目的:探究C反应蛋白/白蛋白(CAR)、血小板/淋巴细胞(PLR)与乳腺癌患者病理特征、新辅助化疗(NAC)疗效的相关性.方法:根据疗效不同将82例乳腺癌患者分为pCR组和non-pCR组,回顾性分析比较两组患者的临床资料、血清学指标和病理学结果.受试者工作特征(ROC)曲线分析CAR、PLR对NAC疗效的预测价值;Pearson相关性分析CAR、PLR与病理特征的关系.结果:两组患者乳腺癌分子亚型、临床分期、雌激素受体(ER)阳性表达、孕激素受体(PR)阳性表达、CRP、白蛋白(Alb)、血小板计数(PLT)和淋巴细胞数(LYMPH#)比较,差异均有统计学意义(P<0.05);pCR组患者CAR和PLR均小于non-pCR组(P<0.05);CAR、PLR及联合检测预测NAC疗效的ROC曲线下面积(AUC)分别为0.755、0.731和0.827;患者不同分子亚型、临床分期、ER阳性表达、PR阳性表达、浸润程度、远端转移和淋巴结转移的CAR和PLR值比较,差异均有统计学意义(P<0.05);CAR、PLR与临床分期、浸润程度、远端转移和淋巴结转移呈正相关,与ER、PR阳性表达呈负相关(P<0.05).结论:CAR、PLR对NAC疗效具有预测价值,其水平与乳腺癌患者临床病理特征具有相关性.

Crizotinib is a tyrosine kinase inhibitor that has been found to be effective in the treatment of c-ros oncogene 1-positive non-small cell lung cancer. Although this targeted agent for treating cancer has shown superiority to standard chemotherapy in some ways, this drug has adverse effects, such as the development of renal abscesses. Some associated renal damage may disappear with crizotinib withdrawal. Hence, we present the case of a 58-year-old man with non-small cell lung cancer on crizotinib therapy who developed bilateral renal abnormal space-occupying lesions, successively which were difficult to identify using various imaging methods; even PET-CT highly suspected the right renal masses as malignant. Finally, the right renal lesions were confirmed as renal abscesses by postoperative pathology. The left renal lesion was considered as renal cysts through the lesion disappearing after crizotinib withdrawal. There have been very few reports in this respect, especially proved by various methods and confirmed by postoperative pathology. It is important to recognize this drug-related complication in order to avoid incorrect diagnosis and inadequate therapy. It is necessary to monitor renal changes after taking crizotinib.

目的:探讨原发性肺癌胃转移的临床表现、鉴别诊断、治疗及预后。方法:回顾性分析2018年4月日照市人民医院收治的1例原发性肺癌胃转移患者资料，并结合文献进行复习。结果:该患者初诊分期为cT 2N 2M x，在行新辅助放化疗、手术后2个月发现肝脏、脑、骨转移，2019年1月腹部CT发现胃底占位。胃镜活组织检查免疫组织化学示：CK7、TTF-1阳性，CK20阴性，明确肺癌胃转移，行免疫、靶向等综合治疗。从胃转移确诊至死亡时间为9.5个月。 结论:肺癌胃转移罕见，临床表现不典型，免疫组织化学是鉴别诊断的常用方法。患者预后差，治疗应遵循晚期肺癌治疗原则。

Breast cancer is one of the most common malignant cancers among women. Cancer cells and adjacent cells determine the development of the disease. Tumor associated macrophages (TAMs) are involved in the regulation of different stages of cancer progression. LncRNAs play an important role in tumor growth and metastasis. However, the function of lncRNA in macrophage and tumor cell interaction is poorly described. Here we reported that lncRNA SNHG1 functioned as a modulator of M2 macrophage polarization and regulated tumor growth and angiogenesis. We indicated that knockdown of SNHG1 inhibited M2 macrophage polarization by suppression of STAT6 phosphorylation. SNHG1 silencing significantly alleviated migration of MCF-7 cells and tube formation of Human Umbilical Vein Endothelial Cells (HUVEC). Furthermore, we found that implantation of cell mixture of MCF-7 cells and macrophages promoted tumor growth and angiogenesis. However, knockdown of SNHG1 in macrophages reversed that effect. Collectively, we demonstrated the important role of lncRNA SNHG1 in macrophages and breast cancer cells interaction. We highlight the essential effect of lncRNA in tumor progression and provide a new method for the prevention and treatment of breast tumor metastasis.

This study aimed to investigate the effect of SIK2 on cisplatin resistance induced by aerobic glycolysis in breast cancer cells and its potential mechanism. qRt-PCR and Western blot were used to detect SIK2 mRNA and protein levels, and cisplatin (DDP) resistant cell lines of breast cancer cells were established. Viability was measured and evaluated via CCK-8, cell invasion capability was evaluated via Transwell, and apoptosis rate was assessed via Flow cytometry. The glycolysis level was evaluated by measuring glucose consumption and lactic acid production. The protein levels of p-PI3K, p- protein kinase B (Akt) and p-mTOR were determined by western blot. SIK2 was highly expressed in breast cancer tissues and cells compared with adjacent tissues and normal human breast epithelial cells, and it had higher diagnostic value for breast cancer. Silencing SIK2 expression can inhibit proliferation and invasion of breast cancer cells and induce their apoptosis. In addition, SIK2 knockdown inhibits glycolysis, reverses the resistance of drug-resistant cells to cisplatin, and inhibits PI3K/AKT/mTOR signaling pathway. When LY294002 was used to inhibit PI3K/AKT/mTOR signaling pathway, the effect of pcDNA3.1-SIK2 on aerobic glycolysis of breast cancer cells could be reversed. SIK2 can promote cisplatin resistance caused by aerobic glycolysis of breast cancer cells through PI3K/AKT/mTOR signaling pathway, which may be a new target to improve cisplatin resistance of breast cancer cells.