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  • 11
    Online Resource
    Online Resource
    Common variants in breast cancer risk loci predispose to distinct tumor subtypes
    Springer Science and Business Media LLC ; 2022
    In:  Breast Cancer Research Vol. 24, No. 1 ( 2022-01-04)
    Details
    In: Breast Cancer Research, Springer Science and Business Media LLC, Vol. 24, No. 1 ( 2022-01-04)
    Abstract: Genome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear. Methods Among 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes. Results Eighty-five of 173 variants were associated with at least one tumor feature (false discovery rate  〈  5%), most commonly ER and grade, followed by PR and HER2. Models for intrinsic-like subtypes found nearly all of these variants (83 of 85) associated at p   〈  0.05 with risk for at least one luminal-like subtype, and approximately half (41 of 85) of the variants were associated with risk of at least one non-luminal subtype, including 32 variants associated with triple-negative (TN) disease. Ten variants were associated with risk of all subtypes in different magnitude. Five variants were associated with risk of luminal A-like and TN subtypes in opposite directions. Conclusion This report demonstrates a high level of complexity in the etiology heterogeneity of breast cancer susceptibility variants and can inform investigations of subtype-specific risk prediction.
    Type of Medium: Online Resource
    ISSN: 1465-542X
    URL: Article
    DOI: 10.1186/s13058-021-01484-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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  • 12
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    Molecular profiling identifies targeted therapy opportunities in pediatric solid cancer
    Springer Science and Business Media LLC ; 2022
    In:  Nature Medicine Vol. 28, No. 8 ( 2022-08), p. 1581-1589
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 28, No. 8 ( 2022-08), p. 1581-1589
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/s41591-022-01856-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1484517-9
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  • 13
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    Abstract B13: Leveraging cloud-based computational resources for gene fusion discovery with potential clinical implications for pediatric solid tumor patients
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 14_Supplement ( 2020-07-15), p. B13-B13
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 14_Supplement ( 2020-07-15), p. B13-B13
    Abstract: Introduction: Gene fusions are important oncogenic drivers with significant clinical impact in some cancer types. This is particularly true in pediatric cancers that often have low mutational burden and lack other diagnostic markers and therapeutic targets. Many gene fusions are rare or private to the individual patient and can be difficult to detect with methods optimized for common fusions. Unbiased sequencing methods and expansive computational resources are needed for expanding our ability to characterize fusions. Building a comprehensive catalog of oncogenic gene fusions will improve our understanding of their diversity and fully harness their potential for clinical impact. Methods: Patients are eligible for the GAIN/iCat2 study if they have been diagnosed with high-risk or recurrent/refractory extracranial solid tumor at age 30 or less and have a sample available for sequencing. Enrolled patients with an unclear diagnosis after standard clinical testing are nominated for transcriptome sequencing by the study investigators. We developed a computational pipeline in Google Cloud for gene fusion discovery utilizing paired end Illumina RNA-Seq data, multiple fusion callers, and a custom algorithm for integrative data analysis. The multicaller fusion detection approach enables us to address the high false-positive rate typical for gene fusion calling in transcriptomic data while improving the sensitivity to detect the more challenging fusions. After filtering, the fusions are annotated using the databases of known fusions and cancer genes. The predicted fusion transcripts are inspected visually, and the fusions are selected based on relevance