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Article ; Online: Osimertinib plus Selumetinib in EGFR-Mutated Non-Small Cell Lung Cancer After Progression on EGFR-TKIs: A Phase Ib, Open-Label, Multicenter Trial (TATTON Part B).

Yang, James Chih-Hsin / Ohe, Yuichiro / Chiu, Chao-Hua / Ou, Xiaoling / Cantarini, Mireille / Jänne, Pasi A / Hartmaier, Ryan J / Ahn, Myung Ju

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 , Page(s) OF1–OF10

Abstract: Background: MEK/ERK inhibition can overcome acquired resistance to osimertinib in preclinical models. Osimertinib [EGFR-tyrosine kinase inhibitor (TKI)] plus selumetinib (MEK1/2 inhibitor) was assessed in the global TATTON study.: Methods: This ... ...

Abstract	Background: MEK/ERK inhibition can overcome acquired resistance to osimertinib in preclinical models. Osimertinib [EGFR-tyrosine kinase inhibitor (TKI)] plus selumetinib (MEK1/2 inhibitor) was assessed in the global TATTON study. Methods: This multicenter, open-label, phase Ib study expansion cohort enrolled patients (aged ≥18 years) with MET-negative, EGFRm advanced NSCLC who had progressed on EGFR-TKIs. Patients were assigned to one of two cohorts by prior first- or second-generation or T790M-directed EGFR-TKI and received osimertinib 80 mg every day and intermittent selumetinib 75 mg twice a day orally. Safety and tolerability (primary objective) and antitumor activity determined by objective response rate (ORR), and progression-free survival (PFS) using RECIST v1.1 were assessed. Data cutoff: March 4, 2020. Results: Forty-seven patients received treatment (prior first- or second-generation EGFR-TKI, n = 12; prior T790M-directed EGFR-TKI, n = 35). Forty-four (94%) patients were Asian; 30 (64%) had baseline exon 19 deletion. Most common AEs were diarrhea (89%), decreased appetite (40%), and stomatitis (32%); 11/47 patients (23%) had an AE Grade ≥3 possibly causally selumetinib-related. ORR was 66.7% [95% confidence interval (CI), 34.9-90.1] in the prior first- or second-generation EGFR-TKI group, 22.9% (95% CI, 10.4-40.1) in the prior T790M-directed EGFR-TKI group, and 34.0% (95% CI, 20.9-49.3) overall; median PFS was 15.0 (95% CI, 2.7-33.0), 2.8 (95% CI, 1.6-5.5), and 4.2 months (95% CI, 2.7-7.2), respectively. Conclusions: In this small study, AEs and tolerability of osimertinib plus selumetinib were as expected, on the basis of previous studies. The combination demonstrated antitumor activity supportive of further investigation in patients with MET-negative, EGFRm advanced NSCLC who had progressed on a previous EGFR-TKI.
Language	English
Publishing date	2022-06-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-4329
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Article ; Online: Author Correction: Candidate mechanisms of acquired resistance to first-line osimertinib in EGFR-mutated advanced non-small cell lung cancer.

Chmielecki, Juliann / Gray, Jhanelle E / Cheng, Ying / Ohe, Yuichiro / Imamura, Fumio / Cho, Byoung Chul / Lin, Meng-Chih / Majem, Margarita / Shah, Riyaz / Rukazenkov, Yuri / Todd, Alexander / Markovets, Aleksandra / Barrett, J Carl / Hartmaier, Ryan J / Ramalingam, Suresh S

Nature communications

2023 Volume 14, Issue 1, Page(s) 3179

Language	English
Publishing date	2023-06-01
Publishing country	England
Document type	Published Erratum
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38999-0
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Article ; Online: Analysis of acquired resistance mechanisms to osimertinib in patients with EGFR-mutated advanced non-small cell lung cancer from the AURA3 trial.

