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  • 1
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    Online Resource
    Abstract 2615: Amplification and/or high expression of Myc family genes sensitizes tumor cells to aurora kinase inhibitors
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2615-2615
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2615-2615
    Abstract: The identification of patient populations predicted to derive clinical benefit from systemic treatment regimens is of critical importance for development of targeted therapies. Collective clinical data available for the Aurora kinase inhibitor class of targeted therapies has indicated that broad single agent clinical activity is not readily apparent. We screened a panel of established lung (mostly non-small cell) and colon cell lines for growth inhibitory sensitivity to PF-03814735, an Aurora family kinase inhibitor, revealing a potential correlation with Myc family amplification or expression. The Aurora kinases A and B have been shown to be functionally linked with Myc family oncoproteins in a number of tumor types. Myc family gene amplification events have been reported in about 30% of small cell lung cancer (SCLC) primary tumors and around 50% of cell lines established from SCLC. We next screened a panel of around 20 SCLC lines for sensitivity to PF-03814735 and its relationship to Myc family gene copy number and gene expression levels. Sensitivity to PF-03814735 in vitro was strongly correlated with amplification events in at least one of the Myc family genes (c-Myc, L-Myc, N-Myc) as well as mRNA expression levels of those genes. Myc family expression demonstrated a significant correlation with gene copy number. Follow up studies to evaluate antitumor efficacy in two SCLC xenograft models, H82 (c-Myc) and H69 (N-Myc), indicated significant tumor growth inhibition by PF-03814735. However, the SCLC models were not appreciably more sensitive to PF-03814735 than several non-Myc amplified tumors studied previously (HCT-116, COLO-205, MDA-MB-231) indicating that further study of optimal dose schedule and/or the molecular basis of sensitivity is warranted. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2615.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-2615
    RVK:
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    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 2
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    Abstract 387: Development of a model of acquired resistance to a multi targeted VEGFR TKI and strategies to target resistance mechanisms through combination
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 387-387
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 387-387
    Abstract: Anti angiogenic agents that target the VEGF pathway (bevacizumab, sorafenib and sunitinib (SU)) have demonstrated improved clinical benefit as single agents or in combination with chemotherapy in a variety of solid tumor types. Although this class of agents has provided an improved treatment option to certain tumor types, it is evident that some patients do not respond to therapy or will relapse despite an initial response to treatment due to an acquired resistance. To better understand this mode of acquired resistance to this class of agents, a model of Renal Cell Carcinoma (RCC) which has shown regression, eventually developed evasive resistance during long term administration of the single agent sunitinib (a small-molecule inhibitor of the VEGF-1, 2, 3, PDGF-α,β, KIT, CSF-1R and FLT-3 receptor tyrosine kinases). Despite the observation that resistant tumors under continuous treatment with sunitinib (60 mg/kg PO, QD) demonstrated a gross phenotypic reduction of micro-vascular density (MVD), they continued to show a progressive increase in size. Because the observed low MVD phenotype was suggestive of an ability of resistant tumor cells to survive in an increasingly hypoxic environment with a reduced functional vasculature, emphasis was placed on identifying tumor cell derived resistance factors. Gene expression and/or proteomic profiling studies accompanied by confirmatory immunoblotting indicated a subset of differentially expressed genes and/or proteins in resistant vs. sensitive treated tumors. Although profiling studies did not clearly elucidate definitive resistance mechanisms, the dysregulation of EGFR, FGFR1, & TGFB1 pathways and downstream signaling through PI3K and MEK were potentially implicated. Comparative genomic hybridization studies did not identify any resistance mechanisms at the cytogenetic level. Sunitinib combination studies designed to target pathways potentially involved in resistance (SU + a PI3K/mTOR inhibitor; SU + a MEK inhibitor) demonstrated the ability to restore sensitivity in the sunitinib resistance model. The ability to identify and characterize resistance mechanisms and circumvent resistance through combination approaches may have utility in developing future combination regimens for anti angiogenic therapies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 387.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-387
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 3
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    Noninvasive Saliva-based EGFR Gene Mutation Detection in Patients with Lung Cancer