to diagnostic classification or therapy to be validated by an orthogonal method. Results: 41 tumor samples were sequenced and analyzed for gene fusions. A total of 203 candidate fusions were detected by two or more fusion callers. Based on functional annotations and potential impact on diagnosis or therapeutic approaches, 12 fusion transcripts of interest were identified, 10 of which were validated by either pre-enrollment testing or an orthogonal method. Of 16 mesenchymal cases, 6 validated fusions had diagnostic relevance and 3 validated fusions had therapeutic implications (ERC1-BRAF, RBPMS-NTRK2, and VCAN-IL23R). Two patients responded to matched targeted therapy. In one case, diagnostic classification was revised. Conclusions: Whole-transcriptome sequencing in this selected patient population identified some fusion transcripts with clinical relevance. Determining the biologic significance of previously unreported fusions will require orthogonal sequencing such as whole genome, functional studies, and analysis of larger patient populations. Improved accuracy and scalability of methods for large-scale gene fusion analysis in the growing public datasets are likely to expand the landscape of gene fusions in cancer. Citation Format: Alma Imamovic, Alanna J. Church, Laura B. Corson, Deirdre Reidy, Navin Pinto, Luke Maese, Theodore W. Laetsch, AeRang Kim, Susan I. Vear, Margaret E. Macy, Mark A. Applebaum, Rochelle Bagatell, Amit J. Sabnis, Daniel A. Weiser, Julia L. Glade-Bender, Gianna R. Strand, Lobin A. Lee, R. Seth Pinches, Catherine M. Clinton, Brian D. Crompton, Neal I. Lindeman, Steven G. DuBois, Katherine A. Janeway, Eliezer M. Van Allen. Leveraging cloud-based computational resources for gene fusion discovery with potential clinical implications for pediatric solid tumor patients [abstract]. In: Proceedings of the AACR Special Conference on the Advances in Pediatric Cancer Research; 2019 Sep 17-20; Montreal, QC, Canada. Philadelphia (PA): AACR; Cancer Res 2020;80(14 Suppl):Abstract nr B13.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.PEDCA19-B13
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 14
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    FANCM missense variants and breast cancer risk: a case-control association study of 75,156 European women
    Springer Science and Business Media LLC ; 2023
    In:  European Journal of Human Genetics Vol. 31, No. 5 ( 2023-05), p. 578-587
    Details
    In: European Journal of Human Genetics, Springer Science and Business Media LLC, Vol. 31, No. 5 ( 2023-05), p. 578-587
    Abstract: Evidence from literature, including the BRIDGES study, indicates that germline protein truncating variants (PTVs) in FANCM confer moderately increased risk of ER-negative and triple-negative breast cancer (TNBC), especially for women with a family history of the disease. Association between FANCM missense variants (MVs) and breast cancer risk has been postulated. In this study, we further used the BRIDGES study to test 689 FANCM MVs for association with breast cancer risk, overall and in ER-negative and TNBC subtypes, in 39,885 cases (7566 selected for family history) and 35,271 controls of European ancestry. Sixteen common MVs were tested individually; the remaining rare 673 MVs were tested by burden analyses considering their position and pathogenicity score. We also conducted a meta-analysis of our results and those from published studies. We did not find evidence for association for any of the 16 variants individually tested. The rare MVs were significantly associated with increased risk of ER-negative breast cancer by burden analysis comparing familial cases to controls (OR = 1.48; 95% CI 1.07–2.04; P  = 0.017). Higher ORs were found for the subgroup of MVs located in functional domains or predicted to be pathogenic. The meta-analysis indicated that FANCM MVs overall are associated with breast cancer risk (OR = 1.22; 95% CI 1.08–1.38; P  = 0.002). Our results support the definition from previous analyses of FANCM as a moderate-risk breast cancer gene and provide evidence that FANCM MVs could be low/moderate risk factors for ER-negative and TNBC subtypes. Further genetic and functional analyses are necessary to clarify better the increased risks due to FANCM MVs.
