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| 1 | Advanced gastric cancer:Current treatment landscape and future perspectives显示文摘Gastric cancer currently ranks fourth in cancer-related mortality worldwide. In the western world, it is most often diagnosed at an advanced stage, after becoming metastatic at distant sites. Patients with advanced disease(locally advanced or metastatic) have a somber prognosis, with a median overall survival of 10-12 mo, and palliative chemotherapy is the mainstay of treatment. In recent years, novel approaches using inhibition of human epidermal growth factor receptor 2(HER2) have demonstrated significant improvements in progression-free and overall survival, compared with chemotherapy alone, in first-line treatment of patients with overexpression of HER2. In addition, both second-line chemotherapy and treatment with the vascular endothelial growth factor receptor-inhibitor ramucirumab demonstrated significant benefits in terms of overall survival, compared with best supportive care, in randomized studies. Moreover, ramucirumab in combination with chemotherapy demonstrated further significant benefits in terms of progression-free and overall survival, compared with chemotherapy alone, in second-line treatment for patients with metastatic gastric cancer. A recently published molecular classification of gastric cancer is expected to improve patient stratification and selection for clinical trials and provide a roadmap for future drug development. Nevertheless, despite these developments the prognosis of patients with advanced gastric cancer remains poor. In this review we discuss current standards of care and outline major topics of drug development in gastric cancer. | Antonia Digklia Anna Dorothea Wagner | 2016 | World Journal of Gastroenterology2016，22，8： | 108 |
| 2 | 双定向超声对比剂在体评价肿瘤血管形成显示文摘目的研制并验证双定向超声对比剂(imagingagent),即将微气泡(MBs)附着到血管内皮生长因子受体2(vascular endothelial growth factor receptor,VEGFR2) | J.K.Willmann A.M.Lutz R.Paulmurugan M.R.Patel J.Rosen-berg 李芳 | 2008 | 国际医学放射学杂志2008，31，A06： | 47 |
| 3 | Management of hepatocellular carcinoma with portal vein tumor thrombosis: Review and update at 2016显示文摘Portal vein tumor thrombosis(PVTT) is a common phenomenon in hepatocellular carcinoma(HCC). Compared to HCC without PVTT, HCC with PVTT is characterized by an aggressive disease course, worse hepatic function, a higher chance of complications related to portal hypertension and poorer tolerance to treatment. Conventionally, HCC with PVTT is grouped together with metastatic HCC during the planning of its management, and most patients are offered palliative treatment with sorafenib or other systemic agents. As a result, most data on the management of HCC with PVTT comes from subgroup analyses or retrospective series. In the past few years, there have been several updates on management of HCC with PVTT. First, it is evident that HCC with PVTT consists of heterogeneous subgroups with different prognoses. Different classifications have been proposed to stage the degree of portal vein invasion/thrombosis, suggesting that different treatment modalities may be individualized to patients with different risks. Second, more studies indicate that more aggressive treatment, including surgical resection or locoregional treatment, may benefit select HCC patients with PVTT. In this review, we aim to discussthe recent conceptual changes and summarize the data on the management of HCC with PVTT. | Stephen L Chan Charing CN Chong Anthony WH Chan Darren MC Poon Kenneth SH Chok | 2016 | World Journal of Gastroenterology2016，22，32： | 44 |
| 4 | Role of autophagy in tumorigenesis,metastasis,targeted therapy and drug resistance of hepatocellular carcinoma显示文摘Autophagy is a 'self-degradative' process and is involved in the maintenance of cellular homeostasis and the control of cellular components by facilitating the clearance or turnover of long-lived or misfolded proteins, protein aggregates, and damaged organelles. Autophagy plays a dual role in cancer, including in tumor progression and tumor promotion, suggesting that autophagy acts as a double-edged sword in cancer cells. Liver cancer is one of the greatest leading causes of cancer death worldwide due to its high recurrence rate and poor prognosis. Especially in China, liver cancer has become one of the most common cancers due to the high infection rate of hepatitis virus. In primary liver cancer, hepatocellular carcinoma (HCC) is the most common type. Considering the perniciousness and complexity of HCC, it is essential to elucidate the function of autophagy in HCC. In this review, we summarize the physiological function of autophagy in cancer, analyze the role of autophagy in tumorigenesis and metastasis, discuss the therapeutic strategies targeting autophagy and the mechanisms of drug-resistance in HCC, and provide potential methods to circumvent resistance and combined anticancer strategies for HCC patients. | Fang Huang Bing-Rong Wang Yi-Gang Wang | 2018 | World Journal of Gastroenterology2018，24，41： | 37 |
