Genes and Cancer最新文献_第6页

Dissecting the expression landscape of cytochromes P450 in hepatocellular carcinoma: towards novel molecular biomarkers. 细胞色素P450在肝细胞癌中的表达:寻找新的分子生物标志物。

Genes and Cancer Pub Date : 2019-05-01 DOI: 10.18632/genesandcancer.190

Camille Martenon Brodeur, Philippe Thibault, Mathieu Durand, Jean-Pierre Perreault, Martin Bisaillon

{"title":"Dissecting the expression landscape of cytochromes P450 in hepatocellular carcinoma: towards novel molecular biomarkers.","authors":"Camille Martenon Brodeur, Philippe Thibault, Mathieu Durand, Jean-Pierre Perreault, Martin Bisaillon","doi":"10.18632/genesandcancer.190","DOIUrl":"https://doi.org/10.18632/genesandcancer.190","url":null,"abstract":"Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths around the world. Recent advances in genomic technologies have allowed the identification of various molecular signatures in HCC tissues. For instance, differential gene expression levels of various cytochrome P450 genes (CYP450) have been reported in studies performed on limited numbers of HCC tissue samples, or focused on a small subset on CYP450s. In the present study, we monitored the expression landscape of all the members of the CYP450 family (57 genes) in more than 200 HCC tissues using RNA-Seq data from The Cancer Genome Atlas. Using stringent statistical filters and data from paired tissues, we identified significantly dysregulated CYP450 genes in HCC. Moreover, the expression level of selected CYP450s was validated by qPCR on cDNA samples from an independent cohort. Threshold values (sensitivity and specificity) based on dysregulated gene expression were also determined to allow for confident identification of HCC tissues. Finally, a global look at expression levels of the 57 members of the CYP450 family across ten different cancer types revealed specific expression signatures. Overall, this study provides useful information on the transcriptomic landscape of CYP450 genes in HCC and on new potential HCC biomarkers.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 3-4","pages":"97-108"},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37378288","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}

引用次数: 7

Inactivated FABP5 suppresses malignant progression of prostate cancer cells by inhibiting the activation of nuclear fatty acid receptor PPARγ. 失活的FABP5通过抑制核脂肪酸受体PPARγ的激活来抑制前列腺癌细胞的恶性进展。

Genes and Cancer Pub Date : 2019-05-01 DOI: 10.18632/genesandcancer.192

Waseem Al-Jameel, Xiaojun Gou, Xi Jin, Jiacheng Zhang, Qiang Wei, Jianzhong Ai, Hong Li, Asmaa Al-Bayati, Angela Platt-Higgins, Andrew Pettitt, Philip S Rudland, Youqiang Ke

{"title":"Inactivated FABP5 suppresses malignant progression of prostate cancer cells by inhibiting the activation of nuclear fatty acid receptor PPARγ.","authors":"Waseem Al-Jameel, Xiaojun Gou, Xi Jin, Jiacheng Zhang, Qiang Wei, Jianzhong Ai, Hong Li, Asmaa Al-Bayati, Angela Platt-Higgins, Andrew Pettitt, Philip S Rudland, Youqiang Ke","doi":"10.18632/genesandcancer.192","DOIUrl":"https://doi.org/10.18632/genesandcancer.192","url":null,"abstract":"Previous study has suggested that the FABP5-PPARγ-signalling transduction pathway gradually replaces the androgen receptor activated pathway in promoting malignant progression of castration-resistant prostate cancer (CRPC) cells. To interfere with this newly discovered FABP5-related signalling pathway, we have produced a highly efficient recombinant FABP5 inhibitor, named dmrFABP5. Treatment with dmrFABP5 significantly supressed the proliferation, migration, invasion and colony formation of the highly malignant prostate cancer cells PC3-M in vitro. To test dmrFABP5's suppressive effect in CRPC, the human PC3-M cells were implanted orthotopically into the prostate gland of immunosuppressed mice to produce tumours. These mice were then treated with dmrFABP5 and produced a highly significant reduction of 100% in metastatic rate and a highly significant reduction of 13-fold in the average size of primary tumours. Immunocytochemial staining showed that the staining intensity of dmrFABP5 treated tumours was reduced by 67%. When tested in vitro, dmrFABP5 suppressed the cancer cells by blocking fatty acid stimulation of PPARγ, and thereby prevented it activating down-stream cancer-promoting or inhibiting cancer-suppressing genes. Our results show that the FABP5 inhibitor dmrFABP5 is a novel molecule for treatment of experimental CRPC and its inhibitory effect is much greater than that produced by SB-FI-26 reported in our previous work.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 3-4","pages":"80-96"},"PeriodicalIF":0.0,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.18632/genesandcancer.192","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37378287","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}