    Type of Medium: Online Resource
    ISSN: 1018-4813 , 1476-5438
    URL: Article
    DOI: 10.1038/s41431-022-01257-w
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
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    SSG: 12
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  • 15
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    Functional epigenetics approach identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers
    Proceedings of the National Academy of Sciences ; 2014
    In:  Proceedings of the National Academy of Sciences Vol. 111, No. 8 ( 2014-02-25), p. 3128-3133
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 111, No. 8 ( 2014-02-25), p. 3128-3133
    Abstract: Defects in epigenetic regulation play a fundamental role in the development of cancer, and epigenetic regulators have recently emerged as promising therapeutic candidates. We therefore set out to systematically interrogate epigenetic cancer dependencies by screening an epigenome-focused deep-coverage design shRNA (DECODER) library across 58 cancer cell lines. This screen identified BRM/SMARCA2, a DNA-dependent ATPase of the mammalian SWI/SNF (mSWI/SNF) chromatin remodeling complex, as being essential for the growth of tumor cells that harbor loss of function mutations in BRG1/SMARCA4. Depletion of BRM in BRG1-deficient cancer cells leads to a cell cycle arrest, induction of senescence, and increased levels of global H3K9me3. We further demonstrate the selective dependency of BRG1 -mutant tumors on BRM in vivo. Genetic alterations of the mSWI/SNF chromatin remodeling complexes are the most frequent among chromatin regulators in cancers, with BRG1/SMARCA4 mutations occurring in ∼10–15% of lung adenocarcinomas. Our findings position BRM as an attractive therapeutic target for BRG1 mutated cancers. Because BRG1 and BRM function as mutually exclusive catalytic subunits of the mSWI/SNF complex, we propose that such synthetic lethality may be explained by paralog insufficiency, in which loss of one family member unveils critical dependence on paralogous subunits. This concept of “cancer-selective paralog dependency” may provide a more general strategy for targeting other tumor suppressor lesions/complexes with paralogous subunits.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1316793111
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2014
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    detail.hit.zdb_id: 1461794-8
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  • 16
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    The Ets transcription factor Elf5 specifies mammary alveolar cell fate
    Cold Spring Harbor Laboratory ; 2008
    In:  Genes & Development Vol. 22, No. 5 ( 2008-03-01), p. 581-586
    Details
    In: Genes & Development, Cold Spring Harbor Laboratory, Vol. 22, No. 5 ( 2008-03-01), p. 581-586
    Abstract: Hormonal cues regulate mammary development, but the consequent transcriptional changes and cell fate decisions are largely undefined. We show that knockout of the prolactin-regulated Ets transcription factor Elf5 prevented formation of the secretory epithelium during pregnancy. Conversely, overexpression of Elf5 in an inducible transgenic model caused alveolar differentiation and milk secretion in virgin mice, disrupting ductal morphogenesis. CD61 + luminal progenitor cells accumulated in Elf5-deficient mammary glands and were diminished in glands with Elf5 overexpression. Thus Elf5 specifies the differentiation of CD61 + progenitors to establish the secretory alveolar lineage during pregnancy, providing a link between prolactin, transcriptional events, and alveolar development.
    Type of Medium: Online Resource
    ISSN: 0890-9369 , 1549-5477
    URL: Article
    DOI: 10.1101/gad.1614608
    RVK:
    WA 15000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2008
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  • 17
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    Identifying ERBB2 Activating Mutations in HER2-Negative Breast Cancer: Clinical Impact of Institute-Wide Genomic Testing and Enrollment in Matched Therapy Trials
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  JCO Precision Oncology , No. 3 ( 2019-12), p. 1-9
    Details
    In: JCO Precision Oncology, American Society of Clinical Oncology (ASCO), , No. 3 ( 2019-12), p. 1-9
    Abstract: The yield of comprehensive genomic profiling in recruiting patients to molecular-based trials designed for small subgroups has not been fully evaluated. We evaluated the likelihood of enrollment in a clinical trial that required the identification of a specific genomic change based on our institute-wide genomic tumor profiling. PATIENTS AND METHODS Using genomic profiling from archived tissue samples derived from patients with metastatic breast cancer treated between 2011 and 2017, we assessed the impact of systematic genomic characterization on enrollment in an ongoing phase II trial (ClinicalTrials.gov identifier: NCT01670877 ). Our primary aim was to describe the proportion of patients with a qualifying ERBB2 mutation identified by our institutional genomic panel (OncoMap or OncoPanel) who enrolled in the trial. Secondary objectives included median time from testing result to trial registration, description of the spectrum of ERBB2 mutations, and survival. Associations were calculated using Fisher’s exact test. RESULTS We identified a total of 1,045 patients with metastatic breast cancer without ERBB2 amplification who had available genomic testing results. Of these, 42 patients were found to have ERBB2 mutation and 19 patients (1.8%) were eligible for the trial on the basis of the presence of an activating mutation, 18 of which were identified by OncoPanel testing. Fifty-eight percent of potentially eligible patients were approached, and 33.3% of eligible patients enrolled in the trial guided exclusively by OncoPanel testing. CONCLUSION More than one half of eligible patients were approached for trial participation and, significantly, one third of those were enrolled in NCT01670877. Our data illustrate the ability to enroll patients in trials of rare subsets in routine clinical practice and highlight the need for these broadly based approaches to effectively support the success of these studies.
