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  • American Association for Cancer Research (AACR)  (7)
  • 1
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    Online Resource
    Abstract 2397: Epigenetic silencing in clear renal cell carcinoma: KEAP1 promoter hypermethylation
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2397-2397
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2397-2397
    Abstract: The Keap1/Nrf2 pathway is a master regulator of the cellular redox state through the induction of several antioxidant defense genes implicated in chemotherapeutic drugs resistance of tumor cells. An increasing body of evidence supports a key role for Keap1/Nrf2 pathway in kidney diseases and renal cell carcinoma, but data concerning the molecular basis and the clinical effect of its deregulation remain incomplete. Here we performed a comprehensive genetic and epigenetic analysis of the KEAP1 gene in 37 tumor/normal paired tissues of clear cell Renal Carcinoma (ccRCCs). Promoter methylation analysis was performed by using a quantitative methylation specific PCR assay in real time, whereas mutation scanning was performed on FFPE tissues by direct sanger sequencing of the exons 4-7 codifying for the DGR domain of the Keap1 protein. A tumor-specific DNA methylation of the KEAP1 gene promoter region was found in 18 out of 37 ccRCCs (48,6%) and a direct effects on the modulation of Keap1 mRNA levels was confirmed by in vitro 5-azacytidine treatment on three different ccRCCs cell lines. Analysis of an independent TGCA data set corroborate the epigenetic findings and reveals a significant correlation in multivariate analysis of epigenetic KEAP1 silencing with Overall Survival in ccRCCs. Our results further suggest that epigenetic deregulation of the Nrf2/Keap1 system could play a pivotal role in the cancerogenesis of ccRCCs. In addition identifying patients with KEAP1 epigenetic abnormalities may contribute to disease progression prediction and response to therapy in ccRCC affected patients. Citation Format: Federico Pio Fabrizio, Manuela Costantini, Massimiliano Copetti, Anna Maria la Torre, Angelo Sparaneo, Andrea Fontana, Maria Luana Poeta, Michele Gallucci, Steno Sentinelli, Paolo Graziano, Paola Parente, Vincenzo Pompeo, Laura De Salvo, Giuseppe Simone, Rocco Papalia, Francesco Picardo, Teresa Balsamo, Gerardo Paolo Flammia, Domenico Trombetta, Angela Pantalone, Klaas Kok, Paranita Ferronika, Lucia Anna Muscarella, Vito Michele Fazio. Epigenetic silencing in clear renal cell carcinoma: KEAP1 promoter hypermethylation [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 2397. doi:10.1158/1538-7445.AM2017-2397
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-2397
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 2
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    Abstract 494: Frequent NRG1 genomic rearrangements in invasive mucinous adenocarcinoma from caucasian patients
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 494-494
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 494-494
    Abstract: Invasive Mucinous Adenocarcinoma (IMA) accounts for 2-5% of lung adenocarcinomas and it is associated with an unfavorable clinical course, mainly due to lack of effective treatments. Current knowledge of the molecular alterations involved in IMAs is limited. Recently, the NRG1 genomic rearrangement was identified as a subtype-specific molecular feature of Asiatic IMA cohorts since it acts as a strong inductor of the aberrant tyrosine kinase activity of ErbB2/ErbB3 heterodimers through PI3K–AKT and MAPK cellular cascades. In light of these premises we explored the occurrence and frequency of NRG1 fusions in a cohort of 90 Formalin Fixed Paraffin Embedded (FFPE) lung adenocarcinoma from Caucasian patients (35 non-IMAs and 55 IMAs) by performing FISH analysis to study the NRG1 genomic region (β-III isoform, chr 8p12). In total, 16 out of 55 (29%) IMAs showed NRG1 rearrangements, whereas in non-mucinous lung adenocarcinoma group it was found with a frequency of 3% (1/35). The functional effect of the genomic rearrangement was confirmed by RT-PCR and sequencing in three cases with available RNA, where NRG1-CD74 fusion transcripts were identified. An aberrant expression of pErbB3 was also observed in these three NRG1 rearranged cases by performing immunohistochemistry analysis, thus confirming the ErbB3 cascade activation. Our results strongly confirm NRG1 rearrangements as potentially treatable oncogenic driver alterations associated with a definite lung adenocarcinoma subtype in Caucasian population and support a clear molecular rationale to novel therapeutic opportunity for these aggressive tumors. Note: This abstract was not presented at the meeting. Citation Format: Domenico Trombetta, Giulio Rossi, Angelo Sparaneo, Federico P. Fabrizio, Maria C. Manzorra, Evaristo Maiello, Vito M. Fazio, Paolo Graziano, Lucia A. Muscarella. Frequent NRG1 genomic rearrangements in invasive mucinous adenocarcinoma from caucasian patients [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 494. doi:10.1158/1538-7445.AM2017-494