引用次数: 20

Tumour Suppressor Genes with Oncogenic Roles in Lung Cancer 肿瘤抑制基因在肺癌中的致癌作用

Genes and Cancer Pub Date : 2019-04-16 DOI: 10.5772/INTECHOPEN.85017

M. Barros-Filho, F. Guisier, Leigha D. Rock, Daiana D. Becker-Santos, Adam P Sage, E. Marshall, W. Lam

引用次数: 6

Chronic low dose arsenic exposure preferentially perturbs mitotic phase of the cell cycle. 慢性低剂量砷暴露优先扰乱细胞周期的有丝分裂期。

Genes and Cancer Pub Date : 2019-02-01 DOI: 10.18632/genesandcancer.185

Suthakar Ganapathy, Jian Liu, Rui Xiong, Tianqi Yu, Alexandros Makriyannis, Changyan Chen

{"title":"Chronic low dose arsenic exposure preferentially perturbs mitotic phase of the cell cycle.","authors":"Suthakar Ganapathy, Jian Liu, Rui Xiong, Tianqi Yu, Alexandros Makriyannis, Changyan Chen","doi":"10.18632/genesandcancer.185","DOIUrl":"https://doi.org/10.18632/genesandcancer.185","url":null,"abstract":"Environmental pollution is a big challenge for human survival. Arsenic compounds are well-known biohazard, the exposure of which is closely linked to onsets of various human diseases, particularly cancers. Upon chronically exposing to arsenic compounds, genomic integrity is often disrupted, leading to tumor development. However, the underlying mechanisms by which chronic, low dose arsenic exposure targets genetic stability to initiate carcinogenesis still remain not fully understood. In this study, human lung epithelial BEAS-2B cells and keratinocytes were treated with 0.5 μM of sodium arsenite for one month (designated as BEAS-2B-SA cells or keratinocytes-SA), and its effect on cell cycle responses was analyzed. After being arrested in mitotic phase of the cell cycle by nocodazole treatment, BEAS-2B-SA cells or keratinocytes-SA were delayed to enter next cytokinesis. The lagging exit of the cells from mitosis was accompanied by a sustained Plk1 phosphorylation, which led to a persistent activation of the mitotic regulators BubR1 and Cdc27. As the result, cyclin B1 (clnB1) degradation was attenuated. BEAS-2B-SA cells or keratinocytes-SA also expressed a constitutively active Akt. The cytogenetic analysis showed an increased numbers of aneuploidy in these cells. The suppression of Akt reversed the aberrant expressions of the mitotic regulators, delay of mitotic exit as well as chromosomal aberrations. Our findings suggest that a long-term exposure to low dose sodium arsenite aberrantly retains the catenation of mitosis, which facilitates establishing genetic instability and predisposes the cells to tumorigenesis.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 1-2","pages":"39-51"},"PeriodicalIF":0.0,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.18632/genesandcancer.185","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37242152","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}

引用次数: 10

Targeting RNA helicase DDX3 in stem cell maintenance and teratoma formation. 靶向RNA解旋酶DDX3在干细胞维持和畸胎瘤形成中的作用。