    Type of Medium: Online Resource
    ISSN: 2473-4284
    URL: Article
    DOI: 10.1200/PO.19.00087
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
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  • 18
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    Effectiveness of sequencing connexin 26 (GJB2) in cases of familial or sporadic childhood deafness referred for molecular diagnostic testing
    Elsevier BV ; 2002
    In:  Genetics in Medicine Vol. 4, No. 4 ( 2002-07), p. 279-288
    Details
    In: Genetics in Medicine, Elsevier BV, Vol. 4, No. 4 ( 2002-07), p. 279-288
    Type of Medium: Online Resource
    ISSN: 1098-3600
    URL: Article
    DOI: 10.1097/00125817-200207000-00006
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2002
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    SSG: 12
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  • 19
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    Abstract A28: Targeted sequencing in 388 patients with high-risk or recurrent/refractory pediatric extracranial solid malignancies: An interim report from the GAIN Consortium/iCat2 Study
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 14_Supplement ( 2020-07-15), p. A28-A28
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 14_Supplement ( 2020-07-15), p. A28-A28
    Abstract: Background: Gene variants with potential therapeutic significance have been reported in 30-60% of childhood malignancies. The 12-institution Genomic Assessment Informs Novel therapy (GAIN) consortium is conducting the individualized cancer therapy 2 (iCat2) study (NCT02520713) with the objective of evaluating the impact of tumor profiling on outcome. We provide an interim report on patients enrolled on the ongoing GAIN/iCat2 study. Methods and Objectives: Patients are eligible if they have a high-risk, recurrent/refractory (RR), or difficult-to-diagnose extracranial solid tumor diagnosed at ≤30 years and adequate sample available for sequencing. A next-generation targeted panel assay is performed. Results are returned with a GAIN report containing clinical interpretation, including an individualized cancer therapy (iCat) recommendation if there is evidence supporting a link between an identified variant and response to molecularly targeted therapy. iCat recommendations are tiered from 1 to 5 based on the level of clinical and preclinical support, with tier 1 being the highest and tier 5 the lowest. Potential extraordinary responders are selected for further review based on having treatment duration of ≥1 year for chemotherapy or ≥4 months or a partial response for targeted therapy. Results: 388 eligible patients were enrolled by 1/1/2019 with the most common diagnoses being osteosarcoma, Ewing sarcoma, and rhabdomyosarcoma. 366 patients (94%) have had at least one successful sequencing result, with 349 having molecular and GAIN reports suitable for inclusion in this analysis. 68% of patients (237/349) have received iCat recommendations, with 41% (143/349) having the highest tier of 1-2 and 27% (94/349) having a highest tier of 3-5. Common genes for which tier 1-2 iCat recommendations were made include TP53 (15%), SMARCB1 (4%), PIK3CA (3%), CDK4 (2%), and KRAS (2%). Common alterations for which tier 3-5 recommendations were made include EWSR1 fusions (12%), MYC/MYCN amplifications (8%), and CDKN2A deletions (7%). Of 170 RR patients with treatment follow-up data entered as of June 2019, 15% (25/170) have received matched targeted therapy. Six of these (24%) are considered extraordinary responders. Of note, extraordinary responses were also seen with some second-line chemotherapy and multitargeted kinase inhibitors. Conclusions: The proportion of patients with clinically significant gene variants is higher in this study than in some previous reports. Providing an iCat recommendation for alterations in genes such as TP53 where evidence is mixed, increased availability of molecularly targeted therapy trials, and more evidence may all be responsible for this increased rate. Reassessment of iCat recommendation tiers based on current evidence is ongoing. Extraordinary responses occur in a subset of children with extracranial solid malignancies who receive matched targeted therapy. Study enrollment is ongoing with further assessments of the impact of tumor profiling on outcome planned. Citation Format: Laura B. Corson, Alanna