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  • American Association for Cancer Research (AACR)  (25)
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  • American Association for Cancer Research (AACR)  (25)
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  • 1
    Online Resource
    Online Resource
    Abstract 494: Stemness characteristics contribute to metastasis and shorter patient survival in nasopharyngeal carcinoma
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 494-494
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 494-494
    Abstract: Nasopharyngeal carcinoma (NPC) has the highest incidence of metastasis among head and neck cancers. The involvement of cancer stem cells (CSCs) in tumorigenesis has been studied in several malignancies, but their presence in NPC has not been extensively evaluated. The range of general characteristics of “stemness” includes increased side-population (SP) fraction, limited functional differentiation or dedifferentiation under the influence of the microenvironment, and expression of putative stem cell markers. We previously isolated a highly metastatic clone (Clone-18) from the NPC cell line CNE-2. Using this clone, we have sought to explore the influence of the stemness characteristics of NPC cells on tumor metastasis. Human tissue samples were collected under informed consent at the Sun Yat-sen University Cancer Center. SP cells were evaluated by flow cytometry. A Transwell assay and a wound-healing assay were used to evaluate the migratory and invasive abilities of the cells. Lung metastasis was evaluated by injecting tumor cells into the tail vein of BALB/c nude mice. Real-time PCR and western blotting were used for a protein kinase C (PKC) pathway study. Tissue microarrays and immunohistochemical staining were used to evaluate the correlation between vimentin and the survival time of patients with nasopharyngeal carcinoma. Clone-18 cells possessed a very high percentage of SP cells (62.1 ± 1.39%) relative to low-metastasis clones (Clone-22, 7.2 ± 1%; Clone-26, 3.9 ± 0.9%) or the parental CNE-2 cells (27.9 ± 2.02%), implying that there were more stem-like cells in the high-metastasis clones. Two stem cell markers, WNT5A and vimentin, were also highly expressed in the high-metastasis clone cells. To confirm the clinical relevance of these findings, human tissue samples were used. The mRNA level for WNT5A was significantly higher in regional metastatic NPC tissues (n = 4) than in primary tumors (n = 20), and it was much higher in liver metastatic NPC (n = 5) than in regional metastatic tissues. In the cohort of 282 NPC patients, a higher vimentin level in the primary tumor, as detected by IHC staining, correlated with shorter overall survival. Suppression of WNT5A by siRNA significantly reduced the migratory and invasive abilities of Clone-18 cells, and this effect was shown to be regulated by activating protein kinase C (PKC). The activated PKC further regulated the expressions of Snail and E-cadherin, which subsequently induced an EMT in NPC cells. In vivo experiments showed that the administration of recombinant WNT5A protein could promote lung metastasis by the low-metastasis Clone-26 cells in the lung metastasis mouse model. In conclusion, the stemness characteristics of NPC cells have been shown to contribute to the migratory, invasive, and metastatic phenotype of this important malignancy, with WNT5A directly regulating these properties and being a critical candidate marker of CSCs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 494. doi:10.1158/1538-7445.AM2011-494
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-494
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 2
    Online Resource
    Online Resource
    ORAI2 Promotes Gastric Cancer Tumorigenicity and Metastasis through PI3K/Akt Signaling and MAPK-Dependent Focal Adhesion Disassembly
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Research Vol. 81, No. 4 ( 2021-02-15), p. 986-1000
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 4 ( 2021-02-15), p. 986-1000