| 5 | Therapeutic management options for stage Ⅲ non-small cell lung cancer显示文摘Lung cancer is the leading cause of cancer death worldwide.Majority of newly diagnosed lung cancers are non-small cell lung cancer(NSCLC), of which up to half are considered locally advanced at the time of diagnosis.Patients with locally advanced stage Ⅲ NSCLC consists of a heterogeneous population, making management for these patients complex.Surgery has long been the preferred local treatment for patients with resectable disease.For select patients, multimodality therapy involving systemic and radiation therapies in addition to surgery improves treatment outcomes compared to surgery alone.For patients with unresectable disease, concurrent chemoradiation is the preferred treatment.More recently, research into different chemotherapy agents, targeted therapies, radiation fractionation schedules, intensity-modulated radiotherapy, and proton therapy have shown promise to improve treatment outcomes and quality of life.The array of treatment approaches for locally advanced NSCLC is large and constantly evolving.An updated review of past and current literature for the roles of surgery, chemotherapeutic agents, radiation therapy, and targeted therapy for stage Ⅲ NSCLC patients are presented. | Stephanie M Yoon Talha Shaikh Mark Hallman | 2017 | World Journal of Clinical Oncology2017，8，1： | 32 |
| 6 | Targeted and immune therapies for hepatocellular carcinoma:Predictions for 2019 and beyond显示文摘Systemic therapy for hepatocellular carcinoma(HCC) has markedly advanced since the survival benefit of a molecular targeted agent, sorafenib, were demonstrated in the SHARP and Asia Pacific trials in 2007. Treatment options for patients with advanced HCC increased by sorafenib, and long-term survival for patients with advanced stage HCC has become possible to some extent. However,development of a more potent first-line novel molecular targeted agent replacing sorafenib and a potent second-line agent after disease progression on or intolerant to sorafenib has been warranted because sorafenib lacks tumor shrinking/necrotizing effects and induces relatively severe adverse events such as hand foot skin reaction. Many agents in the 1 st line and 2 nd line setting were attempted to develop between 2007 and 2016, but all of these clinical trials failed.On the other hand, clinical trials of 4 agents(regorafenib, lenvatinib,cabozantinib, and ramucirumab) succeeded in succession in 2017 and 2018, and their use in clinical practice is possible(regorafenib and lenvatinib) or underway(cabozantinib and ramucirumab). Furthermore, all of 5 clinical trials of combination therapy with transcatheter chemoembolization(TACE) plus a molecular targeted agent failed to date, however, the combination of TACE and sorafenib(TACTICS trials) was reported to be successful and presented at ASCO in 2018. Phase 3 clinical trials of immune checkpoint inhibitors and a combination therapy of immune checkpoint inhibitors and molecular targeted agents are also ongoing, which suggests treatment paradigm of HCC in all stages from early,intermediate and advanced stage, is expected to be changed drastically in the very near future. | Masatoshi Kudo | 2019 | World Journal of Gastroenterology2019，25，7： | 33 |
| 7 | Targeting the untargetable KRAS in cancer therapy显示文摘RAS is one of the most well-known proto-oncogenes. Its gain-of-function mutations occur in approximately 30% of all human cancers. As the most frequently mutated RAS isoform, KRAS is intensively studied in the past years. Despite its well-recognized importance in cancer malignancy,continuous efforts in the past three decades failed to develop approved therapies for KRAS mutant cancer. KRAS has thus long been considered to be undruggable. Encouragingly, recent studies have aroused renewed interest in the development of KRAS inhibitors either directly towards mutant KRAS or against the crucial steps required for KRAS activation. This review summarizes the most recent progress in the exploration of KRAS-targeted anticancer strategies and hopefully provides useful insights for the field. | Pingyu Liu Yijun Wang Xin Li | 2019 | Acta Pharmaceutica Sinica B2019，9，5： | 33 |
| 8 | Liver cancer stem cell markers: Progression and therapeutic implications显示文摘Cancer stem cells(CSCs) are a small subpopulation in cancer, have been proposed to be cancer-initiating cells, and have been shown to be responsible for chemotherapy resistance and cancer recurrence. The identification of CSC subpopulations inside a tumor presents a new understanding of cancer development because it implies that tumors can only be eradicated by targeting CSCs. Although advances in liver cancer detection and treatment have increased the possibility of curing the disease at early stages, unfortunately, most patients will relapse and succumb to their disease. Strategies aimed at efficiently targeting liver CSCs are becoming important for monitoring the progress of liver cancer therapy and for evaluating new therapeutic approaches. Herein, we provide a critical discussion of biological markers described in the literature regarding liver cancer stem cells and the potential of these markers to serve as therapeutic targets. | Jing-Hui Sun Qing Luo Ling-Ling Liu Guan-Bin Song | 2016 | World Journal of Gastroenterology2016，22，13： | 31 |
