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  • 1
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    Online Resource
    Convergent Therapeutic Strategies to Overcome the Heterogeneity of Acquired Resistance in BRAF V600E Colorectal Cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Discovery Vol. 8, No. 4 ( 2018-04-01), p. 417-427
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 8, No. 4 ( 2018-04-01), p. 417-427
    Abstract: Clonal heterogeneity associated with acquired resistance presents a critical therapeutic challenge. Whole-exome sequencing of paired tumor biopsies and targeted sequencing of cell-free DNA (cfDNA) from patients with BRAFV600E colorectal cancer receiving BRAF inhibitor combinations identified 14 distinct alterations in MAPK pathway components driving acquired resistance, with as many as eight alterations in a single patient. We developed a pooled clone system to study clonal outgrowth during acquired resistance, in vitro and in vivo. In vitro, the dynamics of individual resistant clones could be monitored in real time in cfDNA isolated from culture media during therapy. Outgrowth of multiple resistant clones was observed during therapy with BRAF, EGFR, and MEK inhibitor combinations. However, ERK inhibition, particularly in combination with BRAF and EGFR inhibition, markedly abrogated clonal outgrowth in vitro and in vivo. Thus, convergent, up-front therapy may suppress outgrowth of heterogeneous clones harboring clinically observed resistance alterations, which may improve clinical outcome. Significance: We observed heterogeneous, recurrent alterations in the MAPK pathway as key drivers of acquired resistance in BRAFV600E colorectal cancer, with multiple concurrent resistance alterations detectable in individual patients. Using a novel pooled clone system, we identify convergent up-front therapeutic strategies capable of intercepting multiple resistance mechanisms as potential approaches to suppress emergence of acquired resistance. Cancer Discov; 8(4); 417–27. ©2018 AACR. See related commentary by Janku, p. 389. See related article by Corcoran et al., p. 428. This article is highlighted in the In This Issue feature, p. 371
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-17-1227
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 2
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    Abstract LB-A34: Modeling convergent therapeutic strategies to overcome the heterogeneity of acquired resistance in BRAF -mutant colorectal cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Molecular Cancer Therapeutics Vol. 17, No. 1_Supplement ( 2018-01-01), p. LB-A34-LB-A34
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 17, No. 1_Supplement ( 2018-01-01), p. LB-A34-LB-A34
    Abstract: Clonal heterogeneity associated with the emergence of acquired resistance to therapy presents a critical challenge for therapeutic strategies to overcome resistance. We investigated the molecular landscape of acquired resistance in BRAF-mutant colorectal patients treated with BRAF inhibitor combinations. Through whole-exome sequencing of paired pre-treatment and post-progression tumor biopsies and targeted sequencing of pre-treatment and post-progression plasma circulating tumor DNA (ctDNA), we identified 14 unique alterations in MAPK pathway components driving acquired resistance, affecting KRAS, NRAS, BRAF, MEK1 and MEK2. Analysis of ctDNA at the time of disease progression revealed profound tumor heterogeneity associated with acquired resistance, with multiple concurrent resistance alterations detectable in ctDNA in individual patients, with one patient harboring as many as 8 co-existing resistance alterations. These findings necessitate development of a strategy capable of simultaneously overcoming multiple heterogeneous resistance mechanisms. To evaluate potential strategies for convergent targeting of multiple concurrent resistance alterations, we generated individual resistant models harboring the full spectrum of clinically observed mutations driving acquired resistance. Individually, these alterations drove resistance to BRAF inhibitor combinations currently in clinical trials by maintaining MAPK signaling. However, since acquired resistance is thought to arise from pre-existing clones that emerge during treatment, we developed a novel pooled clone model system to study clonal outgrowth under the selective pressure of therapy. In this system, each resistant clone was pooled at an abundance of 1% in a background of the sensitive parental cells and exposed to an array of potential therapies, both in vitro, and in vivo as xenografts. The change in clonal abundance from baseline to the completion of therapy was assessed for each clone by digital PCR to measure the degree of clonal outgrowth. Moreover, in vitro, we were able to monitor clonal dynamics in real-time by isolating