    American Thoracic Society ; 2014
    In:  American Journal of Respiratory and Critical Care Medicine Vol. 190, No. 10 ( 2014-11-15), p. 1117-1126
    Details
    In: American Journal of Respiratory and Critical Care Medicine, American Thoracic Society, Vol. 190, No. 10 ( 2014-11-15), p. 1117-1126
    Type of Medium: Online Resource
    ISSN: 1073-449X , 1535-4970
    URL: Article
    DOI: 10.1164/rccm.201406-1003OC
    RVK:
    XA 21200
    Language: English
    Publisher: American Thoracic Society
    Publication Date: 2014
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  • 4
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    [18F]FLT–PET Imaging Does Not Always “Light Up” Proliferating Tumor Cells
    American Association for Cancer Research (AACR) ; 2012
    In:  Clinical Cancer Research Vol. 18, No. 5 ( 2012-03-01), p. 1303-1312
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 5 ( 2012-03-01), p. 1303-1312
    Abstract: Purpose: [18F]FLT (3′-Fluoro-3′ deoxythymidine)–PET imaging was proposed as a tool for measuring in vivo tumor cell proliferation. The aim of this article was to validate the use of [18F] FLT–PET imaging for measuring xenograft proliferation and subsequent monitoring of targeted therapy. Experimental Design: In exponentially growing xenografts, factors that could impact the outcome of [18F]FLT–PET imaging, such as nucleoside transporters, thymidine kinase 1, the relative contribution of DNA salvage pathway, and the ratio of FLT to thymidine, were evaluated. The [18F] FLT tracer avidity was compared with other proliferation markers. Results: In a panel of proliferating xenografts, [18F]FLT or [3H] thymidine tracer avidity failed to reflect the tumor growth rate across different tumor types, despite the high expressions of Ki67 and TK1. When FLT was injected at the same dose level as used in the preclinical [18F]FLT–PET imaging, the plasma exposure ratio of FLT to thymidine was approximately 1:200. Thymidine levels in different tumor types seemed to be variable and exhibited an inverse relationship with the FLT tracer avidity. In contrast, high-dose administration of bromdeoxyuridine (BrdUrd; 50 mg/kg) yielded a plasma exposure of more than 4-fold higher than thymidine and leads to a strong correlation between the BrdUrd uptake and the tumor proliferation rate. In FLT tracer-avid models, [18F] FLT–PET imaging as a surrogate biomarker predicted the therapeutic response of CDK4/6 inhibitor PD-0332991. Conclusions: Tumor thymidine level is one of the factors that impact the correlation between [18F]FLT uptake and tumor cell proliferation. With careful validation, [18F] FLT–PET imaging can be used to monitor antiproliferative therapies in tracer-avid malignancies. Clin Cancer Res; 18(5); 1303–12. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-11-1433
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 5
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    Initial Clinical Sensitivity and Acquired Resistance to MET Inhibition in MET -Mutated Papillary Renal Cell Carcinoma
    American Society of Clinical Oncology (ASCO) ; 2013
    In:  Journal of Clinical Oncology Vol. 31, No. 16 ( 2013-06-01), p. e254-e258
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 31, No. 16 ( 2013-06-01), p. e254-e258
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2012.46.4289
    RVK:
    XA 52760
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    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2013
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  • 6
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    A Single-Tube Multiplexed Assay for Detecting ALK, ROS1, and RET Fusions in Lung Cancer
    Elsevier BV ; 2014
    In:  The Journal of Molecular Diagnostics Vol. 16, No. 2 ( 2014-03), p. 229-243
    Details
    In: The Journal of Molecular Diagnostics, Elsevier BV, Vol. 16, No. 2 ( 2014-03), p. 229-243
    Type of Medium: Online Resource
    ISSN: 1525-1578
    URL: Article
    DOI: 10.1016/j.jmoldx.2013.11.007
    RVK:
    XA 55072
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2032654-3
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  • 7
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    Abstract LB-220: Molecular predictors of sensitivity to an IGF1R inhibitor in pre-clinical models of lung and colon cancers
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-220-LB-220
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-220-LB-220
    Abstract: Targeting the insulin like growth factor receptor (IGF1R) signaling pathway is a promising approach against a variety of cancers and several clinical trials are now underway designed to evaluate the efficacy of IGF1R inhibitors singly or in combination with chemotherapeutic agents. Identification of the optimal patient population likely to respond is critical to the success of this class of targeted agents. To identify potentially predictive biomarkers, we sought to correlate response to figitumumab (CP-751,871), a fully human monoclonal antibody against IGF1R with molecular characteristics across a panel of cell lines. Growth inhibition to CP-751,871 was assessed in a panel of non-small cell lung carcinoma (NSCLC) (n=27) and colon cancer cell lines (n=21) cultured in anchorage and