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  • American Association for Cancer Research (AACR)  (62)
  • 1
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 8, No. 12 ( 2018-12-01), p. 1548-1565
    Abstract: Malignant pleural mesothelioma (MPM) is a highly lethal cancer of the lining of the chest cavity. To expand our understanding of MPM, we conducted a comprehensive integrated genomic study, including the most detailed analysis of BAP1 alterations to date. We identified histology-independent molecular prognostic subsets, and defined a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity. We also report strong expression of the immune-checkpoint gene VISTA in epithelioid MPM, strikingly higher than in other solid cancers, with implications for the immune response to MPM and for its immunotherapy. Our findings highlight new avenues for further investigation of MPM biology and novel therapeutic options. Significance: Through a comprehensive integrated genomic study of 74 MPMs, we provide a deeper understanding of histology-independent determinants of aggressive behavior, define a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity, and discovered strong expression of the immune-checkpoint gene VISTA in epithelioid MPM. See related commentary by Aggarwal and Albelda, p. 1508. This article is highlighted in the In This Issue feature, p. 1494
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 2
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 29, No. 10 ( 2023-05-15), p. 1984-1995
    Abstract: Inhibitors of Bruton's tyrosine kinase (BTKi) and PI3K (PI3Ki) have significantly improved therapy of chronic lymphocytic leukemia (CLL). However, the emergence of resistance to BTKi has introduced an unmet therapeutic need. Hence, we sought evidence for essential roles of PI3K-δi and PI3K-γi in treatment-naïve and BTKi-refractory CLL. Experimental Design: Responses to PI3K-δi, PI3K-γi, and the dual-inhibitor duvelisib in each B, T, and myeloid cell compartments of CLL were studied in vitro, and in a xenograft mouse model using primary cells from treatment-naïve and ibrutinib-resistant patients, and finally, in a patient with ibrutinib-resistant CLL treated with duvelisib. Results: We demonstrate the essential roles of PI3K-δ for CLL B-cell survival and migration, of PI3K-γ for T-cell migration and macrophage polarization, and of dual inhibition of PI3K-δ,γ for efficacious reduction of leukemia burden. We also show that samples from patients whose disease progressed on ibrutinib were responsive to duvelisib therapy in a xenograft model, irrespective of BTK mutations. In support of this, we report a patient with ibrutinib-resistant CLL, bearing a clone with BTK and PLCγ2 mutations, who responded immediately to single-agent duvelisib with redistribution lymphocytosis followed by a partial clinical remission associated with modulation of T and myeloid cells. Conclusions: Our data define the mechanism of action whereby dual inhibition of PI3K-δ,γ affects CLL B-cell numbers and T and myeloid cell pro-leukemia functions and support the use of duvelisib as a valuable approach for therapeutic interventions, including for patients refractory to BTKi.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 3
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 4933-4933
    Abstract: Duvelisib (IPI-145), a first-in-class, oral, dual PI3K-δ,γ inhibitor, has been approved by the FDA for the treatment of patients with chronic lymphocytic leukemia (CLL), small lymphocytic and follicular lymphoma. Duvelisib potently inhibits PI3K-δ and PI3K-γ, thereby offering a novel therapeutic approach. Here we aimed to understand how duvelisib targets CLL cells and the tumor microenvironment (TME) and hence how it affects CLL, even with BTK-resistant disease. We first assessed the distinct contributions of PI3K-δ and PI3K-γ on CLL cell survival, proliferation, and migration in vitro by using PI3K-δ (PI3K-δi) or PI3K-γ (PI3K-γi) specific inhibitors in addition to duvelisib. We found a significant reduction in viable CLL cells after exposure to PI3K-δi and duvelisib. By measuring Ki67 and p-AKT levels, we found duvelisib and PI3K-δi more potently block CLL cell proliferation than PI3K-γi. PI3K-δi and duvelisib also significantly reduced the migration of CLL B cells into the spleen relative to control. In contrast, PI3K-γi inhibited T cell not B cell homing in vitro and in vivo. We then investigated the impact of single versus dual inhibitory agents on myeloid cells. Tumor-associated macrophages (TAMs) of the “M2 phenotype” contribute to a pro-tumor TME by preventing the induction of T cell mediated anti-tumor immunity. We expanded murine bone marrow derived monocytes and then polarized them to M2 macrophages, in the absence or presence of PI3Ki. At 100nM, PI3K-γi, but not PI3K-δi, significantly inhibited M2 polarization. Duvelisib significantly reduced Arg1 expression at doses equal to or above 10nM. While co-culturing leukemic B cells with M2-polarized murine macrophages increased CLL-cell survival, addition of duvelisib to such co-cultures significantly reduced CLL cell survival. Altogether, duvelisib