Cancer growth and metastasis最新文献

{"title":"In Vitro and In Vivo Tumor Growth Inhibition by Glutathione Disulfide Liposomes.","authors":"Satya S Sadhu,&nbsp;Shenggang Wang,&nbsp;Rakesh Dachineni,&nbsp;Ranjith Kumar Averineni,&nbsp;Yang Yang,&nbsp;Huihui Yin,&nbsp;G Jayarama Bhat,&nbsp;Xiangming Guan","doi":"10.1177/1179064417696070","DOIUrl":"https://doi.org/10.1177/1179064417696070","url":null,"abstract":"<p><p>Glutathione disulfide (GSSG) is an endogenous peptide and the oxidized form of glutathione. The impacts of GSSG on cell function/dysfunction remain largely unexplored due to a lack of method to specifically increase intracellular GSSG. We recently developed GSSG liposomes that can specifically increase intracellular GSSG. The increase affected 3 of the 4 essential steps (cell detachment, migration, invasion, and adhesion) of cancer metastasis in vitro and, accordingly, produced a significant inhibition of cancer metastasis in vivo. In this investigation, the effect of GSSG liposomes on cancer growth was investigated with B16-F10 and NCI-H226 cells in vitro and with B16-F10 cells in C57BL/6 mice in vivo. Experiments were conducted to elucidate the effect on cell death through promotion of apoptosis and the effect on the cell cycle. The in vivo results with C57BL/6 mice implanted subcutaneously with B16-F10 cells showed that GSSG liposomes retarded tumor proliferation more effectively than that of dacarbazine, a chemotherapeutic drug for the treatment of melanoma. The GSSG liposomes by intravenous injection (GLS IV) and GSSG liposomes by intratumoral injection (GLS IT) showed a tumor proliferation retardation of 85% ± 5.7% and 90% ± 3.9%, respectively, compared with the phosphate-buffered saline (PBS) control group. The median survival rates for mice treated with PBS, blank liposomes, aqueous GSSG, dacarbazine, GLS IV, and GLS IT were 7, 7, 7.5, 7.75, 11.5, and 16.5 days, respectively. The effective antimetastatic and antigrowth activities warrant further investigation of the GSSG liposomes as a potentially effective therapeutic treatment for cancer.</p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"10 ","pages":"1179064417696070"},"PeriodicalIF":0.0,"publicationDate":"2017-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179064417696070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34966707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Vitro and In Vivo Antimetastatic Effect of Glutathione Disulfide Liposomes.","authors":"Satya S Sadhu, Shenggang Wang, Rakesh Dachineni, Ranjith Kumar Averineni, Teresa Seefeldt, Jiashu Xie, Hemachand Tummala, G Jayarama Bhat, Xiangming Guan","doi":"10.1177/1179064417695255","DOIUrl":"10.1177/1179064417695255","url":null,"abstract":"<p><p>Cancer metastasis is the major cause of cancer mortality. Despite extensive research efforts, effective treatment for cancer metastasis is still lacking. Cancer metastasis involves 4 essential steps: cell detachment, migration, invasion, and adhesion. Detachment is the first and required step for metastasis. Glutathione disulfide (GSSG) is derived from the oxidation of glutathione (GSH), which is present in biological systems in millimolar concentration. Although GSSG is commercially available, the impact of GSSG on cell functions/dysfunctions has not been fully explored due to the fact that GSSG is not cell membrane permeable and a lack of method to specifically increase GSSG in cells. We have developed GSSG liposomes that effectively deliver GSSG to cells. Unexpectedly, cells treated with GSSG liposomes were resistant to detachment by trypsinization. This observation led to the investigation of the antimetastatic effect of GSSG liposomes. Our data demonstrate that GSSG liposomes at 1 mg/mL completely blocked cell detachment and migration, and significantly inhibited cancer cell invasion. Aqueous GSSG showed no such effect, confirming that the effects on cell detachment, migration, and invasion were caused by the intracellular delivery of GSSG. An in vivo experiment with a murine melanoma experimental metastasis model showed that GSSG liposomes prevented melanoma lung metastasis. The unique antimetastatic mechanism through the effects on detachment and migration, and effective in vitro and in vivo metastasis inhibition, warrants further investigation of the GSSG liposomes as a potential treatment for cancer metastasis.