GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Abstract 4258: Preliminarily results of the Oncohabitats Study: A multicentre validation of overall survival (OS) estimation of patients with glioblastoma (GBM) using vascular biomarkers
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4258-4258
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 4258-4258
    Abstract: We report preliminarily results of an international retrospective study (NCT03439332) analyzing the prognostic value of the early assessment of vascular architecture of glioblastoma (GBM). The initial cohort included 300 pts treated at 7 European hospitals. Multiparametric images were processed by Oncohabitats (www.oncohabitats.upv.es) to obtain the cerebral blood volume (CBV) and cerebral blood flow (CBF) from 4 automatically delimited regions of interest (ROIs): high angiogenic tumor (HAT), low angiogenic tumor (LAT), infiltrating peripherial edema (IPE), and vasogenic peripherial edema (VPE). Uniparametric Cox regression models and Kaplan-Meier analysis were developed to test prognostic and stratification capabilities of each biomarker. 115 pre-surgical MRIs passed quality controls and were included in the analysis. Median follow up was 12.9 months (m) (IQR: 9.2-17.6). 73 pts (63.5%) were male. 54 pts (47%) underwent total resection; 84 pts (73%) received adjuvant temozolomide. Median OS was 13.6 m (95%CI:12.1-15.2). Cox regression analysis yielded a significant correlation between OS and maximum rCBV and rCBF in HAT and LAT (Table), independent of the extent of resection. Median OS by Kaplan-Meier analysis in patients with high and low vascularity is shown in the Table. Our preliminarily results shows that patients with lower vascularity (rCBV or rCBF) in vascular habitats inside enhancing tumor region (HAT and LAT) is associated with higher OS, and could improve patient stratification. Our results are consistent with our pilot study [1], Validation in large multicentric studies is underway. COX REGRESSION ANALYSISKAPLAN-MEIER STRATIFICATION ANALYSISCOX REGRESSION ANALYSISKAPLAN-MEIER STRATIFICATION ANALYSISHAZARD RATIO95% CONFIDENCE INTERVALP-VALUE*NUMBER OF PATIENTSMEDIAN SURVIVAL (months)P-VALUErCBV máximumHigh Angiogenic Tumor10.339[1.09- 1.14]0.0202*[29 86] [16.66 12.78]0.004***Low Angiogenic Tumor10.485[1.17- 1.31] 0.0262*[29 86][17.10 12.78] 0.002***Infiltrating Peripheral Edema0.9835[1.30- 1.71]0.1208[29 86] [14.60 12.91]0.119Vasogenic Peripheral Edema0.7942[1.14- 1.63] 0.6046[29 86][15.23 12.91] 0.220rCBF máximumHigh Angiogenic Tumor0.9997[1.02- 1.03]0.1077[47 68] [14.93 11.65]0.009**Low Angiogenic Tumor10.411[1.21- 1.40] 0.0384*[29 86][15.56 12.75] 0.016*InfiltratingPeripheral Edema0.8923[1.35- 2.04]0.2589[29 86] [15.23 12.83]0.394Vasogenic Peripheral Edema0.6846[1.11- 1.81] 0.7447[29 86][14.60 12.96] 0.508Table: Results of Cox-regression and Kaplan-Meier analysis. (P VALUE*: False discovery rate corrected.)[1]: https://doi.org/10.1148/radiol.2017170845 Citation Format: María del Mar Álvarez-Torres, Fuensanta Bellvís–Bataller, Javier Juan–Albarracín, Elies Fuster–Garcia, David Lorente Estellés, Gaspar Reynes, Fernando Aparici-Robles, Carlos Botella, Jose Muñoz-Langa, Raquel Faubel, Sabina Asensio-Cuesta, Germán Adrían García–Ferrando, Cristina Auger, Alex Rovira, Jose Pineda, Jaime Font de Mora, Enrique Mollà-Olmos, Antonio José Revert-Ventura, Luaba Tshibanda, Didier Martin, Girolamo Crisi, Kyrre Eeg Emblem, Paulina Due-Tonnessen, Torstein R Meling, Juan M García-Gómez. Preliminarily results of the Oncohabitats Study: A multicentre validation of overall survival (OS) estimation of patients with glioblastoma (GBM) using vascular biomarkers [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 4258.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-4258
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    A Tricin Derivative from Deschampsia antarctica Desv. Inhibits Colorectal Carcinoma Growth and Liver Metastasis through the Induction of a Specific Immune Response
    American Association for Cancer Research (AACR) ; 2018
    In:  Molecular Cancer Therapeutics Vol. 17, No. 5 ( 2018-05-01), p. 966-976
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 17, No. 5 ( 2018-05-01), p. 966-976