Genes and Cancer Pub Date : 2019-02-01 DOI: 10.18632/genesandcancer.187

Candace L Kerr, Guus M Bol, Farhad Vesuna, Venu Raman

{"title":"Targeting RNA helicase DDX3 in stem cell maintenance and teratoma formation.","authors":"Candace L Kerr, Guus M Bol, Farhad Vesuna, Venu Raman","doi":"10.18632/genesandcancer.187","DOIUrl":"https://doi.org/10.18632/genesandcancer.187","url":null,"abstract":"DDX3 is an RNA helicase that has antiapoptotic properties, and promotes proliferation and transformation. Besides the role of DDX3 in transformed cells, there is evidence to indicate that DDX3 expression is at its highest levels during early embryonic development and is also expressed in germ cells of adults. Even though there is a distinct pattern of DDX3 expression during embryonic development and in adults, very little is known regarding its role in embryonic stem cells and pluripotency. In this work, we examined the relationship between DDX3 and human embryonic stem cells and its differentiated lineages. DDX3 expression was analyzed by immunohistochemistry in human embryonic stem cells and embryonal carcinoma cells. From the data obtained, it was evident that DDX3 was overexpressed in undifferentiated stem cells compared to differentiated cells. Moreover, when DDX3 expression was abrogated in multiple stem cells, proliferation was decreased, but differentiation was facilitated. Importantly, this resulted in reduced potency to induce teratoma formation. Taken together, these findings indicate a distinct role for DDX3 in stem cell maintenance.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 1-2","pages":"11-20"},"PeriodicalIF":0.0,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6420792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37080309","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}

引用次数: 10

Utilizing cell line-derived organoids to evaluate the efficacy of a novel LIFR-inhibitor, EC359 in targeting pancreatic tumor stroma. 利用细胞系衍生的类器官评估一种新型lifr抑制剂EC359靶向胰腺肿瘤基质的疗效。

Genes and Cancer Pub Date : 2019-02-01 DOI: 10.18632/genesandcancer.184

Bradley R Hall, Andrew Cannon, Christopher Thompson, Bindu Santhamma, Alejandra Chavez-Riveros, Rakesh Bhatia, Hareesh B Nair, Klaus Nickisch, Surinder K Batra, Sushil Kumar

{"title":"Utilizing cell line-derived organoids to evaluate the efficacy of a novel LIFR-inhibitor, EC359 in targeting pancreatic tumor stroma.","authors":"Bradley R Hall, Andrew Cannon, Christopher Thompson, Bindu Santhamma, Alejandra Chavez-Riveros, Rakesh Bhatia, Hareesh B Nair, Klaus Nickisch, Surinder K Batra, Sushil Kumar","doi":"10.18632/genesandcancer.184","DOIUrl":"https://doi.org/10.18632/genesandcancer.184","url":null,"abstract":"Survival of pancreatic cancer (PC) patient is poor due to lack of effective treatment modalities, which is partly due to the presence of dense desmoplasia that impedes the delivery of chemotherapeutics. Therefore, PC stroma-targeting therapies are expected to improve the efficacy of chemotherapeutics. However, in vitro evaluation of stromal-targeted therapies requires a culture system which includes components of both tumor stroma and parenchyma. We aim to generate a cell line-derived 3D organoids to test the efficacy of stromal-targeted, LIFR-inhibitor EC359. Murine PC (FC1245) and stellate (ImPaSC) cells were cultured to generate organoids that recapitulated the histological organization of PC with the formation of ducts by epithelial cells surrounded by activated fibroblasts, as indicated by CK19 and α-SMA staining, respectively. Analysis by qRT-PCR demonstrated a significant downregulation of markers of activated stroma, POSTN, FN1, MMP9, and SPARC (p<0.0001), when treated with gemcitabine in combination with EC359. Concurrently, collagen proteins including COL1A1, COL1A2, COL3A1, and COL5A1 were significantly downregulated (p <0.0001) after treatment with gemcitabine in combination with EC359. Overall, our study demonstrates the utility of cell lines-derived 3D organoids to evaluate the efficacy of stroma-targeted therapies as well as the potential of EC359 to target activated stroma in PC.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 1-2","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.18632/genesandcancer.184","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37080308","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}