</p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"10 ","pages":"1179064417695255"},"PeriodicalIF":0.0,"publicationDate":"2017-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5b/aa/10.1177_1179064417695255.PMC5345945.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34966706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Value of Her2/neu Expression in Gastrointestinal Stromal Tumors: Immunohistochemical Study.","authors":"Ahmed M Abd El-Aziz,&nbsp;Eman A Ibrahim,&nbsp;Ashraf Abd-Elmoghny,&nbsp;Mohammed El-Bassiouny,&nbsp;Zina M Laban,&nbsp;Somaia A Saad El-Din,&nbsp;Youhanna Shohdy","doi":"10.1177/1179064417690543","DOIUrl":"https://doi.org/10.1177/1179064417690543","url":null,"abstract":"<p><strong>Background: </strong>Gastrointestinal stromal tumor (GIST) is a relatively rare type of neoplasms. In Egypt, it represents 2.5% of gastrointestinal tumors and 0.3% of all malignancies. Most of the GISTs develop in the stomach.</p><p><strong>Aim: </strong>To reveal the significance of Her2/neu immunohistochemical expression in GIST and its correlation with other histopathologic parameters and tumor relapse after regular follow-up.</p><p><strong>Patients and methods: </strong>This study is a retrospective and prospective cohort. It included 32 patients with GISTs, who were resectable with no distant metastasis. Immunohistochemical staining by Her2/neu was performed after complete surgical resection of the tumors with preservation of the pseudocapsule.</p><p><strong>Results: </strong>In total, 53.1% of cases were men and 46.9% women. Tumors were classified into low-risk (25%), intermediate-risk (21.9%), and high-risk groups (53.1%). Her2/neu expression was negative in 56.3% of GISTs and positive in 43.7%. Its expression was significantly correlated with risk grade (<i>P</i> = .04), tumor size (<i>P</i> = .001), mitotic count (<i>P</i> = .00), and increased risk of relapse (<i>P</i> = .00). Furthermore, tumor relapse was significantly correlated with the tumor mitotic counts (<i>P</i> = .00). Using kappa agreement test, it showed that 4 mitotic counts/50 high-power fields (HPF) was the cutoff value with which the tumor might be associated more with relapse, with 83% sensitivity, 70% specificity, and <i>P</i> value of .003.</p><p><strong>Conclusions: </strong>Her2/neu might be used as an independent prognostic marker for tumor recurrence after complete resection of GIST, and the cutoff value of mitotic count that might predict tumor relapse is 4/50 HPF. However, more clinical studies with greater number of cases with fluorescent in situ hybridization integration are recommended.</p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"10 ","pages":"1179064417690543"},"PeriodicalIF":0.0,"publicationDate":"2017-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1179064417690543","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34966705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"First-in-Human Phase 1 Trial of Agarose Beads Containing Murine RENCA Cells in Advanced Solid Tumors.","authors":"Barry H Smith, Tapan Parikh, Zoe P Andrada, Thomas J Fahey, Nathaniel Berman, Madeline Wiles, Angelica Nazarian, Joanne Thomas, Anna Arreglado, Eugene Akahoho, David J Wolf, Daniel M Levine, Thomas S Parker, Lawrence S Gazda, Allyson J Ocean","doi":"10.4137/CGM.S39442","DOIUrl":"10.4137/CGM.S39442","url":null,"abstract":"<p><strong>Purpose: </strong>Agarose macrobeads containing mouse renal adenocarcinoma cells (RMBs) release factors, suppressing the growth of cancer cells and prolonging survival in spontaneous or induced tumor animals, mediated, in part, by increased levels of myocyte-enhancing factor (MEF2D) via EGFR-and AKT-signaling pathways. The primary objective of this study was to determine the safety of RMBs in advanced, treatment-resistant metastatic cancers, and then its efficacy (survival), which is the secondary objective.</p><p><strong>Methods: </strong>Thirty-one patients underwent up to four intraperitoneal implantations of RMBs (8 or 16 macrobeads/kg) via laparoscopy in this single-arm trial (FDA BB-IND 10091; NCT 00283075). Serial physical examinations, laboratory testing, and PET-CT imaging were performed before and three months after each implant.