    Abstract: In colorectal carcinoma patients, distant metastatic disease is present at initial diagnosis in nearly 25% of them. The majority of patients with metastatic colorectal carcinoma have incurable disease; therefore, new therapies are needed. Agents derived from medicinal plants have already demonstrated therapeutic activities in human cancer cells. Antartina is an antitumor agent isolated from Deschampsia antarctica Desv. This study aimed to evaluate the antitumor properties of Antartina in colorectal carcinoma models. We used human and murine colorectal carcinoma cell lines for investigating proliferation, apoptosis, and cell-cycle effects of Antartina therapy in vitro. Avatar and immunocompetent colorectal carcinoma animal models were applied for evaluating the effects of Antartina in vivo. Immune response against colorectal carcinoma model was investigated using CTL assay, analyzing dendritic cell activation and intratumor T-cell subpopulation, and by tumor rechallenge experiments. Antartina inhibits in vitro human colorectal carcinoma cell proliferation; however, in vivo experiments in Avatar colorectal carcinoma model Antartina display a limited antitumor effect. In an immunocompetent colorectal carcinoma mice model, Antartina potently inhibited tumor growth and liver metastases, leading to complete tumor regressions in & gt;30% of mice and increased animal survival. In addition, Antartina induced a potent specific cytotoxic T-cell response against colorectal carcinoma and a long-lasting antitumor immunity. Interestingly, Antartina increased tumor immunogenicity and stimulated dendritic cell activation. No toxic effects were observed at the doses employed. Our findings showed that Antartina has the ability to induce antitumor immunity against colorectal carcinoma and can be used to develop new tools for the treatment of colorectal carcinoma. Mol Cancer Ther; 17(5); 966–76. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.MCT-17-0193
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2062135-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Preclinical Efficacy of Endoglin-Targeting Antibody–Drug Conjugates for the Treatment of Ewing Sarcoma
    American Association for Cancer Research (AACR) ; 2019
    In:  Clinical Cancer Research Vol. 25, No. 7 ( 2019-04-01), p. 2228-2240
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 25, No. 7 ( 2019-04-01), p. 2228-2240
    Abstract: Endoglin (ENG; CD105) is a coreceptor of the TGFβ family that is highly expressed in proliferating endothelial cells. Often coopted by cancer cells, ENG can lead to neo-angiogenesis and vasculogenic mimicry in aggressive malignancies. It exists both as a transmembrane cell surface protein, where it primarily interacts with TGFβ, and as a soluble matricellular protein (sENG) when cleaved by matrix metalloproteinase 14 (MMP14). High ENG expression has been associated with poor prognosis in Ewing sarcoma, an aggressive bone cancer that primarily occurs in adolescents and young adults. However, the therapeutic value of ENG targeting has not been fully explored in this disease. Experimental Design: We characterized the expression pattern of transmembrane ENG, sENG, and MMP14 in preclinical and clinical samples. Subsequently, the antineoplastic potential of two novel ENG-targeting monoclonal antibody–drug conjugates (ADC), OMTX503 and OMTX703, which differed only by their drug payload (nigrin-b A chain and cytolysin, respectively), was assessed in cell lines and preclinical animal models of Ewing sarcoma. Results: Both ADCs suppressed cell proliferation in proportion to the endogenous levels of ENG observed in vitro. Moreover, the ADCs significantly delayed tumor growth in Ewing sarcoma cell line–derived xenografts and patient-derived xenografts in a dose-dependent manner. Conclusions: Taken together, these studies demonstrate potent preclinical activity of first-in-class anti-ENG ADCs as a nascent strategy to eradicate Ewing sarcoma.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-18-0936
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    A Novel Method for Rapid Molecular Subgrouping of Medulloblastoma
    American Association for Cancer Research (AACR) ; 2018
    In:  Clinical Cancer Research Vol. 24, No. 6 ( 2018-03-15), p. 1355-1363
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 24, No. 6 ( 2018-03-15), p. 1355-1363