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-494
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Abstract 3750: Design and experimental validation of WG00446_MET_A methylation next generation sequencing panel using ion AmpliSeq technology
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 3750-3750
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 3750-3750
    Abstract: Background: DNA methylation is the most recognized epigenetic mark that leads to a massive distortion in cancer cells. It has been observed that a large number of DNA hypermethylation events co-occur in groups of genes, thus providing a growth advantage to the cell in promoting cell differentiation and neoplastic transformation. Here we designed and performed a first step of validation of a novel next-generation sequencing (NGS) targeted methylation panel that can simultaneously evaluate the methylation levels of multiple cancer-related genes. Methods: The WG00446_MET_A AmpliSeq™ Methylation Panel for Cancer Research was designed using the Ion AmpliSeq technology to amplify 152 regions with an amplicon size range of 125-175bp, that covers a total of 1107 promoter and intragenic CpGs of 18 cancer-related genes. The performance of the panel was assessed by running in duplicate commercially available fully methylated and unmethylated control human gDNA samples and a variable mixture of them to simulate 10%, 25%, 75%, and 90% of global methylation. The libraries (manual preparation using the Ion AmpliSeq Plus Library Kit) were loaded on 530 chips and run on the GeneStudio S5 Sequencer (Thermo Fisher Scientific). The sequencing output was analyzed using the methylation_analysis plugin, available on Ion Torrent Suite v5.16 (Thermo Fisher Scientific). Results: The WG00446_MET_A panel allowed to run 6 samples per 530 chips to reach an observed mean target depth & gt;2,000X (observed reads on-targets: & gt;80%; average number of mapped reads: & gt;450,000/sample). The conversion efficiency, determined by spiking-in Unmethylated Lambda DNA into each sample before the bisulfite conversion process, was & gt;97% for all samples. The observed % of global methylation for all CpGs were & gt;98% and & lt;2% for fully methylated and unmethylated gDNA samples, respectively. The observed results for the variable mixtures were in agreement with what expected. Conclusions: The methylation-specific NGS analysis using the WG00446_MET_A panel represents a feasible method for a fast and multiplexed screening of cancer patients by a high-throughput approach. It will offer the opportunity to design a more robust algorithm for disease prediction for those cancer patients with a low quantity of biological material available. The orthogonal testing on DNA extracted by FFPE and frozen samples is ongoing with a subset of amplicons from the WG00446_MET_A panel. Citation Format: Federico Pio Fabrizio, Stefano Castellana, Angelo Sparaneo, Tommaso Mazza, Flavia Centra, Domenico Trombetta, Vito Michele Fazio, Lucia Anna Muscarella. Design and experimental validation of WG00446_MET_A methylation next generation sequencing panel using ion AmpliSeq technology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3750.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-3750
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
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    Abstract 2251: nrf2-keap1 axis molecular profile in small cell lung cancer cell lines
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2251-2251
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2251-2251
    Abstract: The Keap1/Nrf2 pathway is a master regulator of antioxidants and cellular stress responses implicated in resistance of tumor cells against chemotherapeutic drugs. The link between molecular alterations of this pathway in Non Small Cell Lung Cancer (NSCLC) is well studied and appears to depend on several main factors including the existence of activating mutations in NFE2LE gene and/or loss of function mutations and methylation in the KEAP1 gene. At present, the data concerning the mechanism of alteration of Nrf2-Keap1 pathway in Small Cell Lung Cancer (SCLC) instead are almost incomplete and correlation analysis with therapeutic strategies targeting the molecular dysfunction of this pathway is ongoing. Here we present a comprehensive molecular alteration profile of the main partners of the Nrf2/keap1 axis in 12 SCLC cell lines by integrating data from SNP-Array analysis, immunofluorescence, mutation screening by direct sequencing, methylation by QMSP and expression analyses by RT-qPCR and western blotting. Our analyses confirm the global deregulation of Nrf2/Keap1 pathway in SCLC cell lines, showing an hypermethylation of the CpGs located into the P1 promoter region of the KEAP1 in 42% (5/12) of the cell lines, and a chromosomal amplification involving the NFE2LE gene locus (2q31.1) in two cell lines. Only one just