| 9 | Mechanisms of hepatocellular carcinoma and challenges and opportunities for molecular targeted therapy显示文摘The incidence and mortality of hepatocellular carcinoma(HCC) have fallen dramatically in China and elsewhere over the past several decades. Nonetheless, HCC remains a major public health issue as one of the most common malignant tumors worldwide and one of the leading causes of death caused by cancer in China. Hepatocarcinogenesis is a very complex biological process associated with many environmental risk factors and factors in heredity, including abnormal activation of cellular and molecular signaling pathways such as Wnt/β-catenin, hedgehog, MAPK, AKT, and ERK signaling pathways, and the balance between the activation and inactivation of the proto-oncogenes and anti-oncogenes, and the differentiation of liver cancer stem cells. Molecule-targeted therapy, a new approach for the treatment of liver cancer, blocks the growth of cancer cells by interfering with the molecules required for carcinogenesis and tumor growth, making it both specific and selective. However, there is no one drug completely designed for liver cancer, and further development in the research of liver cancer targeted drugs is now almost stagnant. The purpose of this review is to discuss recent advances in our understanding of the molecular mechanisms underlying the development of HCC and in the development of novel strategies for cancer therapeutics. | Chuan Chen Ge Wang | 2015 | World Journal of Hepatology2015，7，15： | 28 |
| 10 | Role of bevacizumab in colorectal cancer growth and its adverse effects:A review显示文摘Angiogenesis affects both wound healing and malignant cell growth through nutrients and oxygen.Vascular endothelial growth factor(VEGF) is the most important element involved in this complex process.Inhibition of VEGF influences angiogenesis and may restrict tumor growth and metastatic ability.Modern antiangiogenic therapy is based on this theory.Bevacizumab is a recombinant humanized monoclonal antibody(immunoglobulin G1) which binds with VEGF-A forming a large molecule.It can not be bound with VEGF tyrosine kinase receptors preventing VEGF-A incorporation;thus its activity is inhibited inducing blockage of VEGFmediated angiogenesis.Bevacizumab,in combination with chemotherapy or other novel targeted therapeutic agents,is currently used more frequently in clinical practice,mainly for managing advanced colorectal cancer.It is also used for managing other malignancies,such as breast cancer,pancreatic cancer,prostate cancer,non small-cell lung cancer,metastatic renal carcinoma and ovarian tumors.Although it is generally considered a safe treatment,there are reports of some rare side effects which should be taken into account.Recent experiments in rats and mice show promising results with a wider therapeutic range. | Efstathios T Pavlidis Theodoros E Pavlidis | 2013 | World Journal of Gastroenterology2013，19，31： | 24 |
| 11 | Targeted and effective photodynamic therapy for cancer using functionalized nanomaterials显示文摘Photodynamic therapy(PDT) is an emerging, non-invasive therapeutic strategy that involves photosensitizer(PS) drugs and external light for the treatment of diseases. Despite the great progress in PS-mediated PDT, their clinical applications are still hampered by poor water solubility and tissue/cell specificity of conventional PS drugs. Therefore, great efforts have been made towards the development of nanomaterials that can tackle fundamental challenges in conventional PS drug–mediated PDT for cancer treatment. This review highlights recent advances in the development of nano-platforms, in which various functionalized organic and inorganic nanomaterials are integrated with PS drugs, for significantly enhanced efficacy and tumor-selectivity of PDT. | Eun Ji Hong Dae Gun Choi Min Suk Shim | 2016 | Acta Pharmaceutica Sinica B2016，6，4： | 22 |