引用次数: 16

Transcriptomic analysis functionally maps the intrinsically disordered domain of EWS/FLI and reveals novel transcriptional dependencies for oncogenesis. 转录组学分析从功能上绘制了EWS/FLI的内在紊乱结构域，并揭示了肿瘤发生的新的转录依赖性。

Genes and Cancer Pub Date : 2019-02-01 DOI: 10.18632/genesandcancer.188

Emily R Theisen, Kyle R Miller, Iftekhar A Showpnil, Cenny Taslim, Kathleen I Pishas, Stephen L Lessnick

{"title":"Transcriptomic analysis functionally maps the intrinsically disordered domain of EWS/FLI and reveals novel transcriptional dependencies for oncogenesis.","authors":"Emily R Theisen, Kyle R Miller, Iftekhar A Showpnil, Cenny Taslim, Kathleen I Pishas, Stephen L Lessnick","doi":"10.18632/genesandcancer.188","DOIUrl":"https://doi.org/10.18632/genesandcancer.188","url":null,"abstract":"EWS/FLI is the pathognomic fusion oncoprotein that drives Ewing sarcoma. The amino-terminal EWS portion coordinates transcriptional regulation and the carboxy-terminal FLI portion contains an ETS DNA-binding domain. EWS/FLI acts as an aberrant transcription factor, orchestrating a complex mix of gene activation and repression, from both high affinity ETS motifs and repetitive GGAA-microsatellites. Our overarching hypothesis is that executing multi-faceted transcriptional regulation requires EWS/FLI to use distinct molecular mechanisms at different loci. Many attempts have been made to map distinct functions to specific features of the EWS domain, but described deletion mutants are either fully active or completely \"dead\" and other approaches have been limited by the repetitive and disordered nature of the EWS domain. Here, we use transcriptomic approaches to show an EWS/FLI mutant, called DAF, previously thought to be nonfunctional, displays context-dependent and partial transcriptional activity but lacks transforming capacity. Using transcriptomic and phenotypic anchorage-independent growth profiles of other EWS/FLI mutants coupled with reported EWS/FLI localization data, we have mapped the critical structure-function requirements of the EWS domain for EWS/FLI-mediated oncogenesis. This approach defined unique classes of EWS/FLI response elements and revealed novel structure-function relationships required for EWS/FLI activation at these response elements.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 1-2","pages":"21-38"},"PeriodicalIF":0.0,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6420793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37080310","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}

引用次数: 14

A novel 40kDa N-terminal truncated carboxypeptidase E splice variant: cloning, cDNA sequence analysis and role in regulation of metastatic genes in human cancers 一个新的40kDa n端截断羧基肽酶E剪接变异:克隆、cDNA序列分析及其在人类癌症转移基因调控中的作用