</p><p><strong>Results: </strong>RMBs were well tolerated at both dose levels (mean 660.9 per implant). AEs were (Grade 1/2) with no treatment-related SAEs.</p><p><strong>Conclusion: </strong>The data support the safety of RMB therapy in advanced-malignancy patients, and the preliminary evidence for their potential efficacy is encouraging. A Phase 2 efficacy trial is ongoing.</p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"9 ","pages":"9-20"},"PeriodicalIF":0.0,"publicationDate":"2016-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S39442","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34349448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Transfusion on Cancer Growth and Outcome","authors":"H. Goubran, M. Elemary, M. Radosevich, J. Seghatchian, M. El-Ekiaby, T. Burnouf","doi":"10.4137/CGM.S32797","DOIUrl":"https://doi.org/10.4137/CGM.S32797","url":null,"abstract":"For many years, transfusion of allogeneic red blood cells, platelet concentrates, and plasma units has been part of the standard therapeutic arsenal used along the surgical and nonsurgical treatment of patients with malignancies. Although the benefits of these blood products are not a matter of debate in specific pathological conditions associated with life-threatening low blood cell counts or bleeding, increasing clinical evidence is nevertheless suggesting that deliberate transfusion of these blood components may actually lead to negative clinical outcomes by affecting patient’s immune defense, stimulating tumor growth, tethering, and dissemination. Rigorous preclinical and clinical studies are needed to dimension the clinical relevance, benefits, and risks of transfusion of blood components in cancer patients and understand the amplitude of problems. There is also a need to consider validating preparation methods of blood components for so far ignored biological markers, such as microparticles and biological response modifiers. Meanwhile, blood component transfusions should be regarded as a personalized medicine, taking into careful consideration the status and specificities of the patient, rather than as a routine hospital procedure.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"9 1","pages":"1 - 8"},"PeriodicalIF":0.0,"publicationDate":"2016-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S32797","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70689722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANIMAL MODELS OF CANCER BIOLOGY","authors":"N. Yee, N. Ignatenko, N. Finnberg, N. Lee, D. Stairs","doi":"10.4137/CGM.S37907","DOIUrl":"https://doi.org/10.4137/CGM.S37907","url":null,"abstract":"Cancer Growth and Metastasis aims to provide researchers working in this complex, quickly developing field with online, open access to scholarly articles on the growth and metastasis of cancer. In a field where the literature is everexpanding, researchers increasingly need access to up-todate, high quality scholarly articles on areas of specific contemporary interest. This supplement aims to address this by presenting high-quality articles that allow readers to distinguish the signal from the noise. The editor in chief hopes that through this effort, practitioners and researchers will be aided in finding answers to some of the most complex and pressing issues of our time.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"8 1","pages":"115 - 118"},"PeriodicalIF":0.0,"publicationDate":"2015-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S37907","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70690447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Effects of Crizotinib and Temozolomide in Experimental FIG-ROS1 Fusion-Positive Glioblastoma","authors":"Arabinda Das, R. Cheng, M. Hilbert, Yaenette N. Dixon-Moh, Michele L Decandio, W. A. Vandergrift, N. Banik, S. Lindhorst, D. Cachia, A. Varma, Sunil J. Patel, P. Giglio","doi":"10.4137/CGM.S32801","DOIUrl":"https://doi.org/10.4137/CGM.S32801","url":null,"abstract":"Glioblastoma (GB) is the most common malignant brain tumor. Drug resistance frequently develops in these tumors during chemotherapy. Therefore, predicting drug response in these patients remains a major challenge in the clinic. Thus, to improve the clinical outcome, more effective and tolerable combination treatment