    Abstract: The ubiquitous second messenger Ca2+ has long been recognized as a key regulator in cell migration. Locally confined Ca2+, in particular, is essential for building front-to-rear Ca2+ gradient, which serves to maintain the morphologic polarity required in directionally migrating cells. However, little is known about the source of the Ca2+ and the mechanism by which they crosstalk between different signaling pathways in cancer cells. Here, we report that calcium release–activated calcium modulator 2 (ORAI2), a poorly characterized store-operated calcium (SOC) channel subunit, predominantly upregulated in the lymph node metastasis of gastric cancer, supports cell proliferation and migration. Clinical data reveal that a high frequency of ORAI2-positive cells in gastric cancer tissues significantly correlated with poor differentiation, invasion, lymph node metastasis, and worse prognosis. Gain- and loss-of-function showed that ORAI2 promotes cell motility, tumor formation, and metastasis in both gastric cancer cell lines and mice. Mechanistically, ORAI2 mediated SOC activity and regulated tumorigenic properties through the activation of the PI3K/Akt signaling pathways. Moreover, ORAI2 enhanced the metastatic ability of gastric cancer cells by inducing FAK-mediated MAPK/ERK activation and promoted focal adhesion disassembly at rear-edge of the cell. Collectively, our results demonstrate that ORAI2 is a novel gene that plays an important role in the tumorigenicity and metastasis of gastric cancer. Significance: These findings describe the critical role of ORAI2 in gastric cancer cell migration and tumor metastasis and uncover the translational potential to advance drug discovery along the ORAI2 signaling pathway.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-20-0049
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 3
    Online Resource
    Online Resource
    The Landscape of Cell-Free HBV Integrations and Mutations in Cirrhosis and Hepatocellular Carcinoma Patients
    American Association for Cancer Research (AACR) ; 2021
    In:  Clinical Cancer Research Vol. 27, No. 13 ( 2021-07-01), p. 3772-3783
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 13 ( 2021-07-01), p. 3772-3783
    Abstract: Intratumoral hepatitis B virus (HBV) integrations and mutations are related to hepatocellular carcinoma (HCC) progression. Circulating cell-free DNA (cfDNA) has shown itself as a powerful noninvasive biomarker for cancer. However, the HBV integration and mutation landscape on cfDNA remains unclear. Experimental Design: A cSMART (Circulating Single-Molecule Amplification and Resequencing Technology)-based method (SIM) was developed to simultaneously investigate HBV integration and mutation landscapes on cfDNA with HBV-specific primers covering the whole HBV genome. Patients with HCC (n = 481) and liver cirrhosis (LC; n = 517) were recruited in the study. Results: A total of 6,861 integration breakpoints including TERT and KMT2B were discovered in HCC cfDNA, more than in LC. The concentration of circulating tumor DNA (ctDNA) was positively correlated with the detection rate of these integration hotspots and total HBV integration events in cfDNA. To track the origin of HBV integrations in cfDNA, whole-genome sequencing (WGS) was performed on their paired tumor tissues. The paired comparison of WGS data from tumor tissues and SIM data from cfDNA confirmed most recurrent integration events in cfDNA originated from tumor tissue. The mutational landscape across the whole HBV genome was first generated for both HBV genotype C and B. A region from nt1100 to nt1500 containing multiple HCC risk mutation sites (OR & gt; 1) was identified as a potential HCC-related mutational hot zone. Conclusions: Our study provides an in-depth delineation of HBV integration/mutation landscapes at cfDNA level and did a comparative analysis with their paired tissues. These findings shed light on the possibilities of noninvasive detection of virus insertion/mutation.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-21-0002
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 4
    Online Resource
    Online Resource
    Genome-Wide Association Study Identifies a New Locus at 7q21.13 Associated with Hepatitis B Virus–Related Hepatocellular Carcinoma
    American Association for Cancer Research (AACR) ; 2018
    In:  Clinical Cancer Research Vol. 24, No. 4 ( 2018-02-15), p. 906-915
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 24, No. 4 ( 2018-02-15), p. 906-915
    Abstract: Purpose: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. In China, chronic hepatitis B virus (HBV) infection remains the major risk factor for HCC. In this study, we performed a genome-wide association study (GWAS) among Chinese populations to identify novel genetic loci contributing to susceptibility to HBV-related HCC. Experimental Design: GWAS scan is performed in a collection of 205 HBV-related HCC trios (each trio includes an affected proband and his/her both parents), and 355 chronic HBV carriers with HCC (cases) and 360 chronic HBV carriers without HCC (controls), followed by two rounds of replication studies totally consisting of 3,796 cases and 2,544 controls. Results: We identified a novel association signal within the CDK14 gene at 7q21.13 (index