cell-free DNA (cfDNA) from the cell culture media every 3-4 days during therapy. We observed rapid outgrowth of resistant clones during BRAF-EGFR and BRAF-MEK therapy, and delayed, but robust outgrowth during BRAF-MEK-EGFR therapy, all of which are therapies that have been evaluated in recent clinical trials. However, ERK inhibitor alone, and to a greater degree BRAF-ERK and BRAF-ERK-EGFR combinations markedly abrogated the clonal outgrowth of resistant clones. Moreover, in xenograft tumors derived from clonal pools, BRAF-ERK-EGFR triple combination resulted in profound tumor regressions and completely prevented the outgrowth of all resistant clones. In conclusion, we observed the potential for profound heterogeneity of acquired resistance mechanisms in BRAF-mutant colorectal cancer patients, with multiple alterations observed in ctDNA from individual patients. Our data suggest that convergent, upfront therapy with RAF-ERK or RAF-ERK-EGFR inhibitor combinations may suppress outgrowth of clones harboring clinically observed resistant alterations, offering the potential for improved clinical outcome. Citation Format: Mehlika Hazar-Rethinam, Marianna Kleyman, G. Celine Han, David Liu, Leanne G. Ahronian, Heather A. Shahzade, Lifeng Chen, Aparna R. Parikh, Jill N. Allen, Jeffrey W. Clark, Eunice L. Kwak, Jason E. Faris, Janet E. Murphy, Theodore S. Hong, Emily E. Van Seventer, Brandon Nadres, Catriona B. Hong, Joseph M. Gurski Jr., Nicholas A. Jessop, Dora Dias-Santagata, A. John Iafrate, Eli M. Van Allen, Ryan B. Corcoran. Modeling convergent therapeutic strategies to overcome the heterogeneity of acquired resistance in BRAF-mutant colorectal cancer [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2017 Oct 26-30; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2018;17(1 Suppl):Abstract nr LB-A34.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-17-LB-A34
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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    SSG: 12
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  • 3
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    Online Resource
    Integrative Molecular Characterization of Resistance to Neoadjuvant Chemoradiation in Rectal Cancer
    American Association for Cancer Research (AACR) ; 2019
    In:  Clinical Cancer Research Vol. 25, No. 18 ( 2019-09-15), p. 5561-5571
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 25, No. 18 ( 2019-09-15), p. 5561-5571
    Abstract: Molecular properties associated with complete response or acquired resistance to concurrent chemotherapy and radiotherapy (CRT) are incompletely characterized. Experimental Design: We performed integrated whole-exome/transcriptome sequencing and immune infiltrate analysis on rectal adenocarcinoma tumors prior to neoadjuvant CRT (pre-CRT) and at time of resection (post-CRT) in 17 patients [8 complete/partial responders, 9 nonresponders (NR)]. Results: CRT was not associated with increased tumor mutational burden or neoantigen load and did not alter the distribution of established somatic tumor mutations in rectal cancer. Concurrent KRAS/TP53 mutations (KP) associated with NR tumors and were enriched for an epithelial–mesenchymal transition transcriptional program. Furthermore, NR was associated with reduced CD4/CD8 T-cell infiltrates and a post-CRT M2 macrophage phenotype. Absence of any local tumor recurrences, KP/NR status predicted worse progression-free survival, suggesting that local immune escape during or after CRT with specific genomic features contributes to distant progression. Conclusions: Overall, while CRT did not impact genomic profiles, CRT impacted the tumor immune microenvironment, particularly in resistant cases.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-19-0908
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 4
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    Online Resource
    Real-time Genomic Characterization of Advanced Pancreatic Cancer to Enable Precision Medicine
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Discovery Vol. 8, No. 9 ( 2018-09-01), p. 1096-1111
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 8, No. 9 ( 2018-09-01), p. 1096-1111