strategies are needed. Robust experimental evidence has shown that the main reason for failure of treatments is signal redundancy due to coactivation of several functionally linked receptor tyrosine kinases (RTKs), including anaplastic lymphoma kinase (ALK), c-Met (hepatocyte growth factor receptor), and oncogenic c-ros oncogene1 (ROS1: RTK class orphan) fusion kinase FIG (fused in GB)-ROS1. As such, these could be attractive targets for GB therapy. The study subjects consisted of 19 patients who underwent neurosurgical resection of GB tissues. Our in vitro and ex vivo models promisingly demonstrated that treatments with crizotinib (PF-02341066: dual ALK/c-Met inhibitor) and temozolomide in combination induced synergistic antitumor activity on FIG-ROS1-positive GB cells. Our results also showed that ex vivo FIG-ROS1+ slices (obtained from GB patients) when cultured were able to preserve tissue architecture, cell viability, and global gene-expression profiles for up to 14 days. Both in vitro and ex vivo studies indicated that combination blockade of FIG, p-ROS1, p-ALK, and p-Met augmented apoptosis, which mechanistically involves activation of Bim and inhibition of survivin, p-Akt, and Mcl-1 expression. However, it is important to note that we did not see any significant synergistic effect of crizotinib and temozolomide on FIG-ROS1-negative GB cells. Thus, these ex vivo culture results will have a significant impact on patient selection for clinical trials and in predicting response to crizotinib and temozolomide therapy. Further studies in different animal models of FIG-ROS1-positive GB cells are warranted to determine useful therapies for the management of human GBs.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"8 1","pages":"51 - 60"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S32801","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70690386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer Metastases: Early Dissemination and Late Recurrences","authors":"S. Friberg, Andreas M. Nyström","doi":"10.4137/CGM.S31244","DOIUrl":"https://doi.org/10.4137/CGM.S31244","url":null,"abstract":"BACKGROUND Metastatic cells from a primary tumor can occur before the primary cancer is detected. Metastatic cells can also remain in the patient for many years after removal of the primary tumor without proliferating. These dormant malignant cells can awaken and cause recurrent disease decades after the primary treatment. The purpose of this article is to review the clinical evidence for early dissemination and late recurrences in human malignant tumors. We used the following definitions: dormancy of cells may be defined as a nonproliferating state or an arrest in the cell cycle that results in a prolonged G0 phase. If one accepts the term “late metastases” to indicate a period exceeding 10 years from the removal of the primary tumor, then the two malignancies in which this occurs most frequently are cutaneous malignant melanoma (CMM) and renal cell carcinoma (RCC). METHODS PubMed, Web of Science, and Scopus were searched with the keywords “metastases,” “early dissemination,” “late recurrences,” “inadvertently transmitted cancer,” “tumor growth rate,” “dormancy,” “circulating tumor cells,” and “transplantation of cancer.” RESULTS Several case reports of early dissemination and late recurrences of various types of malignancies were found. Analyses of the growth rates of several malignant tumors in the original host indicated that the majority of cancers had metastasized years before they were detected. CMM, RCC, and malignant glioblastoma were the three most common malignancies resulting from an organ transplantation. CMM and RCC were also the two most common malignancies that showed dormancy. In several cases of transplanted CMM and RCC, the donor did not have any known malignancy or had had the malignancy removed so long ago that the donor was regarded as cured. CONCLUSION (1) Metastases can frequently exist prior to the detection of the primary tumor. (2) Metastatic cells may reside in organs in the original host that are not usually the site of detectable secondary tumors, for example, the kidneys and heart. (3) Metastatic cells remain dormant for decades after the primary tumor has been removed. (4) Dormancy might be reversible and lead