sensitizes primary CLL cells to apoptosis and abrogates M2 cell-mediated CLL-cell survival. Finally, in a patient-derived xenograft mouse model (PDX), we demonstrated the essential roles of PI3K-δ and PI3K-γ in the CLL TME. Specifically, we found a more efficacious inhibition in CLL cell burden by dual inhibition of PI3K-δ,γ. Also, samples from patients whose disease progressed on ibrutinib were responsive to duvelisib therapy in PDX, irrespective of BTK mutations. In support of this, we identified an ibrutinib resistant CLL patient, with a clone exhibiting BTK and PLCγ2 mutations who responded immediately to single agent duvelisib with redistribution lymphocytosis followed by a partial clinical remission associated with subsequent modulation of T and myeloid cells. In conclusion, our data define the mechanism of action whereby dual inhibition of PI3K-δ,γ affects CLL B cell numbers and T and myeloid cell pro-leukemia functions, supporting the use of duvelisib as a potentially valuable therapeutic intervention, including for patients refractory to BTKi. Citation Format: Shih-Shih Chen, Jacqueline C. Barrientos, Gerardo Ferrer, Priyadarshini Ravichandran, Michael Ibrahim, Yasmine Kieso, Jeffery L. Kutok, Marisa Peluso, Sujata Sharma, David T. Weaver, Jonathan A. Pachter, Kanti R. Rai, Nicholas Chiorazzi. Duvelisib eliminates CLL B Cells, impairs CLL-supporting cells, and overcomes ibrutinib resistance in a patient-derived xenograft model. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2 023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4933.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 4
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 21, No. 1 ( 2015-01-01), p. 184-192
    Abstract: Purpose: To investigate molecular alterations in choroid plexus tumors (CPT) using a genome-wide high-throughput approach to identify diagnostic and prognostic signatures that will refine tumor stratification and guide therapeutic options. Experimental Design: One hundred CPTs were obtained from a multi-institutional tissue and clinical database. Copy-number (CN), DNA methylation, and gene expression signatures were assessed for 74, 36, and 40 samples, respectively. Molecular subgroups were correlated with clinical parameters and outcomes. Results: Unique molecular signatures distinguished choroid plexus carcinomas (CPC) from choroid plexus papillomas (CPP) and atypical choroid plexus papillomas (aCPP); however, no significantly distinct molecular alterations between CPPs and aCPPs were observed. Allele-specific CN analysis of CPCs revealed two novel subgroups according to DNA content: hypodiploid and hyperdiploid CPCs. Hyperdiploid CPCs exhibited recurrent acquired uniparental disomy events. Somatic mutations in TP53 were observed in 60% of CPCs. Investigating the number of mutated copies of p53 per sample revealed a high-risk group of patients with CPC carrying two copies of mutant p53, who exhibited poor 5-year event-free (EFS) and overall survival (OS) compared with patients with CPC carrying one copy of mutant p53 (OS: 14.3%, 95% confidence interval, 0.71%–46.5% vs. 66.7%, 28.2%–87.8%, respectively, P = 0.04; EFS: 0% vs. 44.4%, 13.6%–71.9%, respectively, P = 0.03). CPPs and aCPPs exhibited favorable survival. Discussion: Our data demonstrate that differences in CN, gene expression, and DNA methylation signatures distinguish CPCs from CPPs and aCPPs; however, molecular similarities among the papillomas suggest that these two histologic subgroups are indeed a single molecular entity. A greater number of copies of mutated TP53 were significantly associated to increased tumor aggressiveness and a worse survival outcome in CPCs. Collectively, these findings will facilitate stratified approaches to the clinical management of CPTs. Clin Cancer Res; 21(1); 184–92. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 5
    In: Cancer Discovery, American Association for Cancer Research (AACR), ( 2023-09-12)
    Abstract: Improved biomarkers are needed for early cancer detection, risk stratification, treatment selection, and monitoring treatment response. While proteins can be useful blood-based biomarkers, many have limited sensitivity or specificity for these applications. Long INterspersed Element-1 (LINE-1) open reading frame 1 protein (ORF1p) is a transposable element protein overexpressed in carcinomas and high-risk precursors during carcinogenesis with negligible expression in normal tissues, suggesting ORF1p could be a highly specific cancer biomarker. To explore ORF1p as a blood-based biomarker, we engineered ultrasensitive digital immunoassays that detect mid-attomolar (10-17 M) ORF1p concentrations in plasma across multiple cancers with high specificity. Plasma ORF1p shows promise for early detection of ovarian cancer, improves diagnostic performance in a multi-analyte panel, provides early therapeutic response monitoring in gastroesophageal cancers, and is prognostic for overall survival in gastroesophageal and colorectal cancers. Together, these observations nominate ORF1p as a multi-cancer biomarker with potential utility for disease detection and monitoring.