| 12 | Treatment options in patients with metastatic gastric cancer:Current status and future perspectives显示文摘Despite advances in the treatment of gastric cancer,it remains the world’s second highest cause of cancer death.As gastric cancer is often diagnosed at an advanced stage,systemic chemotherapy is the mainstay of treatment for these patients.However,no standard palliative chemotherapy regimen has been accepted for patients with metastatic gastric cancer.Palliative chemotherapy including fluoropyrimidine,platin compounds,docetaxel and epirubicin prolongs survival,and improves a high quality of life to a greater extent than best supportive care.The number of clinical investigations associated with targeted agents has recently increased.Agents targeting the epidermal growth factor receptor 1 and human epidermal growth factor receptor 2(HER2)have been widely tested.Trastuzumab was the first target drug developed,and pivotal phaseⅢtrials showed improved survival when trastuzumab was integrated into cisplatin/fluoropyrimidine-based chemotherapy in patients with metastatic gastric cancer.Trastuzumab in combination with chemotherapy was thus approved to be a new standard of care for patients with HER2-positive advanced esophagogastric adenocarcinoma.Thus,the evaluation of HER2 status in all patients with metastatic gastroesophageal adenocarcinoma should be considered.Other agents targeting vascular endothelial growth factor,mammalian target of rapamycin,and other biological pathways have also been investigated in clinical trials,but showed little impact on the survival of patients.In this review,systemic chemotherapy and targeted therapies for metastatic gastric cancer in the first-and second-line setting are summarized in the light of recent advances. | Ahmet Bilici | 2014 | World Journal of Gastroenterology2014，20，14： | 23 |
| 13 | Relationship between expression of EGFR in gastric cancer tissue and clinicopathological features显示文摘Objective:To investigate the relationship between the expression of epidermal growth factor receptor(ECFR) in gastric cancer and the clinicopalhological features and prognosis. Methods:A total of 78 paraffin specimens of gastric cancer operation were collected.The immunohistochemical method was used to detect the expression of ECFR in 78 cases of gastric cancer and 20 cases of adjacent normal tissue.The relationship between the high expression of ECFR and clinicopathological features was analyzed.Results:ECFR positive expression rate in the 78 cases of gastric cancer tissue was 57.7%(43/78),while ECFR was not expressed in 20 cases of adjacent normal tissue.The high ECFR expression was positively correlated with the position of gastric cancer,tumor size,cell differentiation,invasive depth,lymph node metastasis and TNM staging,yet having no obvious relation with gender or age.Conclusions:ECFR expression level in gastric cancer is closely related to the incidence and development of gastric cancer,which can provide a theoretical basis for the targeted therapy for gastric cancer with ECFR as the target. | Ming Gao Xiu-Ju Liang Zi-Sen Zhang Wang Ma Zhi-Wei Chang Ming-Zhi Zhang | 2013 | Asian Pacific Journal of Tropical Medicine2013，6，4： | 20 |
| 14 | Current and emerging therapies in unresectable and recurrent gastric cancer显示文摘Gastric cancer is one of the most lethal cancers worldwide despite many advances and options in therapy. As it is often diagnosed at an advanced stage, prognosis is poor with a median overall survival of less than twelve months. Chemotherapy remains the mainstay of treatment for these patients but it confersonly a moderate survival advantage. There remains a need for new targeted treatment options and a way to better define patient populations who will benefit from these agents. In the past few years, there has been a better understanding of the biology, molecular profiling, and heterogeneity of gastric cancer. Our increased knowledge has led to the identification of gastric cancer subtypes and to the development of new targeted therapeutic agents. There are now two new targeted agents, trastuzumab and ramucirumab, that have recently been approved for the treatment of advanced and metastatic gastric cancer. There are also many other actively investigated targets, including epidermal growth factor receptor, the phosphatadylinositol 3-kinase/protein kinase B/mammalian target of rapamycin pathway, c-Met, poly ADP-ribose polymerase, and immune checkpoint inhibition. In this review, we discuss the current management of advanced gastric cancer as well as emerging targeted therapies and immunotherapy. | Erin Jou Lakshmi Rajdev | 2016 | World Journal of Gastroenterology2016，22，20： | 20 |
| 15 | Molecular pathogenesis of bone metastases in breast cancer: Proven and emerging therapeutic targets显示文摘Metastatic occurrence is the principal cause of death in breast cancer patients. The high osteotropism makes breast cancer the most common primary tumor type associated with metastatic bone disease. The peculiar clinical aspects associated with metastases limited to the skeletal system suggest considering these cases as a distinctive subset of metastatic patients with a better prognosis. Because bone is frequently the first metastatic site in disease relapse, it is feasible that the next improvement in therapeutic options for bone metastatic disease could be associated with an improvement of survival expectation and quality of life in breast cancer patients. Study of the molecular basis of bone remodeling and breast cancer osteotropism has allowed identification of several therapeutic candidates involved in formation and progression of bone metastases. These targets are frequently the determinants of positive feedback between the tumor and bone cells whose clinical outcome is osteolytic lesions. In this review, we discuss the physiopathologic features underlying targeted therapeutic strategies aimed at interfering with the aberrant bone remodeling associated with breast cancer metastases. | Nadia Rucci Patrizia Sanità Simona Delle Monache Edoardo Alesse Adriano Angelucci | 2014 | World Journal of Clinical Oncology2014，5，3： | 18 |