    Abstract: Clinically relevant subtypes exist for pancreatic ductal adenocarcinoma (PDAC), but molecular characterization is not yet standard in clinical care. We implemented a biopsy protocol to perform time-sensitive whole-exome sequencing and RNA sequencing for patients with advanced PDAC. Therapeutically relevant genomic alterations were identified in 48% (34/71) and pathogenic/likely pathogenic germline alterations in 18% (13/71) of patients. Overall, 30% (21/71) of enrolled patients experienced a change in clinical management as a result of genomic data. Twenty-six patients had germline and/or somatic alterations in DNA-damage repair genes, and 5 additional patients had mutational signatures of homologous recombination deficiency but no identified causal genomic alteration. Two patients had oncogenic in-frame BRAF deletions, and we report the first clinical evidence that this alteration confers sensitivity to MAPK pathway inhibition. Moreover, we identified tumor/stroma gene expression signatures with clinical relevance. Collectively, these data demonstrate the feasibility and value of real-time genomic characterization of advanced PDAC. Significance: Molecular analyses of metastatic PDAC tumors are challenging due to the heterogeneous cellular composition of biopsy specimens and rapid progression of the disease. Using an integrated multidisciplinary biopsy program, we demonstrate that real-time genomic characterization of advanced PDAC can identify clinically relevant alterations that inform management of this difficult disease. Cancer Discov; 8(9); 1096–111. ©2018 AACR. See related commentary by Collisson, p. 1062. This article is highlighted in the In This Issue feature, p. 1047
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-18-0275
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 5
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    Care Patterns and Overall Survival in Patients With Early-Onset Metastatic Colorectal Cancer
    American Society of Clinical Oncology (ASCO) ; 2021
    In:  JCO Oncology Practice Vol. 17, No. 12 ( 2021-12), p. e1846-e1855
    Details
    In: JCO Oncology Practice, American Society of Clinical Oncology (ASCO), Vol. 17, No. 12 ( 2021-12), p. e1846-e1855
    Abstract: Colorectal cancer (CRC) incidence in patients younger than 50 years of age, commonly defined as early-onset (EO-CRC), is rising. EO-CRC often presents with distinct clinicopathologic features. However, data on prognosis are conflicting and outcomes with modern treatment approaches for metastatic disease are still limited. MATERIALS AND METHODS: We prospectively enrolled patients with metastatic CRC (mCRC) to a biobanking and clinical data collection protocol from 2014 to 2018. We grouped the cohort based on age at initial diagnosis: 〈 40 years, 40-49 years, and ≥ 50 years. We used regression models to examine associations among age at initial diagnosis, treatments, clinicopathologic features, and survival. RESULTS: We identified 466 patients with mCRC (45 [10%] age 〈 40 years, 109 [23%] age 40-49 years, and 312 [67%] age ≥ 50 years). Patients 〈 40 years of age were more likely to have received multiple metastatic resections (odds ratio [OR] , 3.533; P = .0066) than their older counterparts. Patients with EO-CRC were more likely to receive triplet therapy than patients 〉 50 years of age (age 〈 40 years: OR, 6.738; P = .0002; age 40-49 years: OR, 2.949; P = .0166). Patients 40-49 years of age were more likely to have received anti-EGFR therapy (OR, 2.633; P = .0016). Despite differences in care patterns, age did not predict overall survival. CONCLUSION: Despite patients with EO-CRC receiving more intensive treatments, survival was similar to the older counterpart. However, EO-CRC had clinical and molecular features associated with worse prognoses. Improved biologic understanding is needed to optimize clinical management of EO-CRC. The cost-benefit ratio of exposing patients with EO-CRC to more intensive treatments has to be carefully evaluated.
    Type of Medium: Online Resource
    ISSN: 2688-1527 , 2688-1535
    URL: Article
    DOI: 10.1200/OP.20.01010
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2021
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  • 6
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    Liquid versus tissue biopsy for detecting acquired resistance and tumor heterogeneity in gastrointestinal cancers
    Springer Science and Business Media LLC ; 2019
    In:  Nature Medicine Vol. 25, No. 9 ( 2019-09), p. 1415-1421
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 25, No. 9 ( 2019-09), p. 1415-1421
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/s41591-019-0561-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
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  • 7
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    Author Correction: Liquid versus tissue biopsy for detecting acquired resistance and tumor heterogeneity in gastrointestinal cancers
    Springer Science and Business Media LLC ; 2019
    In:  Nature Medicine Vol. 25, No. 12 ( 2019-12), p. 1949-1949
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 25, No. 12 ( 2019-12), p. 1949-1949
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/s41591-019-0698-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 1484517-9
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  • 8
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    Prediction model for detecting circulating tumor DNA (ctDNA) in metastatic colorectal cancer (mCRC).