described point mutation in the kelch-repeat 2 was observed in one of the cell line analysed. Our gene-alteration profile of SCLC cell lines provides new insights into the mechanism of deregulation of Nrf2-Keap1 detoxification pathway in this group of high grade neuroendocrine lung cancers, suggesting the NFE2LE gene amplification and the KEAP1 promoter hypermethylation as alternative mechanisms of dysfunctional Nrf2/Keap1 in SCLCs.Analyses on tumor tissues are ongoing to confirm these observations. Moreover, the provided full molecular data from cell lines will be useful for in vitro functional studies aimed to establish new combined therapeutic strategies in targeted cancer treatments of this aggressive lung tumor histotype. Citation Format: Lucia Anna Muscarella, Annamaria la Torre, Angelo Sparaneo, Orazio Palumbo, Clelia Tiziana Storlazzi, Teresa Balsamo, Domenico Trombetta, Fabio Pellegrini, Raffaela Barbano, Barbara Pasculli, Paolo Graziano, Montse Sanchez-cespedes, Maria Teresa Landi, Paola Parrella, Vito Michele Fazio. nrf2-keap1 axis molecular profile in small cell lung cancer cell lines. [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 2251. doi:10.1158/1538-7445.AM2014-2251
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-2251
    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
    detail.hit.zdb_id: 410466-3
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  • 5
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    Abstract 4887: Recurrent NRG1 rearrangements in Caucasian pulmonary mucinous adenocarcinoma: results from an Italian multi-center cohort
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4887-4887
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4887-4887
    Abstract: Invasive Mucinous Adenocarcinoma (IMA) is a rare histotype of lung adenocarcinoma associated with an unfavorable prognosis due to the lack of effective treatment. The NRG1 rearrangement is a new subtype-specific molecular feature of IMA and acts as a strong oncogenic inductor of the aberrant tyrosine kinase activity of ErbB2/ErbB3 heterodimers through PI3K-AKT/MAPK cellular cascades. We recently described for the first time the occurrence of NRG1 rearrangements in 31% of Caucasian lung IMAs and highlighted a strong association between NRG1 rearrangements and ErbB3 activation. Here we extended our lung IMA samples cohort by enrolling a total of 71 patients from three different Italian Centers and collected clinical-pathological information and molecular profile, included the mutational status of KRAS, EGFR and ALK genes. We screened all samples by fluorescent in situ hybridization (FISH) for the detection of putative NRG1 rearrangements and by immunohistochemistry (IHC) for the expression of phosphorylated-ErbB3 (pErbB3) receptor. Finally, we customized a new targeted RNA Custom Panel to detect all 9 NRG1-fusion variants published to date to molecular characterize the NRG1 fusion variants in NRG1 rearranged IMAs. Results showed NRG1 rearrangements in 32% of lung IMAs, displaying both NRG1 FISH split signals and deletions of the 5' portion of the gene. IHC confirmed our previous findings of association between pErbB3 immunoreactivity and NRG1 rearrangements, and the heterogeneity of fluorescent signal distribution and immunostaining along the tissue sections. The CD74-NRG1 remains the most common fusion variant identified in lung IMA samples. Correlation analysis among clinical-pathological data, pErbB3 expression and NRG1 rearrangements are ongoing. Our results confirm the usefulness of IHC/FISH combined approach for NRG1 broken tumors identification and highlight the role of NRG1 rearrangement as master molecular marker of lung IMAs, potentially useful to select patients for the emerging target therapies. Citation Format: Domenico Trombetta, Paolo Graziano, Angelo Sparaneo, Giulio Rossi, Antonio Rossi, Marcello Tiseo, Massimo Di Maio, Federico P. Fabrizio, Maria C. Manzorra, Flavia Centra, Leonarda Di Candia, Marco Audisio, Evaristo Maiello, Vito M. Fazio, Lucia A. Muscarella. Recurrent NRG1 rearrangements in Caucasian pulmonary mucinous adenocarcinoma: results from an Italian multi-center cohort [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4887.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-4887
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
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    Abstract 3843: Nrf2-keap1 axis: uncovers molecular profile in lung carcinoids
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 3843-3843
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 3843-3843