anchorage-independent conditions. Mutation status, whole-genome mRNA expression and DNA copy number were correlated to drug sensitivity. In addition, RNA expression of key genes in relevant signaling pathways was also interrogated via real time PCR. In the present studies, the frequency of response was greater in colon cancer cell lines than in NSCLC. Tissue or cell origin-specific expression levels of insulin-like growth factor binding proteins (IGFBPs) were associated with sensitivity. Low IGFBP3 expression [p=0.0035] correlated with response in NSCLC cell lines whereas low IGFBP6 [p=0.013] and IGF2BP3 [p=0.038] expression correlated with response in colon cancer lines. Increased IGF1R mRNA [p=0.045] levels, microsatellite stability, and PIK3CA wild-type status were also correlated with sensitivity in colon cancer lines. In addition, high expression of erbB2 [p=0.04] and erbB3 [p=0.04] were also associated with sensitivity of colon cancer lines. Collectively, findings from these studies are of potential value to identify patient populations with increased probability of benefit from IGF1R targeted agents. Our results further indicate that molecular predictors associated with the IGF1R pathway are potentially distinct between lung and colon cancer lines and additional studies to extend to other tumor types are warranted. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-220.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-LB-220
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 8
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    Abstract 2749: Liquid biopsy testing allows highly-sensitive detection of plasma cfDNA mutations in 87 breast cancer-related genes
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2749-2749
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2749-2749
    Abstract: Liquid biopsies have the potential to revolutionize the way physicians select personalized anti-cancer therapies, monitor patient responses to treatment, and characterize acquired resistance to cancer drugs. New tests that use a simple peripheral blood draw offer snapshots of a patient‘s total tumor DNA mutation profile and are attractive because of their minimally-invasive modality and because they integrate information from both primary and metastatic disease. Currently, most plasma cell-free DNA (cfDNA) mutation detection tests used in clinical research detect known hotspot mutations in a limited number of genes. Technologies that interrogate multi-gene panels in cfDNA are advancing, but commercially-available options suitable for clinical use are limited, come at a high cost, and are not customizable. We designed and developed a customized, next generation sequencing-based, liquid biopsy assay capable of detecting somatic mutations in 87 breast cancer genes involved in cell cycle and estrogen receptor signaling. Targeted regions (147 Kb) were enriched using hybrid capture resulting in an average capture specificity and uniformity of 65.93% and 96.38%, respectively. When tested on cfDNA from healthy donors (n=14), we demonstrated a level of specificity & gt;99.99%. Analytical sensitivity of 0.1% was established on HapMap and reference mutant cell line DNA. Using a pool of HapMap genomic DNA (n=10), 96% (48/50) of SNPs with expected allele frequency of 0.1% were detected. In reference mutant cell line DNA with 1% or 0.1% mutant allele frequencies, we were able to reliably detect all mutations present at 1% and mutations at 0.1% in 50% of the cases. Assay validation on plasma cfDNA with matching tumor from ER+, HER2- breast cancer patients will be presented. In conclusion, we developed a highly sensitive and specific liquid biopsy assay to interrogate 87 breast cancer-related genes. The high level of specificity and sensitivity makes the test ideal not only for detecting known cancer gene hotspot mutations but also for detection of novel gene mutations that may arise during treatment as a result of acquired drug resistance. Citation Format: Maruja E. Lira, Tao Xie, Shibing Deng, Jennifer Kinong, Jingjin Gao, Zhou Zhu, Nathan Lee, Paul Rejto, Jadwiga Bienkowska, James Hardwick, Kai Wang, Stephen Huang. Liquid biopsy testing allows highly-sensitive detection of plasma cfDNA mutations in 87 breast cancer-related genes [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2749. doi:10.1158/1538-7445.AM2017-2749
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-2749
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 9
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    Abstract 3492: γ-secretase inhibitor PF-03084014 diminishes the tumor-initiating cells and demonstrates synergy with docetaxel in breast cancer xenograft models
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 3492-3492
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 3492-3492