Chmielecki, Juliann / Mok, Tony / Wu, Yi-Long / Han, Ji-Youn / Ahn, Myung-Ju / Ramalingam, Suresh S / John, Thomas / Okamoto, Isamu / Yang, James Chih-Hsin / Shepherd, Frances A / Bulusu, Krishna C / Laus, Gianluca / Collins, Barbara / Barrett, J Carl / Hartmaier, Ryan J / Papadimitrakopoulou, Vassiliki

Nature communications

2023 Volume 14, Issue 1, Page(s) 1071

Abstract: Osimertinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), potently and selectively inhibits EGFR-TKI-sensitizing and EGFR T790M resistance mutations. This analysis evaluates acquired resistance mechanisms to second-line ... ...

Abstract	Osimertinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), potently and selectively inhibits EGFR-TKI-sensitizing and EGFR T790M resistance mutations. This analysis evaluates acquired resistance mechanisms to second-line osimertinib (n = 78) in patients with EGFR T790M advanced non-small cell lung cancer (NSCLC) from AURA3 (NCT02151981), a randomized phase 3 study comparing osimertinib with chemotherapy. Plasma samples collected at baseline and disease progression/treatment discontinuation are analyzed using next-generation sequencing. Half (50%) of patients have undetectable plasma EGFR T790M at disease progression and/or treatment discontinuation. Fifteen patients (19%) have >1 resistance-related genomic alteration; MET amplification (14/78, 18%) and EGFR C797X mutation (14/78, 18%).
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; ErbB Receptors/genetics ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Mutation ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Disease Progression
Chemical Substances	osimertinib (3C06JJ0Z2O) ; ErbB Receptors (EC 2.7.10.1) ; Protein Kinase Inhibitors ; EGFR protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-02-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-35962-x
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Article ; Online: Candidate mechanisms of acquired resistance to first-line osimertinib in EGFR-mutated advanced non-small cell lung cancer.

Nature communications

2023 Volume 14, Issue 1, Page(s) 1070

Abstract: Osimertinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), potently and selectively inhibits EGFR-TKI-sensitizing and EGFR T790M resistance mutations. In the Phase III FLAURA study (NCT02296125), first-line osimertinib ... ...

Abstract	Osimertinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), potently and selectively inhibits EGFR-TKI-sensitizing and EGFR T790M resistance mutations. In the Phase III FLAURA study (NCT02296125), first-line osimertinib improved outcomes vs comparator EGFR-TKIs in EGFRm advanced non-small cell lung cancer. This analysis identifies acquired resistance mechanisms to first-line osimertinib. Next-generation sequencing assesses circulating-tumor DNA from paired plasma samples (baseline and disease progression/treatment discontinuation) in patients with baseline EGFRm. No EGFR T790M-mediated acquired resistance are observed; most frequent resistance mechanisms are MET amplification (n = 17; 16%) and EGFR C797S mutations (n = 7; 6%). Future research investigating non-genetic acquired resistance mechanisms is warranted.
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; ErbB Receptors/genetics ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Mutation ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	osimertinib (3C06JJ0Z2O) ; ErbB Receptors (EC 2.7.10.1) ; Protein Kinase Inhibitors ; EGFR protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-02-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-35961-y
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Article ; Online: Graduate students bring clinical know-how into their lab work through the HHMI Med into Grad program.

Hartmaier, Ryan J / Shaffer, Donald R

Disease models & mechanisms

2009 Volume 2, Issue 11-12, Page(s) 531–532

MeSH term(s)	Biomedical Research/education ; Curriculum ; Education, Medical, Graduate ; Humans ; Organizations, Nonprofit ; Program Development ; Research Support as Topic ; Students
Language	English
Publishing date	2009-11
Publishing country	England
Document type	News
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.004531
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Article ; Online: Early Clearance of Plasma Epidermal Growth Factor Receptor Mutations as a Predictor of Outcome on Osimertinib in Advanced Non-Small Cell Lung Cancer; Exploratory Analysis from AURA3 and FLAURA.

