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Barrett's esophagus (BE) is the precursor to esophageal adenocarcinoma (EAC). Progression to cancer typically occurs in a stepwise fashion through worsening dysplasia and ultimately, invasive neoplasia. Established EAC with deep involvement of the esophageal wall and/or metastatic disease is invariably associated with poor long-term survival rates. This guides the rationale of surveillance of Barrett’s in an attempt to treat lesions at an earlier, and potentially curative stage. The last two decades have seen a paradigm shift in management of Barrett’s with rapid expansion in the role of endoscopic eradication therapy (EET) for management of dysplastic and early neoplastic BE, and there have been substantial changes to international consensus guidelines for management of early BE based on evolving evidence. This review aims to assist the physician in the therapeutic decision-making process with patients by comprehensive review and summary of literature surrounding natural history of Barrett’s by histological stage, and the effectiveness of interventions in attenuating the risk posed by its natural history. Key findings were as follows. Non-dysplastic Barrett’s is associated with extremely low risk of progression, and interventions cannot be justified. The annual risk of cancer progression in low grade dysplasia is between 1%-3%; EET can be offered though evidence for its benefit remains confined to highly select settings. High-grade dysplasia progresses to cancer in 5%-10% per year; EET is similarly effective to and less morbid than surgery and should be routinely performed for this indication. Risk of nodal metastases in intramucosal cancer is 2%-4%, which is comparable to operative mortality rate, so EET is usually preferred. Submucosal cancer is associated with nodal metastases in 14%-41% hence surgery remains standard of care, except for select situations.  相似文献   
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In post-menopausal women, intra-mammary estrogen, which is converted from extra-ovarian estrone (E1), promotes the growth of breast cancer. Since the aromatase inhibitor letrozole does not suppress 17β-estradiol (E2) production from E1, high intra-mammary E1 concentrations impair letrozole''s therapeutic efficacy. Progesterone receptor membrane component 1 (Pgrmc1) is a non-classical progesterone receptor associated with breast cancer progression. In the present study, we introduced a Pgrmc1 heterozygous knockout (hetero KO) murine model exhibiting low Pgrmc1 expression, and observed estrogen levels and steroidogenic gene expression. Naïve Pgrmc1 hetero KO mice exhibited low estrogen (E2 and E1) levels and low progesterone receptor (PR) expression, compared to wild-type mice. In contrast, Pgrmc1 hetero KO mice that have been ovariectomized (OVX), including letrozole-treated OVX mice (OVX-letrozole), exhibited high estrogen levels and PR expression. Increased extra-ovarian estrogen production in Pgrmc1 hetero KO mice was observed with the induction of steroid sulfatase (STS). In MCF-7 cell, letrozole suppressed PR expression, but PGRMC1 knockdown increased PR and STS expression. Our presented results highlight the important role of Pgrmc1 in modulating estrogen production when ovary-derived estrogen is limited, thereby suggesting a potential therapeutic approach for letrozole resistance.  相似文献   
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Journal of Assisted Reproduction and Genetics - Oocyte in vitro maturation (IVM) is an assisted reproductive technology designed to obtain mature oocytes following culture of immature...  相似文献   
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Breast Cancer Research and Treatment - Studies that report equivalent oncologic outcomes of sentinel lymph node biopsy (SLNB) alone versus axillary lymph node dissection (ALND) for T1-2N1mi breast...  相似文献   
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BACKGROUNDChondrosarcoma, a cartilage matrix producing tumor, is the second most commonly observed primary bone tumor after osteosarcoma, accounting for 15% of all chest wall malignancies. We herein report the case of a patient with chondrosarcoma of the sternum and our management of the chest wall defects that presented following radical tumor resection.CASE SUMMARYA 31-year-old patient presented to our hospital with dull pain and a protruding mass overlying the chest for 3 mo. The presence of nocturnal pain and mass size progression was reported, as were overhead arm elevation-related limitations. Computed tomography showed a focal osteoblastic mass in the sternum with bony exostosis and adjacent soft tissue calcification. Positron emission tomography-computed tomography revealed hypermetabolic activity with a mass located over the upper sternum. Magnetic resonance imaging showed a focal ill-defined bony mass of the sternum with cortical destruction and periosteal reaction. Preoperative biopsy showed a consistent result with chondrosarcoma with immunohistochemical positivity for S100 and focal positivity for IDH-1. The grade II chondrosarcoma diagnosis was confirmed by postoperative pathology. The patient underwent radical tumor resection and chest wall reconstruction with a locking plate and cement spacer. The patient was discharged 1 wk after surgery without any complications. At the 1-year follow-up, there was no local recurrence on imaging. The functional scores, including Constant Score, Nottingham Clavicle Score, and Oxford Shoulder Score, showed the absence of pain in the performance of daily activities or substantial functional disabilities.CONCLUSIONThe diagnosis of chondrosarcoma must be considered when chest wall tumors are encountered. The surgical reconstructive materials, with a locking plate and cement spacer, used in our study are cost-effective and readily-available for the sternum defect.  相似文献   
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