| 16 | Impact of Taurine on the proliferation and apoptosis of human cervical carcinoma cells and its mechanism显示文摘Background:Cervical cancer has the fourth highest incidence and mortality rate of all cancers in women worldwide;让seriously harms their physical and mental health.The aim of this study was to observe the roles and preliminary mechanism of Taurine(Tau)-induced apoptosis in cervical cancer cells.Methods:Cells from the human cervical cancer cell line SiHa were transfected with the recombinant plasmid pEGFP-N1-MST1(mammalian sterile 20-like kinase 1);then,the cell proliferation activity was analyzed by the MTT assay,cell apoptosis by flow cytometry,and the related protein levels by Western blotting.Results:Tau inhibited the proliferation of SiHa cells and induced apoptosis in these cells(the apoptotic rate was 21.95%in the Tau 160 mmol/L group and 30%in the Tau 320 mmol/L group),upregulated the expression of the MST1(control,0.53;Tau 40-320 mmol/L groups,0.84-1.45)and Bax(control,0.45;Tau 40-320 mmol/L groups,0.64-1.51)proteins(P<0.01),and downregulated the expression of Bcl-2(control,1.28,Tau 40-320 mmol/L groups,0.93-0.47)(P<0.01).The overexpression of MST1 promoted the apoptosis of SiHa cells,enhanced the apoptosis-inductive effects of Tau(P<0.01),upregulated the expression of the proapoptotic proteins p73,p53,PUMA(p53 upregulated modulator of apoptosis),and caspase-3,and promoted the phosphorylation of YAP(Yes-associated protein).Conclusions:Tau inhibited the proliferation and induced the apoptosis of cervical cancer SiHa cells.The MST1 protein plays an important role in the Tau-induced apoptosis of cervical cancer cells. | Hua Li Wen-Jing Ruan Li-Qiao Liu Hui-Fang Wan Xiao-Hong Yang Wei-Feng Zhu Le-Han Yu Xia-Li Zhang Fu-Sheng Wan | 2019 | Chinese Medical Journal2019，，8： | 18 |
| 17 | Systemic treatment strategies for triple-negative breast cancer显示文摘Triple-negative breast cancer(TNBC) is defined by the lack of immunohistochemical expression of the estrogen and progesterone receptors and human epidermal growth factor receptor 2(EGFR2). Most TNBC has a basal-like molecular phenotype by gene expression profiling and shares clinical and pathological features with hereditary BRCA1 related breast cancers. This review evaluates the activity of available chemotherapy and targeted agents in TNBC. A systematic review of PubM ed and conference databases was carried out to identify randomised clinical trials reporting outcomes in women with TNBC treated with chemotherapy and targeted agents. Our review identified TNBC studies of chemotherapy and targeted agents with different mechanisms of action, including induction of synthetic lethality and inhibition of angiogenesis, growth and survival pathways. TNBC is sensitive to taxanes and anthracyclins. Platinum agents are effective in TNBC patients with BRCA1 mutation, either alone or in combination with poly adenosine diphosphate polymerase 1 inhibitors. Combinations of ixabepilone and capecitabine have added to progression-free survival(PFS) without survival benefit in metastatic TNBC. Antiangiogenic agents, tyrosine kinase inhibitors and EGFR inhibitorsin combination with chemotherapy produced only modest gains in PFS and had little impact on survival. TNBC subgroups respond differentially to specific targeted agents. In future, the treatment needs to be tailored for a specific patient, depending on the molecular characteristics of their malignancy. TNBC being a chemosensitive entity, combination with targeted agents have not produced substantial improvements in outcomes. Appropriate patient selection with rationale combinations of targeted agents is needed for success. | Budhi Singh Yadav Suresh C Sharma Priyanka Chanana Swaty Jhamb | 2014 | World Journal of Clinical Oncology2014，5，2： | 18 |