to late recurrences.","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"8 1","pages":"43 - 49"},"PeriodicalIF":0.0,"publicationDate":"2015-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S31244","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70690067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutant K-RAS Promotes Invasion and Metastasis in Pancreatic Cancer Through GTPase Signaling Pathways.","authors":"Julianna Padavano,&nbsp;Rebecca S Henkhaus,&nbsp;Hwudaurw Chen,&nbsp;Bethany A Skovan,&nbsp;Haiyan Cui,&nbsp;Natalia A Ignatenko","doi":"10.4137/CGM.S29407","DOIUrl":"https://doi.org/10.4137/CGM.S29407","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma is one of the most aggressive malignancies, characterized by the local invasion into surrounding tissues and early metastasis to distant organs. Oncogenic mutations of the K-RAS gene occur in more than 90% of human pancreatic cancers. The goal of this study was to investigate the functional significance and downstream effectors of mutant K-RAS oncogene in the pancreatic cancer invasion and metastasis. We applied the homologous recombination technique to stably disrupt K-RAS oncogene in the human pancreatic cell line MiaPaCa-2, which carries the mutant K-RAS (G12C) oncogene in both alleles. Using in vitro assays, we found that clones with disrupted mutant K-RAS gene exhibited low RAS activity, reduced growth rates, increased sensitivity to the apoptosis inducing agents, and suppressed motility and invasiveness. In vivo assays showed that clones with decreased RAS activity had reduced tumor formation ability in mouse xenograft model and increased survival rates in the mouse orthotopic pancreatic cancer model. We further examined molecular pathways downstream of mutant K-RAS and identified RhoA GTP activating protein 5, caveolin-1, and RAS-like small GTPase A (RalA) as key effector molecules, which control mutant K-RAS-dependent migration and invasion in MiaPaCa-2 cells. Our study provides rational for targeting RhoA and RalA GTPase signaling pathways for inhibition of pancreatic cancer metastasis. </p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"8 Suppl 1","pages":"95-113"},"PeriodicalIF":0.0,"publicationDate":"2015-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S29407","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34297561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current State of Animal (Mouse) Modeling in Melanoma Research.","authors":"Omer F Kuzu,&nbsp;Felix D Nguyen,&nbsp;Mohammad A Noory,&nbsp;Arati Sharma","doi":"10.4137/CGM.S21214","DOIUrl":"https://doi.org/10.4137/CGM.S21214","url":null,"abstract":"<p><p>Despite the considerable progress in understanding the biology of human cancer and technological advancement in drug discovery, treatment failure remains an inevitable outcome for most cancer patients with advanced diseases, including melanoma. Despite FDA-approved BRAF-targeted therapies for advanced stage melanoma showed a great deal of promise, development of rapid resistance limits the success. Hence, the overall success rate of melanoma therapy still remains to be one of the worst compared to other malignancies. Advancement of next-generation sequencing technology allowed better identification of alterations that trigger melanoma development. As development of successful therapies strongly depends on clinically relevant preclinical models, together with the new findings, more advanced melanoma models have been generated. In this article, besides traditional mouse models of melanoma, we will discuss recent ones, such as patient-derived tumor xenografts, topically inducible BRAF mouse model and RCAS/TVA-based model, and their advantages as well as limitations. Although mouse models of melanoma are often criticized as poor predictors of whether an experimental drug would be an effective treatment, development of new and more relevant models could circumvent this problem in the near future. </p>","PeriodicalId":88440,"journal":{"name":"Cancer growth and metastasis","volume":"8 Suppl 1","pages":"81-94"},"PeriodicalIF":0.0,"publicationDate":"2015-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4137/CGM.S21214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34101858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}