rs10272859, OR = 1.28, P = 9.46 × 10−10). Furthermore, we observed that the at-risk rs10272859[G] allele was significantly associated with higher mRNA expression levels of CDK14 in liver tissues. Chromosome conformation capture assays in liver cells confirmed that a physical interaction exists between the promoter region of CDK14 and the risk-associated SNPs in strong linkage disequilibrium with the index rs10272859 at 7q21.13. This index rs10272859 also showed significant association with the survival of HCC patients. Conclusions: Our findings highlight a novel locus at 7q21.13 conferring both susceptibility and prognosis to HBV-related HCC, and suggest the CDK14 gene to be the functional target of the 7q21.13 locus. Clin Cancer Res; 24(4); 906–15. ©2017 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-17-2537
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 5
    Online Resource
    Online Resource
    Effects of Infection-Induced Fever and the Interaction with IL6 rs1800796 Polymorphism on the Prognosis of Breast Cancer
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 31, No. 11 ( 2022-11-02), p. 2030-2037
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 31, No. 11 ( 2022-11-02), p. 2030-2037
    Abstract: Previous studies have found that acute febrile infection may decrease the risk of breast cancer. Meanwhile, it is well known that interleukin-6 (IL6) played dual roles in the tumor microenvironment. Fever may stimulate IL6 production, and IL6 rs1800796 also influences the expression of IL6. However, the impact of fever and its interaction with IL6 rs1800796 on breast cancer survival remains to be explored. Methods: This was a prospective cohort study of 4,223 breast cancer patients. Exposures were pre-/postdiagnostic infection-induced fever and rs1800796 polymorphism. The endpoints were overall survival (OS) and progression-free survival (PFS). Adjusted hazard ratios were obtained using multivariate Cox proportional hazards regression models. Results: Compared with women without prediagnostic fever, the adjusted hazard ratio (HR) of progression for those with prediagnostic fever was 0.81 (95% CI, 0.66–0.99), particularly for the CC genotype of IL6 rs1800796 (HR, 0.53; 95% CI, 0.36–0.79). OS was also better (HR, 0.59; 95% CI, 0.36–0.99) among women with the CC genotype exposed to prediagnostic fever, accompanied by a significant interaction (P = 0.021). Postdiagnostic fever conferred better PFS for breast cancer (HR, 0.72; 95% CI, 0.52–1.00). Irrespective of the genotype of IL6, lymph node–positive women with postdiagnostic fever (HR, 0.57; 95% CI, 0.37–0.89) had a lower risk of progression than lymph node–negative women (HR, 1.12; 95% CI, 0.70–1.79). Conclusions: Infection-induced fever was beneficial to breast cancer survival, particularly for women who were the CC genotype of IL6 rs1800796 or node positive. Impact: This study provides new insight into the roles of infection-induced fever as a potential prognostic marker and therapy regimen for breast cancer.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-22-0498
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 6
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    Online Resource
    A Randomized Controlled Trial Comparing Two Different Schedules for Cisplatin Treatment in Patients with Locoregionally Advanced Nasopharyngeal Cancer
    American Association for Cancer Research (AACR) ; 2021
    In:  Clinical Cancer Research Vol. 27, No. 15 ( 2021-08-01), p. 4186-4194
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 15 ( 2021-08-01), p. 4186-4194
    Abstract: Previous studies suggest that a cumulative cisplatin dose of 200 mg/m2 might be adequate in the intensity-modulated radiation therapy (IMRT) era for locoregionally advanced nasopharyngeal carcinoma (LANPC). However, two cycles of once-every-3-weeks cisplatin at 100 mg/m2 has never been prospectively compared with standard once-a-week cisplatin regimen. Patients and Methods: This trial was conducted at three hospitals from 2011 to 2016. Patients who met the eligibility criteria were recruited (ChiCTR-TRC-12001979) and randomly assigned (1:1) via a computer-generated sequence to receive once-every-3-weeks cisplatin at 100 mg/m2 for two cycles or once-a-week cisplatin at 40 mg/m2 for six cycles concurrently with IMRT. Primary endpoint was failure-free survival and between-group absolute difference of 10% as the noninferiority margin. Results: A total of 510 patients were enrolled. Median follow-up time was 58.3 months with 85.4% of 3-year failure-free survival in the once-every-3-weeks group and 85.6% in the once-a-week group. An absolute difference of −0.2% (95% confidence