Genes and Cancer Pub Date : 2019-01-01 DOI: 10.18632/genesandcancer.193

Xuyu Yang, H. Lou, Ya-Ting Chen, Shui-Feng Huang, Y. Loh

{"title":"A novel 40kDa N-terminal truncated carboxypeptidase E splice variant: cloning, cDNA sequence analysis and role in regulation of metastatic genes in human cancers","authors":"Xuyu Yang, H. Lou, Ya-Ting Chen, Shui-Feng Huang, Y. Loh","doi":"10.18632/genesandcancer.193","DOIUrl":"https://doi.org/10.18632/genesandcancer.193","url":null,"abstract":"Carboxypeptidase E (CPE), a prohormone processing enzyme, is a 476- amino acid protein with a signal peptide in its N-terminus and is expressed in the nervous and the endocrine systems. Recent evidence indicate CPE plays various non-enzymatic roles in the endocrine and nervous systems and in various cancers. Besides wild type (WT) CPE, a 40-kDa CPE protein that localizes in the nucleus and cytoplasm has been described in embryonic mouse brain. In this study we have cloned this CPE variant encoding the 40kDa CPE-ΔN protein from human cancer cells. RACE assay and sequence analysis confirmed existence of this CPE variant mRNA, which has 198 nucleotides removed within the first exon and 589 nucleotides from the 3’-UTR, respectively, compared to WT-CPE mRNA. Bioinformatic analysis revealed that this CPE variant mRNA has a shortened open reading frame, which starts coding from the 3rd ATG relative to WT-CPE mRNA and encodes a 40kDa N-terminus truncated CPE protein. RT-PCR and Western blot analysis showed that 40kDa CPE-ΔN is expressed in multiple cancer cell lines and tumor tissues. Overexpression of this 40kDa CPE-ΔN variant up-regulated expression of multiple metastatic genes encompassing different signaling pathways, suggesting potentially an important role of CPE-ΔN in tumor metastasis.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 1","pages":"160 - 170"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67544359","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}

引用次数: 7

Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer. 在三阴性乳腺癌中，Smad3水平升高和Smad2水平降低介导TGF-β通过TMEPAI/PMEPA1从生长抑制因子向生长和转移促进因子的功能转换。

Genes and Cancer Pub Date : 2019-01-01 DOI: 10.18632/genesandcancer.194

Prajjal K Singha, Srilakshmi Pandeswara, Hui Geng, Rongpei Lan, Manjeri A Venkatachalam, Albert Dobi, Shiv Srivastava, Pothana Saikumar

{"title":"Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer.","authors":"Prajjal K Singha, Srilakshmi Pandeswara, Hui Geng, Rongpei Lan, Manjeri A Venkatachalam, Albert Dobi, Shiv Srivastava, Pothana Saikumar","doi":"10.18632/genesandcancer.194","DOIUrl":"https://doi.org/10.18632/genesandcancer.194","url":null,"abstract":"Screening of several TNBC cell lines showed altered Smad2 and Smad3 protein levels compared to normal mammary epithelial cells, suggesting the possibility that it could play an important role in the escape of cancer cells from TGF-β mediated growth inhibition. To assess the functional relevance of these endogenous molecules, Smad2 or Smad3 expression was knocked down individually and assessed their effects on pro-oncogenic properties of TGF-β. Smad3 deficiency reduced growth and invasion capacity of breast cancer cells in comparison to Smad2 which had no effect. Smad3 deficiency was also found to be associated with a reduction in the expressions of TMEPAI/PMEPA1 and EMT inducing transcription factors, E-Cadherin and increased expression of cell cycle inhibitors and Vimentin. On the other hand, Smad2 deficiency had opposite effect on these regulators. Interestingly, the decreased growth, invasion and associated gene expressions were largely reversed by overexpressing TMEPAI in Smad3 knockdown cells, suggesting that Smad3-TMEPAI axis may be involved in subverting growth suppressive effects of TGF-β into growth promotion. Similarly, altered levels of Smad proteins and TMEPAI were also noted in primary TNBC tumor tissues. Analysis of the existing databases provided additional support in terms of TMEPAI and Smad2 expression impacting the survival of TNBC patients. Taken together, our data demonstrate a novel role for Smad3 in cancer transformation and cancer progression through TMEPAI and further suggest that selective targeting of TGF-β-Smad3-TMEPAI axis may be beneficial in triple negative breast cancer therapy and prevention.","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"10 5-6","pages":"134-149"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10001373","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}

引用次数: 22

John Mendelsohn: A visionary scientist, oncologist and leader 约翰·门德尔松:一位有远见的科学家、肿瘤学家和领导者

Genes and Cancer Pub Date : 2019-01-01 DOI: 10.18632/genesandcancer.195

Rakesh Kumar, F. Murad, O. Bogler, B. O’Malley, G. Hortobagyi

引用次数: 3