| 18 | Changing role of histopathology in the diagnosis and management of hepatocellular carcinoma显示文摘Hepatocellular carcinoma (HCC) is one of the most common and fatal cancer in the world. HCC frequently presents with advanced disease, has a high recurrence rate and limited treatment options, which leads to very poor prognosis. This warrants urgent improvement in the diagnosis and treatment. Liver biopsy plays very important role in the diagnosis and prognosis of HCC, but with technical advancements and progression in the field of imaging, clinical guidelines have restricted the role of biopsy to very limited situations. Biopsy also has its own problems of needle tract seeding of tumor, small risk of complications, technical and sampling errors along with interpretative errors. Despite this, tissue analysis is often required because imaging is not always specific, limited expertise and lack of advanced imaging in many centers and limitations of imaging in the diagnosis of small, mixed and other variant forms of HCC. In addition, biopsy confirmation is often required for clinical trials of new drugs and targeted therapies. Tissue biomarkers along with certain morphological features, phenotypes and immune-phenotypes that serve as important prognostic and outcome predictors and as decisive factors for therapy decisions, add to the continuing role of histopathology. Advancements in cancer biology and development of molecular classification of HCC with clinic pathological correlation, lead to discovery of HCC phenotypic surrogates of prognostic and therapeutically significant molecular signatures. Thus tissue characteristics and morphology based correlates of molecular subtypes provide invaluable information for management and prognosis. This review thus focuses on the importance of histopathology and resurgence of role of biopsy in the diagnosis, management and prognostication of HCC. | Archana Rastogi | 2018 | World Journal of Gastroenterology2018，24，35： | 17 |
| 19 | Mechanisms and therapeutic advances in the management of endocrine-resistant breast cancer显示文摘The estrogen receptor(ER) pathway plays a critical role in breast cancer development and progression. Endocrine therapy targeting estrogen action is the most important systemic therapy for ER positive breast cancer. However its efficacy is limited by intrinsic and acquired resistance. Mechanisms responsible for endocrine resistance include deregulation of the ER pathway itself, including loss of ER expression, posttranslational modification of ER, deregulation of ER coactivators; increased receptor tyrosine kinase signaling leading to activation of various intracellular pathways involved in signal transduction, proliferation and cell survival, including growth factor receptor tyrosine kinases human epidermal growth factor receptor-2, epidermal growth factor receptor, PI3K/AKT/mammalian target of rapamycin(m TOR), Mitogen activated kinase(MAPK)/ERK, fibroblast growth factor receptor, insulin-like growth factor-1 receptor; alterations in cell cycle and apoptotic machinery; Epigenetic modificationincluding dysregulation of DNA methylation, histone modification, and nucleosome remodeling; and altered expression of specific micro RNAs. Functional genomics has helped us identify a catalog of genetic and epigenetic alterations that may be exploited as potential therapeutic targets and biomarkers of response. New treatment combinations targeting ER and such oncogenic signaling pathways which block the crosstalk between these pathways have been proven effective in preclinical models. Results of recent clinical studies suggest that subsets of patients benefit from the combination of inhibitor targeting certain oncogenic signaling pathway with endocrine therapy. Especially, inhibition of the m TOR signaling pathway, a key component implicated in mediating multiple signaling cascades, offers a promising approach to restore sensitivity to endocrine therapy in breast cancer. We systematically reviewed important publications cited in Pub Med, recent abstracts from ASCO annual meetings and San Antonio Breast Cancer Symposium, and relevant trials registered at Clinical Trials.gov. We present the molecular mechanisms contributing to endocrine resistance, in particular focusing on the biological rationale for the clinical development of novel targeted agents in endocrine resistant breast cancer. We summarize clinical trials utilizing novel strategies to overcome therapeutic resistance, highlighting the need to better identify the appropriate patients whose diseases are most likely to benefit from these specific strategies. | Meng Zhao Bhuvaneswari Ramaswamy | 2014 | World Journal of Clinical Oncology2014，5，3： | 17 |
| 20 | Neoadjuvant treatment of esophageal cancer显示文摘The management of esophageal cancer has been evolving over the past 30 years. In the United States, multimodality treatment combining chemotherapy and radiotherapy (RT) prior to surgical resection has come to be accepted by many as the standard of care, although debate about its overall effect on survival still exists, and rightfully so. Despite recent improvements in detection and treatment, the overall survival of patients with esophageal cancer remains lower than most solid tumors, which highlights why further advances are so desperately needed. The aim of this article is to provide a complete review of the history of esophageal cancer treatment with the addition of chemotherapy, RT, and more recently, targeted agents to the surgical management of resectable disease. | Nicholas P Campbell Victoria M Villaflor | 2010 | World Journal of Gastroenterology2010，16，30： | 16 |
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