interval, −6.3 to 5.9; Pnoninferiority = 0.0016). Acute toxicities of grade 3 or higher occurred in 55.8% in the once-every-3-weeks group and 66.3% in the once-a-week group (P = 0.015). The most common acute toxicities were hematologic abnormalities, including leukopenia (16% vs. 27%; P = 0.0022) and thrombocytopenia (1% vs. 5%; P = 0.015). The late grade 3–4 auditory loss rate was significantly lower in the once-every-3-weeks group than the once-a-week group (6% vs. 13%; P = 0.0039). Conclusions: Once-every-3-weeks cisplatin as concurrent chemoradiotherapy is noninferior to once-a-week cisplatin in the treatment efficacy in the LANPC. Although both regimens are well tolerated, severe acute toxicities and late-onset auditory loss are higher in the once-a-week group.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-20-4532
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 7
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    Online Resource
    AMPK Phosphorylates ZDHHC13 to Increase MC1R Activity and Suppress Melanomagenesis
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7 ( 2023-04-04), p. 1062-1073
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7 ( 2023-04-04), p. 1062-1073
    Abstract: Inherited genetic variations in the melanocortin-1 receptor (MC1R) responsible for human red hair color (RHC) variants are associated with impaired DNA damage repair and increased melanoma risk. MC1R signaling is critically dependent on palmitoylation, primarily mediated by the protein acyltransferase zinc finger DHHC-type palmitoyltransferase 13 (ZDHHC13). A better understanding of how ZDHHC13 is physiologically activated could help identify approaches to prevent melanomagenesis in redheads. Here, we report that AMP-activated protein kinase (AMPK) phosphorylates ZDHHC13 at S208 to strengthen the interaction between ZDHHC13 and MC1R-RHC, leading to enhanced MC1R palmitoylation in redheads. Consequently, phosphorylation of ZDHHC13 by AMPK increased MC1R-RHC downstream signaling. AMPK activation and MC1R palmitoylation repressed UVB-induced transformation of human melanocytes in vitro and delayed melanomagenesis in vivo in C57BL/6J-MC1R-RHC mice. The importance of AMPK to MC1R signaling was validated in human melanomas where AMPK upregulation correlated with expression of factors downstream from MC1R signaling and with prolonged patient survival. These findings suggest AMPK activation as a promising strategy to reduce melanoma risk, especially for individuals with red hair. Significance: Phosphorylation of ZDHHC13 by AMPK at S208 promotes MC1R activation and suppresses melanocyte transformation, indicating activation of AMPK as a potential approach to prevent melanoma in people with red hair.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-22-2595
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 8
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    Oxidative Stress Activates SIRT2 to Deacetylate and Stimulate Phosphoglycerate Mutase
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 13 ( 2014-07-01), p. 3630-3642
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 13 ( 2014-07-01), p. 3630-3642
    Abstract: Glycolytic enzyme phosphoglycerate mutase (PGAM) plays an important role in coordinating energy production with generation of reducing power and the biosynthesis of nucleotide precursors and amino acids. Inhibition of PGAM by small RNAi or small molecule attenuates cell proliferation and tumor growth. PGAM activity is commonly upregulated in tumor cells, but how PGAM activity is regulated in vivo remains poorly understood. Here we report that PGAM is acetylated at lysine 100 (K100), an active site residue that is invariably conserved from bacteria, to yeast, plant, and mammals. K100 acetylation is detected in fly, mouse, and human cells and in multiple tissues and decreases PGAM2 activity. The cytosolic protein deacetylase sirtuin 2 (SIRT2) deacetylates and activates PGAM2. Increased levels of reactive oxygen species stimulate PGAM2 deacetylation and activity by promoting its interaction with SIRT2. Substitution of endogenous PGAM2 with an acetylation mimetic mutant K100Q reduces cellular NADPH production and inhibits cell proliferation and tumor growth. These results reveal a mechanism of PGAM2 regulation and NADPH homeostasis in response to oxidative stress that impacts cell proliferation and tumor growth. Cancer Res; 74(13); 3630–42. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-13-3615
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
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  • 9
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    CYP3A5 Functions as a Tumor Suppressor in Hepatocellular Carcinoma by Regulating mTORC2/Akt Signaling
