6%(53/72)、26 7%(8/30)、14 3%(3/21),三者间比较差异有统计学意义(χ~2=33 15,P<0 01)

6%(53/72)、26.7%(8/30)、14.3%(3/21),三者间比较差异有统计学意义(χ~2=33.15,P<0.01)。VASH1的表达在NSCLC的淋巴结转移、TNM分期和分化程度方面差异有统计学意义(均P
Preclinical 更多 modelling studies are beginning to aid development of therapies targeted against key regulators of pancreatic cancer progression. Pancreatic cancer is an aggressive, stromally-rich tumor, from which few people survive. Within the tumor microenvironment cellular and extracellular components exist, shielding tumor cells from immune cell clearance, and chemotherapy, enhancing progression of the disease. The cellular component

of this microenvironment consists mainly of stellate cells and inflammatory cells. New findings suggest that manipulation of the cellular component of the tumor microenvironment is possible to promote

immune cell killing of tumor cells. Here we explore possible immunogenic therapeutic strategies. Additionally extracellular stromal elements play a key role in protecting tumor cells from chemotherapies targeted at the pancreas. We describe the experimental findings and the pitfalls associated with translation of stromally targeted therapies to clinical trial. Finally, we discuss the key inflammatory signal transducers activated subsequent to driver mutations in oncogenic Kras in pancreatic cancer. We present the preclinical findings that have led to successful Checkpoint activation early trials of STAT3 inhibitors in pancreatic adenocarcinoma.
Since the discovery that non-small cell lung cancer(NSCLC) is driven by epidermal

growth factor receptor(EGFR) mutations, the EGFR tyrosine kinase inhibitors(EGFR-TKIs, e.g., ge fi tinib and elrotinib) have been effectively used for clinical treatment. However, patients eventually develop drug resistance. Resistance to EGFR-TKIs is inevitable 还有 due to various mechanisms, such as the secondary mutation(T790M), activation of alternative pathways(c-Met, HGF, AXL), aberrance of the downstream pathways(K-RAS mutations, loss of PTEN), impairment of the EGFR-TKIs-mediated apoptosis pathway(BCL2-like 11/BIM deletion polymorphism), histologic transformation, ATP binding cassette(ABC) transporter effusion, etc. Here we review and summarize the known resistant mechanisms to EGFR-TKIs and provide potential targets for development of new therapeutic strategies.
2014年8月,对肺右下叶2 cm结节施行单切口胸腔镜亚肺叶切除术,术后病理诊断为肺炎性肌纤维母细胞瘤(inflammatory myofibroblastic tumor,IMT),随访1年余,无复发、转移。
Gastric cancer is one of the most lethal cancers worldwide despite many advances and options in therapy.

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