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
    detail.hit.zdb_id: 2607892-2
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  • 6
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    Online Resource
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Immunology Research Vol. 9, No. 2_Supplement ( 2021-02-01), p. PO085-PO085
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 9, No. 2_Supplement ( 2021-02-01), p. PO085-PO085
    Abstract: Acute myeloid leukemia (AML) is a hematopoietic malignancy with limited therapeutic options. Standard-of-care chemotherapy depletes AML cells to induce remission, but often precedes disease relapse. To promote robust and durable immunity against AML, we developed a macroporous cryogel-based vaccine which provided a sustained release of GM-CSF to concentrate dendritic cells (DCs), TLR agonist CpG-ODN, and leukemia antigen. Prophylactic vaccination in mice against AML cell lysates or peptide antigen induced a potent anti-tumor adaptive immune response and prevented the engraftment of AML cells. This immunity was transferable, as bone marrow transplanted from vaccinated mice immunized recipients against AML. In models of established disease, only the combination of chemotherapy and biomaterial vaccination entirely eradicated AML in all mice and generated long-term T cell immunity preventing relapse. Notably, in combination with chemotherapy, a cryogel vaccine delivering no antigen (only GM-CSF and CpG-ODN) generated robust AML-specific T cell immunity, depleted leukemia, and enabled long-term survival. In this setting, tumor antigens were likely sourced from chemotherapy-induced AML cell death, as AML cells expressing high levels of apoptotic markers were found in the vaccine site and draining lymph node, co-localizing with DCs activated by the vaccine. These results demonstrate the capacity of a biomaterial-based vaccine to induce a potent immune response depleting AML and preventing relapse, even without defined antigen targets. Citation Format: Alexander J. Najibi, Nisarg J. Shah, Ting-Yu Shih, Angelo S Mao, Azeem Sharda, David T. Scadden, David J. Mooney. Cryogel-based cancer vaccine to treat acute myeloid leukemia [abstract]. In: Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; 2020 Oct 19-20. Philadelphia (PA): AACR; Cancer Immunol Res 2021;9(2 Suppl):Abstract nr PO085.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. NG14-NG14
    Abstract: Deficient DNA mismatch repair (dMMR) induces a hypermutator phenotype, leaving a genomic scar known as microsatellite instability (MSI). MSI is observed in approximately 30% of endometrial cancers, 20% of gastric cancers, 15% of colorectal cancers, and in a smaller fraction of other tumor types. This hypermutator phenotype is thought to produce large numbers of immunogenic neoantigens, leading to the approval of MSI status as a clinical biomarker for immunotherapy. However, more than 60% of patients with MSI tumors fail to respond to immune checkpoint therapy. To uncover alternative therapeutic vulnerabilities for these patients, we used transcriptome signature-guided approaches to identify MLN4924 (pevonedistat), a Nedd8-activating enzyme inhibitor, as a potential therapy for dMMR/MSI cancers. We discover that destabilizing mutations from the dMMR mutation process lead to rampant proteome instability in MSI tumors, resulting in an abundance of misfolded protein aggregates. To compensate, MSI cancer cells activate a Nedd8-mediated degradation pathway to facilitate clearance of misfolded proteins, which is blocked by treatment with MLN4924. The accumulation of misfolded proteins in MSI cancer cells following MLN4924 treatment activated the unfolded protein response, promoted immune cell migration, and induced immunogenic cell death. Antitumor vaccination with MLN4924-treated cells stimulated the generation of endogenous tumor antibodies and prevented tumor incidence upon re-challenge. Based on this immunostimulation, we combined MLN4924 with PD1 blockade, finding that the combination increased