BRCA1/2 mutation carriers and non-carriers.
Zhang, Y, Huang, M, Zhu, Z
Molecular biology reports. 2012;(6):6881-6
Abstract
The AIB1 gene (amplified in breast cancer 1), coding for a member of steroid receptor co-activator p160 protein family is involved in regulation of estrogen receptor transactivation influencing the estrogen-dependent gene expression. It contains a glutamine repeat polymorphism and several single nucleotide polymorphisms that may alter the transcriptional activation of the receptor and affect susceptibility to breast cancer. Previous studies have shown that these polymorphisms may modify the breast cancer risk in women carrying BRCA1/2 mutations. However, the results remained controversial. This meta-analysis of literatures was performed to derive a more precise estimation of the relationship. A total of 22 studies were identified, including 3,742 cases and 3,491 controls for AIB1 polyglutamine repeat polymorphism, 2,170 cases and 3,309 controls for Q586H polymorphism, and 2,183 cases and 3,319 controls for T960T polymorphism. Overall, we found no evidence of association for individuals who carried at least one AIB1 allele of 28 or 29 or more repeat with breast cancer risk. But we found increased breast cancer risk in BRCA1/2 mutation carriers for individuals with both alleles ≥29 polyglutamine repeat (OR, 1.64; 95% CI 1.24-2.17). And reduced risk was found to be associated with the Q586H polymorphism among the variant homozygote genotype carriers (OR, 0.42; 95% CI 0.23-0.77). Our results do not support the direct association of AIB1 polyglutamine repeat length and breast cancer. However, we found that BRCA1/2 mutation carriers with both alleles ≥29 repeats have a higher risk of breast cancer.
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A novel calmodulin antagonist O-(4-ethoxyl-butyl)-berbamine overcomes multidrug resistance in drug-resistant MCF-7/ADR breast carcinoma cells.
Liu, R, Zhang, Y, Chen, Y, Qi, J, Ren, S, Xushi, MY, Yang, C, Zhu, H, Xiong, D
Journal of pharmaceutical sciences. 2010;(7):3266-75
Abstract
Multidrug resistance (MDR) mediated by the overexpression of the drug efflux protein P-glycoprotein is one of the major obstacles to successful cancer chemotherapy. The development of safe and effective MDR-reversing agents is an important approach to addressing this problem clinically. In this study, we evaluated the P-gp-modulatory potential of O-(4-ethoxyl-butyl)-berbamine (EBB), a novel calmodulin antagonist and derivative of bisbenzylisoquinoline alkaloid, which significantly improved the chemosensitivity of P-glycoprotein-mediated multidrug-resistant cells to doxorubicin compared with the efficacy of a conventional P-glycoprotein inhibitor, verapamil. EBB not only blocked the function of P-glycoprotein confirmed by the fact that EBB increased intracellular accumulation of rhodamine 123 and doxorubicin but also inhibited the expression of P-glycoprotein actualized by downregulating P-glycoprotein. Furthermore, our results showed that cotreatment with EBB and doxorubicin resulted in marked G(2)/M arrest and apoptosis of MCF-7/ADR cells, accompanied by down-regulation of the proteins cdc2/p34 and cyclin B1 and increased the levels of calcium ions. Taken together, these results suggest that cotreatment with EBB and doxorubicin could strongly potentiate the antitumor activity of doxorubicin, thus may have significant clinical application in cancer chemotherapy.