    Abstract: Notch signaling is known to be a survival pathway for tumor-initiating cells. In this report, we demonstrate that the γ-secretase inhibitor PF-03084014 significantly enhances the antitumor activity of docetaxel in multiple xenograft models of triple-negative breast cancer. Mechanistic evaluation revealed that PF-03084014 perturbs the Notch signaling pathway and suppresses the function of tumor initiating cells (TIC). In MDA-MB-231Luc model, treatment of docetaxel led to a significant increase of CD133+/CD44+ and ALDH+ subpopulations by FACS analysis. In combination with PF-03084014, these two unique cell subpopulations were significantly diminished. Correspondingly, the functional analyses by tumor re-implant and mammosphere-forming efficiency assays revealed that docetaxel-therapy promoted the tumor initiating capability of the remaining cells, in which an increased stem cell property and Notch pathway activation were observed through gene signature changes. In contrast, PF-03084014 co-treatment with docetaxel substantially hampered the self-renewal ability of these cells. Notch target gene analysis demonstrated the biological relevance of PF-03084014-induced activity. To characterize the function of CD133+/CD44+ subpopulation, MDA-MB-231Luc tumors were de-bulked by the treatment with docetaxel. Subsequently, the CD133+/CD44+ and CD133-/CD44- subpopulatons were isolated and re-implanted in SCID-bg mice using a limiting dilution approach. The results showed that CD133+/CD44+ cells gave rise to tumors with a 100 % take rate (10/10), whereas CD133-/CD44- cells were not tumorgenic (0/10). In addition, CD133+/CD44+ cells exhibited much higher tumorigenicity compared with the respective adherent parental cell line. PF-03084014 treatment caused a significant delay of CD133+/CD44+ tumor growth. The ability of PF-03084014 to suppress TICs was also observed in other breast cancer xenografts, including patient derived models. This data suggests that anti-TIC is one of the contributing mechanisms for the synergistic activities of PF-03084014 in combination with docetaxel. Our work provides potential therapeutic opportunities for PF-03084014 to improve conventional cytotoxic therapy by inhibiting Notch signaling in tumor-initiating cells and other bulk tumor cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3492. doi:1538-7445.AM2012-3492
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-3492
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 10
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    Abstract 764: Rational combination of PF-06463922 (next-generation ALK inhibitor) with PI3K pathway inhibitors overcomes ALKi resistance in EML4-ALK+ NSCLC models
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 764-764
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 764-764
    Abstract: Crizotinib (PF-02341066) is a small molecule tyrosine kinase inhibitor of ALK, ROS1 and c-MET that is approved in over 70 countries for the treatment of ALK fusion positive non-small cell lung cancer (ALK+ NSCLC). Crizotinib achieved robust objective response rates of approximately 60% in ALK+ NSCLC and significantly improved progression free survival compared to chemotherapy. The emergence of secondary mutations within the ALK kinase domain or the activation of compensatory signaling pathways in crizotinib and other ALKi refractory tumors prompted searches for next generation of ALKi active against resistance mutations as single agents or in combination with other treatments. Such effort led to our recent discovery of PF-06463922, an ALK/ROS1 inhibitor with greatly improved ALK potency, brain penetration, and broad spectrum activity against all known clinical ALKi-resistant mutations. PF-06463922 is being tested in a Phase I clinical trial in both ALK+ and ROS1 fusion positive NSCLC in treatment naive or ALKi relapsed patients. In our current preclinical study, we explored rational combination strategies to further improve the efficacy of PF-06463922 in ALKi resistant cells or tumors. Our results show that compared to PF-06463922 alone, the combination of this compound with PI3K pathway inhibitors, such as PF-05212384 (PI3K/mTOR), GDC0941 (pan-PI3K) or GDC0032 (beta-sparing) leads to more robust anti-proliferative activity in vitro and greater duration of efficacy in vivo in the ALKi resistant models. These PI3K pathway inhibitors also partially overcome EGF or HGF ligand-induced resistance to PF-06463922. Interestingly, in addition to AKT signaling, both compounds inhibit ERK signaling as well, which may be essential for their enhancement of PF-06463922 cell activity or tumor efficacy in combination settings. Studies are ongoing to identify optimal partners for PF-06463922 combination using isoform selective PI3Ki, AKTi and mTORi. We are also exploring the breadth of efficacy of this combination in overcoming resistance to crizotinib, PF-06463922 or other ALKi. The findings provide important evidence that will help define the clinical development path for PF-06463922. This research effort may ultimately lead to more effective approaches to treat ALKi refractory patients in the clinic. Citation Format: Ping Wei, Ming Qiu, Nathan Lee, Joan Cao, Hui Wang, Konstantinos Tsaparikos, Conglin Fan, Timothy Sargis, Justine Lam, Maruja E. Lira, Goldie Lui, James Hardwick, Valeria Fantin, Paul Rejto, Tod Smeal. Rational combination of PF-06463922 (next-generation ALK inhibitor) with PI3K pathway inhibitors overcomes ALKi resistance in EML4-ALK+ NSCLC models. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 764. doi:10.1158/1538-7445.AM2015-764
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-764
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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