recruitment of CD8+ lymphocytes and improved therapeutic efficacy beyond either treatment alone. Taken together, our results indicate that targeting proteome instability is a novel therapeutic avenue for MSI patients and may potentiate immune checkpoint blockade, potentially increasing the depth and duration of response, as well as the fraction of dMMR/MSI patients who can benefit. Citation Format: Nidhi Sahni, Daniel J. McGrail, Jeannine Garnett, Jun Yin, Hui Dai, David J. H. Shih, Guang Peng, David Menter, Melinda S. Yates, Scott Kopetz, Karen Lu, Russell Broaddus, Gordon B. Mills, Shiaw Y. Lin. Proteome instability is an immunogenic therapeutic vulnerability in mismatch repair deficient cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr NG14.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2303-2303
    Abstract: Background: An increased risk of prostate cancer was observed in Parkinson’s disease (PD) patients treated with entacapone during a pre-approval randomized clinical trial. Objective: To investigate a potential association between entacapone use and prostate cancer in an ambulatory setting. Methods: Using data from the Department of Veterans Affairs (VA) healthcare system, new-user cohorts were created of PD patients treated with add-on entacapone or add-on dopamine agonist/monoamine oxidase B inhibitors between January 2000 and December 2014. Patients were followed on-treatment for occurrence of prostate cancer, identified via VA cancer registry linkage. Cox proportional hazards regression with time-dependent exposure was used to calculate hazard ratios (HR) and 95% confidence intervals (CI). Confounding was controlled by using inverse probability treatment weighting calculated from propensity scores. Results: Mean follow-up time was 3.1 and 4.0 years in the entacapone and control cohort, respectively. There were 17,666 subjects meeting study criteria (mean age, 74 (SD 8.6) years); the group treated with entacapone comprised 5,257 subjects. Twenty-three prostate cancers occurred in the entacapone cohort and 97 in the control cohort. The overall incidence of prostate cancer was 1.8 per 1000 person-years of risk. There was no difference in risk of prostate cancer between the cohorts for increased duration of entacapone intake (adjusted HR: 1.08; 95% confidence interval: 0.46-2.51 for cumulative exposure of ≥2 years). Time since starting drug therapy and cumulative dose (mg) were also examined. Conclusion: In this cohort of PD patients, extended duration of entacapone use was not associated with an increased incidence of prostate cancer. Note: This abstract was not presented at the meeting. Citation Format: Jacqueline M. Major, Francesca Cunningham, Diane Dong, Kunthel By, Kwan Hur, David C. Shih, Simone P. Pinheiro, Gerald D. Podskalny, David J. Graham. Entacapone and prostate cancer in patients with Parkinson’s disease: A large Veterans Health Administration study [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 2303. doi:10.1158/1538-7445.AM2017-2303
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 9
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    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 14 ( 2009-07-15), p. 5699-5706
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 14 ( 2009-07-15), p. 5699-5706
    Abstract: Understanding the molecular details associated with aberrant high mobility group A2 (HMGA2) gene expression is key to establishing the mechanism(s) underlying its oncogenic potential and effect on the development of therapeutic strategies. Here, we report the involvement of HMGA2 in impairing DNA-dependent protein kinase (DNA-PK) during the nonhomologous end joining (NHEJ) process. We showed that HMGA2-expressing cells displayed deficiency in overall and precise DNA end-joining repair and accumulated more endogenous DNA damage. Proper and timely activation of DNA-PK, consisting of Ku70, Ku80, and DNA-PKcs subunits, is essential for the repair of DNA double strand breaks (DSB) generated endogenously or by exposure to genotoxins. In cells