J. Church, Deirdre Reidy, Pei-Chi Kao, Wenjun Kang, Navin Pinto, Luke Maese, Theodore W. Laetsch, AeRang Kim, Susan I. Vear, Margaret E. Macy, Mark A. Applebaum, Lobin A. Lee, Duong Doan, R. Seth Pinches, Seong Choi, Suzanne J. Forrest, Catherine M. Clinton, Brian D. Crompton, Laura E. MacConaill, Samuel L. Volchenboum, Neal I. Lindeman, Steven G. DuBois, Wendy B. London, Katherine A. Janeway. Targeted sequencing in 388 patients with high-risk or recurrent/refractory pediatric extracranial solid malignancies: An interim report from the GAIN Consortium/iCat2 Study [abstract]. In: Proceedings of the AACR Special Conference on the Advances in Pediatric Cancer Research; 2019 Sep 17-20; Montreal, QC, Canada. Philadelphia (PA): AACR; Cancer Res 2020;80(14 Suppl):Abstract nr A28.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.PEDCA19-A28
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 20
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    Abstract A59: Sequencing identifies diagnostically relevant alterations in pediatric solid tumor patients
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 14_Supplement ( 2020-07-15), p. A59-A59
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 14_Supplement ( 2020-07-15), p. A59-A59
    Abstract: Introduction: Molecular techniques have been incorporated into the diagnostic algorithms for many specific tumors, but the diagnostic role of next-generation sequencing has not been described at a population level. We report diagnostically relevant alterations identified by large-scale sequencing in a prospective cohort of pediatric solid tumors. Methods and Objectives: Patients are eligible for the GAIN / iCat2 study if they have a high-risk, recurrent, or refractory extracranial solid tumor diagnosed at age 30 or less and have an adequate sample for sequencing available. After informed consent, tumor was sequenced using a next-generation sequencing assay that evaluates 447 genes and includes data about sequence variants, copy number alterations, and, in selected genes, translocations. Some cases received additional sequencing via RNASeq or targeted RNA sequencing for further evaluation of fusions. Diagnostic relevance was determined according to AMP/ASCO/CAP standards and guidelines for the reporting of sequence variants in cancer. Results: 349 patients were enrolled as of December 31, 2018, and had tumor tissue successfully sequenced. These patients represent 60 unique diagnoses according to the WHO ICD-O classification. The most common single diagnoses were osteosarcoma (n=64), Ewing sarcoma (n=44), and alveolar rhabdomyosarcoma (n=32). For 349 patients, 184 (53%) had one or more genetic alterations that were diagnostically relevant, of which 159 (86%) were structural variants, 16 (8%) were sequence variants, and 9 (5%) were copy number variations. Alterations of high diagnostic relevance include CIC-DUX4 fusions in sarcoma (n=8), TP53 intron 1 rearrangements in osteosarcoma (n=26), DICER1 sequence variants in various tumors (n=7), and BCOR internal tandem duplications in clear-cell sarcoma of kidney and primitive myxoid mesenchymal tumor of infancy (n=3). Conclusions: Diagnostically relevant alterations were identified in over half of pediatric solid tumor patients evaluated. Gene fusions are particularly prevalent. These results support a role for sequencing that includes robust fusion assessment to inform diagnosis in patients with pediatric solid tumors. Citation Format: Alanna J. Church, Laura B. Corson, Alma Imamovic-Tuco, Gianna R. Strand, Dierdre Reidy, Duong Doan, Robert S. Pinches, Mark A. Applebaum, Rochelle Bagatell, Brian D. Crompton, Steven G. DuBois, Julia L. Glade Bender, Theodore W. Laetsch, Lobin A. Lee, Neal I. Lindeman, Marian H. Harris, Margaret E. Macy, Luke Maese, Navin Pinto, Amit J. Sabnis, Eliezer M. Van Allen, Susan I. Vear, Daniel A. Weiser, Catherine M. Clinton, Katherine A. Janeway. Sequencing identifies diagnostically relevant alterations in pediatric solid tumor patients [abstract]. In: Proceedings of the AACR Special Conference on the Advances in Pediatric Cancer Research; 2019 Sep 17-20; Montreal, QC, Canada. Philadelphia (PA): AACR; Cancer Res 2020;80(14 Suppl):Abstract nr A59.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.PEDCA19-A59
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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