    Abstract: Purpose: The classification of medulloblastoma into WNT, SHH, group 3, and group 4 subgroups has become of critical importance for patient risk stratification and subgroup-tailored clinical trials. Here, we aimed to develop a simplified, clinically applicable classification approach that can be implemented in the majority of centers treating patients with medulloblastoma. Experimental Design: We analyzed 1,577 samples comprising previously published DNA methylation microarray data (913 medulloblastomas, 457 non-medulloblastoma tumors, 85 normal tissues), and 122 frozen and formalin-fixed paraffin-embedded medulloblastoma samples. Biomarkers were identified applying stringent selection filters and Linear Discriminant Analysis (LDA) method, and validated using DNA methylation microarray data, bisulfite pyrosequencing, and direct-bisulfite sequencing. Results: Using a LDA-based approach, we developed and validated a prediction method (EpiWNT-SHH classifier) based on six epigenetic biomarkers that allowed for rapid classification of medulloblastoma into the clinically relevant subgroups WNT, SHH, and non-WNT/non-SHH with excellent concordance ( & gt;99%) with current gold-standard methods, DNA methylation microarray, and gene signature profiling analysis. The EpiWNT-SHH classifier showed high prediction capacity using both frozen and formalin-fixed material, as well as diverse DNA methylation detection methods. Similarly, we developed a classifier specific for group 3 and group 4 tumors, based on five biomarkers (EpiG3-G4) with good discriminatory capacity, allowing for correct assignment of more than 92% of tumors. EpiWNT-SHH and EpiG3-G4 methylation profiles remained stable across tumor primary, metastasis, and relapse samples. Conclusions: The EpiWNT-SHH and EpiG3-G4 classifiers represent a new simplified approach for accurate, rapid, and cost-effective molecular classification of single medulloblastoma DNA samples, using clinically applicable DNA methylation detection methods. Clin Cancer Res; 24(6); 1355–63. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-17-2243
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    A Three-Gene Expression Signature Model for Risk Stratification of Patients with Neuroblastoma
    American Association for Cancer Research (AACR) ; 2012
    In:  Clinical Cancer Research Vol. 18, No. 7 ( 2012-04-01), p. 2012-2023
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 7 ( 2012-04-01), p. 2012-2023
    Abstract: Purpose: Neuroblastoma is an embryonal tumor with contrasting clinical courses. Despite elaborate stratification strategies, precise clinical risk assessment still remains a challenge. The purpose of this study was to develop a PCR-based predictor model to improve clinical risk assessment of patients with neuroblastoma. Experimental Design: The model was developed using real-time PCR gene expression data from 96 samples and tested on separate expression data sets obtained from real-time PCR and microarray studies comprising 362 patients. Results: On the basis of our prior study of differentially expressed genes in favorable and unfavorable neuroblastoma subgroups, we identified three genes, CHD5, PAFAH1B1, and NME1, strongly associated with patient outcome. The expression pattern of these genes was used to develop a PCR-based single-score predictor model. The model discriminated patients into two groups with significantly different clinical outcome [set 1: 5-year overall survival (OS): 0.93 ± 0.03 vs. 0.53 ± 0.06, 5-year event-free survival (EFS): 0.85 ± 0.04 vs. 0.042 ± 0.06, both P & lt; 0.001; set 2 OS: 0.97 ± 0.02 vs. 0.61 ± 0.1, P = 0.005, EFS: 0.91 ± 0.8 vs. 0.56 ± 0.1, P = 0.005; and set 3 OS: 0.99 ± 0.01 vs. 0.56 ± 0.06, EFS: 0.96 ± 0.02 vs. 0.43 ± 0.05, both P & lt; 0.001]. Multivariate analysis showed that the model was an independent marker for survival (P & lt; 0.001, for all). In comparison with accepted risk stratification systems, the model robustly classified patients in the total cohort and in different clinically relevant risk subgroups. Conclusion: We propose for the first time in neuroblastoma, a technically simple PCR-based predictor model that could help refine current risk stratification systems. Clin Cancer Res; 18(7); 2012–23. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-11-2483