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  Journal of Clinical Oncology Vol. 37, No. 15_suppl ( 2019-05-20), p. 3590-3590
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 37, No. 15_suppl ( 2019-05-20), p. 3590-3590
    Abstract: 3590 Background: While tissue-based assays have yields above 90% in solid tumors, there is less known about factors that influence the sensitivity of ctDNA for detecting mutations. Methods:We retrospectively evaluated mCRC patients (pts) who had plasma-derived NGS utilizing a highly-sensitive targeted 68-73-gene ctDNA assay. In a case-control design, pts with a known mutation on tissue and radiologic evidence of metastatic disease but no detectable ctDNA mutation were matched 1:3 with randomly selected pts with detectable mutations and compared according to clinical, laboratory, and radiologic characteristics. A prediction score for ctDNA detection was built using a binary logistic backward stepwise regression analysis and tested in two independent data sets from different institutions. Area under the curve (AUC) from receiver operating characteristics curves (ROC) were used for internal and external validation. Results: From 416 pts who met inclusion criteria, plasma-derived NGS did not find tumor mutations in 66 cases (15.9%); 198 pts with detectable alterations were selected as controls. After multivariate analysis, the detection of ctDNA was associated with increasing age (OR 1.05; 95%CI 1.02-1.09; p = .001), presence of liver (OR 5.82; 95%CI 2.55-12.49; p 〈 .001) and lymph node metastases (OR 3.28; 95%CI 1.51-7.60; p = .004), archival TP53 mutations (OR = 2.88; 95%CI 1.37-6.17; p = .006). A key determinant was timing of collection relative to disease status: plasma collected in newly diagnosed metastatic disease or after evidence of progression was substantially more likely to have detectable alterations (OR 9.24; 95%CI 4.11-22.40; p 〈 .001); The simplified prediction model performed well in internal (AUC = 0.88) and external validation (AUC = 0.95; 163 pts). Conclusions: Our validated prediction model provides clinicians and researchers with a tool to screen for patients in whom ctDNA testing can outperform tissue-based testing in detecting genomic alterations.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2019.37.15_suppl.3590
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
    detail.hit.zdb_id: 2005181-5
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  • 9
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    Circulating tumor derived cell-free DNA (ctDNA) to predict recurrence of metastatic colorectal cancer (mCRC) following curative intent surgery or radiation.
    American Society of Clinical Oncology (ASCO) ; 2021
    In:  Journal of Clinical Oncology Vol. 39, No. 15_suppl ( 2021-05-20), p. 3565-3565
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 39, No. 15_suppl ( 2021-05-20), p. 3565-3565
    Abstract: 3565 Background: Over half of patients (pts) with oligometastatic CRC treated with curative intent surgery or radiotherapy experience cancer recurrence with or without adjuvant chemotherapy. ctDNA detection post-definitive treatment could identify high risk pts for additional intervention to eliminate molecular residual disease. Here we report results of a prospective observational study aiming to determine ctDNA detection rates using a sensitive liquid biopsy and to correlate post-procedure ctDNA detection (post-ctDNA (+)) with radiographic mCRC recurrence. Methods: Pts with mCRC intending to undergo a curative intent procedure were prospectively recruited at two US sites. ctDNA was collected pre-procedure, 3 weeks post-procedure, and at multiple structured follow-up timepoints. The presence of ctDNA was evaluated using a plasma-only integrated genomic and epigenomic assay (Guardant Reveal, Guardant Health). A bioinformatic classifier was applied to differentiate tumor derived versus non-tumor derived cell-free DNA. Results: Among 52 enrolled pts, post-ctDNA data is available for 45 pts (87%), with a median of 4 (range 1-10) timepoints per pt. The sample analysis failure rate was 1% (2/217). As of 1/1/2021, the radiographic recurrence rate was 60% with a median follow-up time of 50 (range 4-192) weeks. 23 of 25 pts with post-ctDNA(+) have had recurrence (Positive Predictive Value [PPV], 92%). On average, ctDNA was detected 28 weeks before radiographic recurrence (mean 12 vs. 40 weeks, respectively). The two pts with post-ctDNA(+) but no recurrence have 〉 3 years follow-up; one pt received adjuvant chemotherapy and cleared ctDNA. With a median event-free follow-up time of 97 (range 4-192) weeks, 4 of 20 pts with no post-ctDNA detection (-) have recurred (Negative Predictive Value, 80%). 