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 7 ( 2015-04-01), p. 1470-1481
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 7 ( 2015-04-01), p. 1470-1481
    Abstract: CYP3A5 is a cytochrome P450 protein that functions in the liver metabolism of many carcinogens and cancer drugs. However, it has not been thought to directly affect cancer progression. In this study, we challenge this perspective by demonstrating that CYP3A5 is downregulated in many hepatocellular carcinomas (HCC), where it has an important role as a tumor suppressor that antagonizes the malignant phenotype. CYP3A5 was downregulated in multiple cohorts of human HCC examined. Lower CYP3A5 levels were associated with more aggressive vascular invasion, poor differentiation, shorter time to disease recurrence after treatment, and worse overall patient survival. Mechanistic investigations showed that CYP3A5 overexpression limited MMP2/9 function and suppressed HCC migration and invasion in vitro and in vivo by inhibiting AKT signaling. Notably, AKT phosphorylation at Ser473 was inhibited in CYP3A5-overexpressing HCC cells, an event requiring mTORC2 but not Rictor/mTOR complex formation. CYP3A5-induced ROS accumulation was found to be a critical upstream regulator of mTORC2 activity, consistent with evidence of reduced GSH redox activity in most clinical HCC specimens with reduced metastatic capacity. Taken together, our results defined CYP3A5 as a suppressor of HCC pathogenesis and metastasis with potential utility a prognostic biomarker. Cancer Res; 75(7); 1470–81. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-14-1589
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 10
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    Abstract 1212: Studying cancer drug resistance in patient derived xenograft tumor models
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1212-1212
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1212-1212
    Abstract: Anti-cancer drugs, either targeted therapies or cytotoxic chemotherapies, have proven to be effective in treating certain cancer patients. However, in most cases, tumors recur and become resistant to the treatment after a period of time. There are urgent needs to understand the underlying drug resistance mechanisms, to discover drug resistance targets and drug resistance biomarkers and to develop new therapies or combination therapies to tackle this widely occurring clinical problem. Currently the main approaches to study cancer drug resistance include analyzing clinical samples and developing drug resistance models in vitro. Numerous potential resistance mechanisms have been revealed. However, validation of these findings in a clinical-like setting and to test therapies in preclinical studies requires in vivo tumor models of drug resistance. At GenenDesign, we have developed cancer drug resistance PDX tumor models through short term drug testing or long term treatment of xenograft tumor mice. Cancer drugs investigated in our studies include major classes of targeted therapeutic modalities such as Her2 inhibitors, EGFR inhibitors, FGFR inhibitors and cMet/ALK inhibitors, as well as several standard of care (SoC) chemotherapies. From these studies, we have identified de novo resistance models, acquired resistance models and reversible resistance models in multiple cancer types including lung cancer and gastric cancer. In analyzing more than a dozen of Her2 positive but Herceptin resistance PDX models, we have uncovered molecular abnormalities such as Pten deletion, PI3K mutation, amplification of EGFR, cMet and cyclin E, which have been reported previously to be associated with Herceptin resistance in early studies. Studies are on-going to test whether combination therapies will be effective in overcoming Herceptin resistance. In drug response profiling of our PDX models, we also found wide spread phenotypical and functional heterogeneity in individual tumors. The heterogeneity within each tumor, in some cases, contributed to evolving of drug resistance from initially responsive tumors. Citation Format: Tengfei Yu, Ying Yan, Wei Du, Yuefei Yang, Tingting Tan, Xuqin Yang, Jiali Gu, Liang Hua, Xin K. Ye, Zhenyu Gu. Studying cancer drug resistance in patient derived xenograft tumor models. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1212. doi:10.1158/1538-7445.AM2014-1212
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-1212
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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    detail.hit.zdb_id: 1432-1
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