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Pancreatic Cancer Risk in Relation to Lifetime Smoking Patterns, Tobacco Type, and Dose–Response Relationships
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 29, No. 5 ( 2020-05-01), p. 1009-1018
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 5 ( 2020-05-01), p. 1009-1018
    Abstract: Despite smoking being a well-established risk factor for pancreatic cancer, there is a need to further characterize pancreatic cancer risk according to lifespan smoking patterns and other smoking features, such as tobacco type. Our aim was to deeply investigate them within a large European case–control study. Methods: Tobacco smoking habits and other relevant information were obtained from 2,009 cases and 1,532 controls recruited in the PanGenEU study using standardized tools. Multivariate logistic regression analysis was performed to evaluate pancreatic cancer risk by smoking characteristics and interactions with other pancreatic cancer risk factors. Fractional polynomials and restricted cubic splines were used to test for nonlinearity of the dose–response relationships and to analyze their shape. Results: Relative to never-smokers, current smokers [OR = 1.72; 95% confidence interval (95% CI), 1.39–2.12], those inhaling into the throat (OR = 1.48; 95% CI, 1.11–1.99) or chest (OR = 1.33; 95% CI, 1.12–1.58), and those using nonfiltered cigarettes (OR = 1.69; 95% CI, 1.10–2.61), were all at an increased pancreatic cancer risk. Pancreatic cancer risk was highest in current black tobacco smokers (OR = 2.09; 95% CI, 1.31–3.41), followed by blond tobacco smokers (OR = 1.43; 95% CI, 1.01–2.04). Childhood exposure to tobacco smoke relative to parental smoking was also associated with increased pancreatic cancer risk (OR = 1.24; 95% CI, 1.03–1.49). Dose–response relationships for smoking duration, intensity, cumulative dose, and smoking cessation were nonlinear and showed different shapes by tobacco type. Effect modification by family history of pancreatic cancer and diabetes was likely. Conclusions: This study reveals differences in pancreatic cancer risk by tobacco type and other habit characteristics, as well as nonlinear risk associations. Impact: This characterization of smoking-related pancreatic cancer risk profiles may help in defining pancreatic cancer high-risk populations.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-19-1027
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Abstract P1-15-02: An educational cancer genetics course to increase knowledge on hereditary breast cancer syndromes among physicians-in-training at a teaching hospital in Mexico City
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 4_Supplement ( 2020-02-15), p. P1-15-02-P1-15-02
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 4_Supplement ( 2020-02-15), p. P1-15-02-P1-15-02
    Abstract: Background: Breast cancer incidence is increasing globally, and a significant proportion of the disease has been linked to genetic susceptibility. Genetic knowledge and skills are essential for achieving optimal cancer care and prevention. However, in low- and middle-income countries the availability of physicians and other providers specializing in cancer genetics is very limited, and cancer genetics is not included in most undergraduate or graduate medical programs. Providing physicians-in-training with education on hereditary breast and ovarian cancer (HBOC) syndromes has the potential to improve the early identification of patients at a higher risk of breast cancer. This study aimed to assess the effect of a short HBOC course given to fellows from a single teaching hospital in Mexico City. Methods: We evaluated the basal practice patterns and knowledge on HBOC among fellows enrolled in internal medicine, general surgery, medical oncology and clinical genetics fellowship programs using a validated cancer genetics questionnaire composed of 13 questions and graded on a 0-100% scale. Fellows received a cancer genetics course (three lectures) from oncologists and geneticists with training in cancer genetics, and changes in knowledge post-course were evaluated using the same questionnaires. Descriptive statistics were utilized to describe the included subjects, and T-tests were used to compare pre and post questionnaire scores. Results: 110 fellows with a median age of 26.9 years (range 24-31) completed the basal questionnaire. 