3 of 4 pts with recurrence despite post-ctDNA(-) also were pre-ctDNA(-). We observed a sensitivity of 85% and a specificity of 89% for the ctDNA assay. The median time to radiographic recurrence was 36 wks for ctDNA(+) vs. not reached for ctDNA(-) (Hazard Ratio, 7.7; 95% CI, 2.6-22.5; P 〈 .001). Conclusions: In mCRC pts undergoing curative intent surgery or radiotherapy, detection of ctDNA post-procedure had a high PPV for cancer recurrence, with a median lead time of 6 months compared to surveillance imaging. Thus, ctDNA holds promise as a biomarker for pt enrollment on clinical trials and as an endpoint for monitoring of response to experimental therapies in this oligometastatic CRC population.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2021.39.15_suppl.3565
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2021
    detail.hit.zdb_id: 2005181-5
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  • 10
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    Abstract LB-257: Liquid biopsy versus tissue biopsy to assess acquired resistance and tumor heterogeneity in gastrointestinal cancers
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. LB-257-LB-257
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. LB-257-LB-257
    Abstract: The inevitable emergence of acquired resistance is a major limitation to the clinical benefit of precision medicine strategies. Single-lesion tumor biopsies have long been the mainstay of understanding acquired resistance, but recent data suggest tumor biopsies may under-represent the molecular heterogeneity of acquired resistance. Alternatively, studies have suggested that liquid biopsy approaches analyzing cell-free DNA (cfDNA) may offer significant advantages, but extensive prospective comparisons of matched liquid vs. tumor biopsies obtained at the time of acquired resistance are lacking. Here, we assess systematic liquid biopsy upon acquired resistance to targeted therapy in 44 patients across seven molecularly defined subtypes of gastrointestinal cancers. Liquid biopsy at disease progression identified at least one functionally validated molecular mechanism of resistance in 75% of patients, wherein 52% exhibited & gt;1 resistance alteration (range 2-9, median 3 per patient). In 23 patients in whom a matched post-progression tumor biopsy could be obtained, tumor biopsy was less effective than liquid biopsy in identifying resistance mechanisms, with resistance alterations detected in only 48% of patients, and multiple resistance mechanisms detected in only 9% of cases. In matched cases, liquid biopsy detected at least one resistance alteration not detected in tumor biopsy in 78% of cases. Targeted analysis and whole-exome sequencing of serial cfDNA, multiple post-progression biopsies, and rapid autopsy specimens from select cases revealed key insights into the geographic and complex characteristics of heterogeneity captured by liquid biopsy in the setting of acquired resistance. These data illustrate that acquired resistance is characterized by frequent and profound tumor heterogeneity, and suggests that liquid biopsy may more effectively identify heterogeneous clinically relevant resistance alterations compared to standard tumor biopsy. Citation Format: Aparna R. Parikh, Ignaty Leshchiner, Liudmila Elagina, Lipika Goyal, Chaya Levovitz, Giulia Siravegna, Dimitri Livitz, Kahn Rhrissorrakrai, Liz Martin, Emily E. Van Seventer, Megan Hanna, Kara Slowik, Filippo Utro, Christopher J. Pinto, Alicia Wong, Brian P. Danysh, Ferran Fece de la Cruz, Isobel J. Fetter, Brandon Nadres, Heather A. Shahzade, Jill N. Allen, Lawrence S. Blaszkowsky, Jeffrey W. Clark, Bruce Giantonio, Janet E. Murphy, Ryan D. Nipp, Eric Roeland, David P. Ryan, Colin D. Weekes, Eunice L. Kwak, Jason E. Faris, Francois Aguet, Ipsita Guha, Mehlika Hazar-Rethinam, Dora Dias-Santagata, David T. Ting, Andrew X. Zhu, Theodore S. Hong, Todd R. Golub, A J. Iafrate, Viktor Adalsteinsson, Alberto Bardelli, Laxmi Parida, Dejan Juric, Gad Getz, Ryan B. Corcoran. Liquid biopsy versus tissue biopsy to assess acquired resistance and tumor heterogeneity in gastrointestinal cancers [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 LB-257.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-LB-257
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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