    Abstract: Introduction. The Keap1/Nrf2 pathway is a master regulator of antioxidants and cellular stress re-sponses implicated in resistance of tumour cells against chemotherapeutic drugs. Recent data suggest that genetic and epigenetic mechanisms may play a pivotal role in the regulation of KEAP1 expression in Non Small Cell Lung Cancer. At present, the data concerning the mechanism of alteration of Nrf2-Keap1 pathway in the Carcinoids of the lung remain almost incomplete. Materials and methods. Here we report a comprehensive molecular characterization of Keap1/Nrf2 axis in cell lines and 48 tissues from Lung Carcinoid affected patients by integrating data from altera-tions at DNA, transcript and protein levels. Results. An hypermethylation of the CpGs island located into the P1 promoter region of the KEAP1 was detected in 16 out of the 32 Typical Carcinoids (50%) and 8 out of the 16 Atypical Carcinoids (50%). No somatic mutations were detected both in the kelch-repeats region of the KEAP1 gene and in the Nhe2 domain of NFE2L2 gene, whereas LOH at the KEAP1 locus (19p13.2) was found in more than 50% of cases, suggesting that biallelic inactivation of KEAP1 in lung cancer is a common event in lung carcinoids. Decreased of the KEAP1 expression in methylated cancer cells induced greater nuclear accumulation of Nrf2, causing enhanced transcriptional xenobiotic metabolism enzymes. Conclusions. This is the first study to our knowledge that provides new insights into the mechanism of deregulation of Nrf2/Keap1 detoxification pathway in lung carcinoids. Loss of KEAP1 function leading to constitutive activation of Nrf2-mediated gene expression in cancer suggests that deregulation of the Keap1/Nrf2 system could play a pivotal role in the pathogenesis of carcinoids. Citation Format: Angelo Sparaneo, Annamaria la Torre, Domenico Trombetta, Leonarda Di Candia, Massimiliano Copetti, Teresa Balsamo, Evaristo Maiello, Paolo Graziano, Vito M. Fazio, Lucia A. Muscarella, Montse Sanchez-Cespedes. Nrf2-keap1 axis: uncovers molecular profile in lung carcinoids. [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 3843. doi:10.1158/1538-7445.AM2015-3843
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-3843
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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    Abstract 3841: Effects of KEAP1 genetic and epigenetic silencing in SCLC cell lines
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 3841-3841
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 3841-3841
    Abstract: Introduction. Nuclear factor erythroid-2 related factor 2 (Nrf2) is a redox-sensitive transcription factor that positively regulates the expression of genes encoding antioxidants, xenobiotic detoxification enzymes, and drug efflux pumps, and confers cytoprotection against oxidative stress and xenobiotics in normal cells. Kelch-like ECH-associated protein 1 (Keap1) negatively regulates Nrf2 activity by targeting it to proteasomal degradation. We have just described a Keap1/Nrf2 axis full genetic and epigenetic characterization of SCLC cell lines that revealed unreported molecular alterations of the Keap1/Nrf2 axis. Materials and methods. The downstream effects of the genetic and epigenetic alterations of the KEAP1 gene were investigated in 12 cell lines derived from human small cell lung carcinoma in terms of modulation of the KEAP1 transcript and protein levels, nuclear accumulation of Nrf2 and enhancing transcriptional induction of xenobiotic metabolism enzymes. Additional functional analysis of short interfering RNA (siRNA) inhibition of the KEAP1 and treatment 5-aza-2′-deoxycytidine (DAC) were conducted. Results. Our analysis revealed that the Keap1 mRNA and protein level decreased significantly in genetic and epigenetic alterated SCLC cell lines compared with those without any alterations. Con-versely Nrf2 levels and protein nuclear localization were increased and these modifications were associated with a parallel increase in the expression of AKR1C1, TXN1 and NQO1 at the cellular lev-el. Silencing RNA experiments in vitro in H1184, H69V and were performed to confirm the cause-effect relation between the gain of Nrf2 and the increase in AKR1C1, TXN1 and NQO1 expression. Treatments with 5-aza-2′-deoxycytidine restored the expression of KEAP1 in SCLC cells and replace the functional Keap1/Nrf2 equilibrium. Conclusions. Our data provide new insights into the potential downstream effects of genetic and epigenetic Keap1/Nrf2 molecular deregulation in SCLCs, suggesting that the impairment of Keap1 activity actually induces the expression of cytoprotective enzymes also in small cell lung cancer cells. Validations on tissues from SCLC affected patients combined with in vitro pharmacological studies are demanded to establish new combined therapeutic strategies in targeted cancer treat-ments of this aggressive lung tumour histotype. Citation Format: Domenico Trombetta, Annamaria la Torre, Angelo Sparaneo, Teresa Balsamo, Massimiliano Copetti, Montse Sanchez-Cespedes, Evaristo Maiello, Paolo Graziano, Vito M. Fazio, Lucia A. Muscarella. Effects of KEAP1 genetic and epigenetic silencing in SCLC cell lines. [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 3841. doi:10.1158/1538-7445.AM2015-3841
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-3841
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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