Clinical cancer research : an official journal of the American Association for Cancer Research

2023 Volume 29, Issue 17, Page(s) 3340–3351

Abstract: Purpose: Plasma circulating tumor DNA (ctDNA) analysis is used for genotyping advanced non-small cell lung cancer (NSCLC); monitoring dynamic ctDNA changes may be used to predict outcomes.: Patients and methods: This was a retrospective, exploratory ... ...

Abstract	Purpose: Plasma circulating tumor DNA (ctDNA) analysis is used for genotyping advanced non-small cell lung cancer (NSCLC); monitoring dynamic ctDNA changes may be used to predict outcomes. Patients and methods: This was a retrospective, exploratory analysis of two phase III trials [AURA3 (NCT02151981), FLAURA (NCT02296125)]. All patients had EGFR mutation-positive (EGFRm; ex19del or L858R) advanced NSCLC; AURA3 also included T790M-positive NSCLC. Osimertinib (FLAURA, AURA3), or comparator EGFR-tyrosine kinase inhibitor (EGFR-TKI; gefitinib/erlotinib; FLAURA), or platinum-based doublet chemotherapy (AURA3) was given. Plasma EGFRm was analyzed at baseline and Weeks 3/6 by droplet digital PCR. Outcomes were assessed by detectable/non-detectable baseline plasma EGFRm and plasma EGFRm clearance (non-detection) at Weeks 3/6. Results: In AURA3 (n = 291), non-detectable versus detectable baseline plasma EGFRm had longer median progression-free survival [mPFS; HR, 0.48; 95% confidence interval (CI), 0.33-0.68; P < 0.0001]. In patients with Week 3 clearance versus non-clearance (n = 184), respectively, mPFS (months; 95% CI) was 10.9 (8.3-12.6) versus 5.7 (4.1-9.7) with osimertinib and 6.2 (4.0-9.7) versus 4.2 (4.0-5.1) with platinum-pemetrexed. In FLAURA (n = 499), mPFS was longer with non-detectable versus detectable baseline plasma EGFRm (HR, 0.54; 95% CI, 0.41-0.70; P < 0.0001). For Week 3 clearance versus non-clearance (n = 334), respectively, mPFS was 19.8 (15.1 to not calculable) versus 11.3 (9.5-16.5) with osimertinib and 10.8 (9.7-11.1) versus 7.0 (5.6-8.3) with comparator EGFR-TKI. Similar outcomes were observed by Week 6 clearance/non-clearance. Conclusions: Plasma EGFRm analysis as early as 3 weeks on-treatment has the potential to predict outcomes in EGFRm advanced NSCLC.
Language	English
Publishing date	2023-06-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-3146
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Zs.A 4223: Show issues

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Article ; Online: Improving ChIP-seq peak-calling for functional co-regulator binding by integrating multiple sources of biological information

Osmanbeyoglu Hatice / Hartmaier Ryan J / Oesterreich Steffi / Lu Xinghua

BMC Genomics, Vol 13, Iss Suppl 1, p S

2012 Volume 1

Abstract: Abstract Background Chromatin immunoprecipitation coupled with massively parallel sequencing (ChIP-seq) is increasingly being applied to study genome-wide binding sites of transcription factors. There is an increasing interest in understanding the ... ...