48.9% were enrolled in internal medicine, 21.8% in general surgery, 13.6% in medical oncology and 7.2% in clinical genetics. All respondents reported to routinely interrogate patients about their family history of cancer, and 70% said they had referred patients to the genetics clinic at their institution. The average score on the basal survey was 62% (SD 17). After the cancer genetics course was completed, 85 fellows answered the questionnaire. We found a relative increase in knowledge from pre to post-intervention of 12% (post-intervention average score 70% [SD 14]), which was statistically significant (p & lt;0.01). After the course, 36% of fellows said they would feel capable to provide recommendations to patients at risk of HBOC, compared to 17% before the course (p & lt;0.01). Conclusions: Although knowledge about HBOC among Mexican fellows is suboptimal, we found that providing short educational courses on cancer genetics may lead to a significant increase in knowledge on HBOC, as well as to an increase in confidence regarding recommendations. This study reinforces the need to develop focused and cost-effective educational strategies in low- and middle-income countries where specialists in cancer genetics are scarce, in order to provide physicians-in-training with knowledge and tools to recognize, refer, and counsel patients at risk of HBOC. Citation Format: Yanin Chavarri Guerra, Hector De la Mora Molina, Rosa Elena Caballero Landinez, Arantxa Lagunas Salazar, Andrea De la O Murillo, Rafael Reyes Arciniega, Enrique Soto Perez de Celis, Jose Luis Rodriguez Olivares, Osvaldo M Mutchinick, Jazmin Arteaga Vazquez. An educational cancer genetics course to increase knowledge on hereditary breast cancer syndromes among physicians-in-training at a teaching hospital in Mexico City [abstract]. In: Proceedings of the 2019 San Antonio Breast Cancer Symposium; 2019 Dec 10-14; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(4 Suppl):Abstract nr P1-15-02.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS19-P1-15-02
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Epigenetic EGFR Gene Repression Confers Sensitivity to Therapeutic BRAFV600E Blockade in Colon Neuroendocrine Carcinomas
    American Association for Cancer Research (AACR) ; 2020
    In:  Clinical Cancer Research Vol. 26, No. 4 ( 2020-02-15), p. 902-909
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 4 ( 2020-02-15), p. 902-909
    Abstract: The limited knowledge of the molecular alterations that characterize poorly differentiated neuroendocrine carcinomas has limited the clinical development of targeted agents directed to driver mutations. Here we aim to identify new molecular targets in colon neuroendocrine carcinomas (co-NEC) and proof the efficacy of matching drugs. Experimental Design: We performed a multi-omic analysis of co-NEC to identify genetic or epigenetic alterations that could be exploited as effective drug targets. We compared co-NEC samples with colorectal carcinomas (CRC) to identify neuroendocrine-specific traits. Patients with co-NEC and patient-derived xenografts were treated with a BRAFV600E-blocking drug to demonstrate sensitivity. Results: co-NEC and CRC are similar in their mutational repertoire, although co-NECs are particularly enriched in BRAFV600E mutations. We report for the first time that V600EBRAF-mutant co-NECs may benefit from BRAF inhibition in monotherapy and how EGFR status is essential to predict innate sensitivity and acquired resistance by a differential methylation of its gene regulatory regions. Conclusions: The identification of V600E BRAF mutations in high-grade co-NECs has allowed the description of radiological responses to combination therapy of BRAF and MEK inhibitors in basket clinical trials. However, the molecular rationale for this treatment combination was based on the presence of the BRAF mutation and the efficacy observed in other cancer types such as melanoma. Future drug development in this setting should test BRAF inhibitors upfront and the addition of anti-EGFR antibodies instead of MEK inhibitors for an efficient blockade of acquired resistance.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-19-1266
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...