overexpressing HMGA2, accumulation of histone 2A variant X phosphorylation at Ser-139 (γ-H2AX) was associated with hyperphosphorylation of DNA-PKcs at Thr-2609 and Ser-2056 before and after the induction of DSBs. Also, the steady-state complex of Ku and DNA ends was altered by HMGA2. Microirradiation and real-time imaging in living cells revealed that HMGA2 delayed the release of DNA-PKcs from DSB sites, similar to observations found in DNA-PKcs mutants. Moreover, HMGA2 alone was sufficient to induce chromosomal aberrations, a hallmark of deficiency in NHEJ-mediated DNA repair. In summary, a novel role for HMGA2 to interfere with NHEJ processes was uncovered, implicating HMGA2 in the promotion of genome instability and tumorigenesis. [Cancer Res 2009;69(14):5699–706]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
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  • 10
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 618-618
    Abstract: While massively parallel sequencing technology has greatly expanded the number of molecular genetic tests available in oncology, little is known about the spectrum and clinical utility of findings obtained from testing tumors and circulating tumor material in specific patient populations. Here we report findings from the METAMORPH study, in which stage IV breast cancer patients had metastatic tumor biopsies (metDNA) and concurrently collected cell-free circulating tumor DNA (cfDNA). Illumina TruSeq Cancer Panel (for metDNA) and Guardant360 (for cfDNA) were performed. 28 patients had both tests; results are shown in the Table. 68% of patients had at least one alteration in metDNA and 86% in cfDNA. PIK3CA mutations were most common, occurring in 43% and 36% of patients’ metDNA and cfDNA, respectively. Overall, 16 of 28 (57%) of patients had the same alterations identified in both metDNA and cfDNA. Excluding ERBB2 amplifications in HER2+ patients, 43% of patients’ metDNA and 57% of patients’ cfDNA contained pathogenic mutations or variants of uncertain significance (VUS) for which there are approved targeted therapies or clinical trials. Overall, 80 alterations were identified, 23 of which were detected by both assays. Multiple reasons for discordance in calls between metDNA and cfDNA assays were identified. While biological phenomena (e.g. tumor heterogeneity) may contribute to discordance, technical issues played an important role. Additional studies using whole exome sequencing and other platforms to further assess biological evolution of metastatic disease and clinical utility of molecular profiling of metastatic tumors and cell-free DNA are needed. Table 1 Tumor DNA (metDNA)Cell-free DNA (cfDNA)# pts with alteration (%)19/28 (68%)24/28 (86%)ER+/Her2- (n = 17)10/1715/17Her2+ (n = 4)4/42/4TNBC (n = 7)5/77/7Total # alterations in # genes31 in 7 genes72 in 19 genesGenes w/alterations (total); Bold: genes for which exists a possible targeted therapeuticPIK3CA (13), TP53 (10), ERBB2 (4), EGFR, RB1, SMAD4, STK11PIK3CA (14), TP53 (14), EGFR (9), ERBB2 (6), BRAF (6), MET (6), JAK2 (3), NOTCH1 (2), FBXW7 (2), ARAD, FGFR2, JAK3, KRAS, MYC, NPM1, PROC, RET, SMAD4, SMARCB1Variants only covered by one assay033Variants detected in both but only reported by one assay3 (2 indels, 1 VUS)1 (1 synonymous)Variants detected by only one assay1 amplification at 7-fold; 4 SNVs (AF range 19-75%)2 amplifications at & lt;3-fold; 13 SNVs (AF range 0.1-0.8%) Citation Format: Kara N. Maxwell, Danielle J. Soucier-Ernst, Erica L. Carpenter, Andrea B. Troxel, Christopher Colameco, Candace Clark, Michael D. Feldman, Bijal Kakrecha, Melissa Langer, Joy Lee, David A. Lewis, David Lieberman, Jennifer Morrissette, Tien-chi Pan, Stephanie S. Yee, Natalie Shih, Lewis A. Chodosh, Angela M. DeMichele. Comparison of mutational spectra in metastatic tumors and cell-free DNA in breast cancer patients. [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 618. doi:10.1158/1538-7445.AM2015-618
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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