Abstract	Abstract Background Chromatin immunoprecipitation coupled with massively parallel sequencing (ChIP-seq) is increasingly being applied to study genome-wide binding sites of transcription factors. There is an increasing interest in understanding the mechanism of action of co-regulator proteins, which do not bind DNA directly, but exert their effects by binding to transcription factors such as the estrogen receptor (ER). However, due to the nature of detecting indirect protein-DNA interaction, ChIP-seq signals from co-regulators can be relatively weak and thus biologically meaningful interactions remain difficult to identify. Results In this study, we investigated and compared different statistical and machine learning approaches including unsupervised, supervised, and semi-supervised classification (self-training) approaches to integrate multiple types of genomic and transcriptomic information derived from our experiments and public database to overcome difficulty of identifying functional DNA binding sites of the co-regulator SRC-1 in the context of estrogen response. Our results indicate that supervised learning with naïve Bayes algorithm significantly enhances peak calling of weak ChIP-seq signals and outperforms other machine learning algorithms. Our integrative approach revealed many potential ERα/SRC-1 DNA binding sites that would otherwise be missed by conventional peak calling algorithms with default settings. Conclusions Our results indicate that a supervised classification approach enables one to utilize limited amounts of prior knowledge together with multiple types of biological data to enhance the sensitivity and specificity of the identification of DNA binding sites from co-regulator proteins.
Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	006
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Who's driving anyway? Herculean efforts to identify the drivers of breast cancer.

Hartmaier, Ryan J / Priedigkeit, Nolan / Lee, Adrian V

Breast cancer research : BCR

2012 Volume 14, Issue 5, Page(s) 323

Abstract: The continuing advancement of sequencing technologies has made the systematic identification of all driving somatic events in cancer a possibility. In the June 2012 issue of Nature, five papers show some significant headway in this endeavor, each a ... ...

Abstract	The continuing advancement of sequencing technologies has made the systematic identification of all driving somatic events in cancer a possibility. In the June 2012 issue of Nature, five papers show some significant headway in this endeavor, each a herculean effort of genome sequencing, and transcriptome and copy number analysis resulting in data on thousands of breast cancers. Integrating these massive datasets, the authors were able to further subdivide breast cancer and identify a number of novel driver genes. While the studies represent a leap forward in describing the genomics of breast cancer, and clearly highlight the tremendous diversity between tumors, the studies only scrape the surface of molecular changes in breast tumors, with more granularity to come from the study of epigenomics, single cell sequencing, and so on. The immediate importance of the data to clinical care is currently unknown, and will depend upon detailed identification and functional analysis of driver mutations.
MeSH term(s)	Aromatase/metabolism ; Aromatase Inhibitors/therapeutic use ; Breast Neoplasms/classification ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Transformation, Neoplastic/genetics ; DNA Copy Number Variations/genetics ; Evolution, Molecular ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genome, Human/genetics ; Humans ; Mutagenesis/genetics ; Mutation/genetics ; Oncogenes/genetics ; Translocation, Genetic/genetics
Chemical Substances	Aromatase Inhibitors ; Aromatase (EC 1.14.14.1)
Language	English
Publishing date	2012-10-31
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/bcr3325
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Zs.A 5494: Show issues

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Article ; Online: The genomic landscape of metastatic breast cancer: Insights from 11,000 tumors.

Rinaldi, Jacob / Sokol, Ethan S / Hartmaier, Ryan J / Trabucco, Sally E / Frampton, Garrett M / Goldberg, Michael E / Albacker, Lee A / Daemen, Anneleen / Manning, Gerard

PloS one

2020 Volume 15, Issue 5, Page(s) e0231999

Abstract: Background: Metastatic breast cancer is the leading cause of cancer death in women, but the genomics of metastasis in breast cancer are poorly studied.: Methods: We explored a set of 11,616 breast tumors, including 5,034 metastases, which had ... ...

Abstract	Background: Metastatic breast cancer is the leading cause of cancer death in women, but the genomics of metastasis in breast cancer are poorly studied. Methods: We explored a set of 11,616 breast tumors, including 5,034 metastases, which had undergone targeted sequencing during standard clinical care. Results: Besides the known hotspot mutations in ESR1, we observed a metastatic enrichment of previously unreported, lower-prevalence mutations in the ligand-binding domain, implying that these mutations may also be functional. Furthermore, individual ESR1 hotspots are significantly enriched in specific metastatic tissues and histologies, suggesting functional differences between these mutations. Other alterations enriched across all metastases include loss of function of the CDK4 regulator CDKN1B, and mutations in the transcription factor CTCF. Mutations enriched at specific metastatic sites generally reflect biology of the target tissue and may be adaptations to growth in the local environment. These include PTEN and ASXL1 alterations in brain metastases and NOTCH1 alterations in skin. We observed an enrichment of KRAS, KEAP1, STK11 and EGFR mutations in lung metastases. However, the patterns of other mutations in these tumors indicate that these are misdiagnosed lung primaries rather than breast metastases. Conclusions: An order-of-magnitude increase in samples relative to previous studies allowed us to detect novel genomic characteristics of metastatic cancer and to expand and clarify previous findings.
MeSH term(s)	Adult ; Biomarkers, Tumor/genetics ; Breast Neoplasms/epidemiology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Case-Control Studies ; Estrogen Receptor alpha/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Gene Frequency ; Genes, erbB-2 ; Genomics ; Germ-Line Mutation ; High-Throughput Nucleotide Sequencing ; Humans ; Lymphatic Metastasis ; Middle Aged ; Mutation ; Neoplasm Metastasis ; Prevalence
Chemical Substances	Biomarkers, Tumor ; Estrogen Receptor alpha
Language	English
Publishing date	2020-05-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0231999
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Article ; Online: Osimertinib + Savolitinib to Overcome Acquired MET-Mediated Resistance in Epidermal Growth Factor Receptor-Mutated, MET-Amplified Non-Small Cell Lung Cancer: TATTON.

Cancer discovery

2022 Volume 13, Issue 1, Page(s) 98–113

Abstract: MET-inhibitor and EGFR tyrosine kinase inhibitor (EGFR-TKI) combination therapy could overcome acquired MET-mediated osimertinib resistance. We present the final phase Ib TATTON (NCT02143466) analysis (Part B, n = 138/Part D, n = 42) assessing oral ... ...

Abstract	MET-inhibitor and EGFR tyrosine kinase inhibitor (EGFR-TKI) combination therapy could overcome acquired MET-mediated osimertinib resistance. We present the final phase Ib TATTON (NCT02143466) analysis (Part B, n = 138/Part D, n = 42) assessing oral savolitinib 600 mg/300 mg once daily (q.d.) + osimertinib 80 mg q.d. in patients with MET-amplified, EGFR-mutated (EGFRm) advanced non-small cell lung cancer (NSCLC) and progression on prior EGFR-TKI. An acceptable safety profile was observed. In Parts B and D, respectively, objective response rates were 33% to 67% and 62%, and median progression-free survival (PFS) was 5.5 to 11.1 months and 9.0 months. Increased antitumor activity may occur with MET copy number ≥10. EGFRm circulating tumor DNA clearance on treatment predicted longer PFS in patients with detectable baseline ctDNA, while acquired resistance mechanisms to osimertinib + savolitinib were mediated by MET, EGFR, or KRAS alterations. Significance: The savolitinib + osimertinib combination represents a promising therapy in patients with MET-amplified/overexpressed, EGFRm advanced NSCLC with disease progression on a prior EGFR-TKI. Acquired resistance mechanisms to this combination include those via MET, EGFR, and KRAS. On-treatment ctDNA dynamics can predict clinical outcomes and may provide an opportunity to inform earlier decision-making. This article is highlighted in the In This Issue feature, p. 1.
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Proto-Oncogene Proteins p21(ras)/genetics ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Mutation ; Aniline Compounds/therapeutic use ; ErbB Receptors
Chemical Substances	osimertinib (3C06JJ0Z2O) ; 1-(1-(imidazo(1,2-a)pyridin-6-yl)ethyl)-6-(1-methyl-1H-pyrazol-4-yl)-1H-(1,2,3)triazolo(4,5-b)pyrazine (2A2DA6857R) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Protein Kinase Inhibitors ; Aniline Compounds ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2022-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-22-0586
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