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Article ; Online: Breast Cancer,

Bose, Ron / Ma, Cynthia X

2021 Volume 385, Issue 13, Page(s) 1241–1243

MeSH term(s)	Breast Neoplasms/genetics ; Drug Resistance, Neoplasm ; Female ; Humans ; Mutation ; Protein Kinase Inhibitors/therapeutic use ; Quinolines/therapeutic use ; Receptor, ErbB-2/antagonists & inhibitors ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Receptor, ErbB-3/genetics ; Receptor, ErbB-3/metabolism ; Signal Transduction
Chemical Substances	Protein Kinase Inhibitors ; Quinolines ; Receptor, ErbB-2 (EC 2.7.10.1) ; Receptor, ErbB-3 (EC 2.7.10.1) ; neratinib (JJH94R3PWB)
Language	English
Publishing date	2021-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMcibr2110552
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Article ; Online: A neu view of invasive lobular breast cancer.

Bose, Ron

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

2013 Volume 19, Issue 13, Page(s) 3331–3333

Abstract: Genome sequencing of relapsed, invasive lobular breast cancer identified actionable mutations in 86% of the cases. HER2 alterations occur in 27% of the cases, including 4 cases with activating HER2 mutations and 1 with a novel HER2-GRB7 gene fusion. This ...

Abstract	Genome sequencing of relapsed, invasive lobular breast cancer identified actionable mutations in 86% of the cases. HER2 alterations occur in 27% of the cases, including 4 cases with activating HER2 mutations and 1 with a novel HER2-GRB7 gene fusion. This fusion links the HER2 tyrosine kinase domain to the GRB7 src homology 2 (SH2) domain.
MeSH term(s)	Breast Neoplasms/genetics ; Cadherins/genetics ; Carcinoma, Ductal, Breast/genetics ; Carcinoma, Lobular/genetics ; Female ; Humans ; Mutation ; Receptor, ErbB-2/genetics
Chemical Substances	Cadherins ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2013-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-13-1031
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Zs.A 4223: Show issues

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Article ; Online: Analysis of somatic mutations across the kinome reveals loss-of-function mutations in multiple cancer types.

Kumar, Runjun D / Bose, Ron

Scientific reports

2017 Volume 7, Issue 1, Page(s) 6418

Abstract: In this study we use somatic cancer mutations to identify important functional residues within sets of related genes. We focus on protein kinases, a superfamily of phosphotransferases that share homologous sequences and structural motifs and have many ... ...

Abstract	In this study we use somatic cancer mutations to identify important functional residues within sets of related genes. We focus on protein kinases, a superfamily of phosphotransferases that share homologous sequences and structural motifs and have many connections to cancer. We develop several statistical tests for identifying Significantly Mutated Positions (SMPs), which are positions in an alignment with mutations that show signs of selection. We apply our methods to 21,917 mutations that map to the alignment of human kinases and identify 23 SMPs. SMPs occur throughout the alignment, with many in the important A-loop region, and others spread between the N and C lobes of the kinase domain. Since mutations are pooled across the superfamily, these positions may be important to many protein kinases. We select eleven mutations from these positions for functional validation. All eleven mutations cause a reduction or loss of function in the affected kinase. The tested mutations are from four genes, including two tumor suppressors (TGFBR1 and CHEK2) and two oncogenes (KDR and ERBB2). They also represent multiple cancer types, and include both recurrent and non-recurrent events. Many of these mutations warrant further investigation as potential cancer drivers.
MeSH term(s)	Animals ; Checkpoint Kinase 2/genetics ; Databases, Genetic ; Humans ; Loss of Function Mutation ; Mice ; NIH 3T3 Cells ; Neoplasms/enzymology ; Neoplasms/genetics ; Phosphotransferases/chemistry ; Phosphotransferases/genetics ; Phosphotransferases/metabolism ; Receptor, ErbB-2/genetics ; Receptor, Transforming Growth Factor-beta Type I/genetics ; Reproducibility of Results ; Vascular Endothelial Growth Factor Receptor-2/genetics
Chemical Substances	Phosphotransferases (EC 2.7.-) ; Checkpoint Kinase 2 (EC 2.7.1.11) ; ERBB2 protein, human (EC 2.7.10.1) ; KDR protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; CHEK2 protein, human (EC 2.7.11.1) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; TGFBR1 protein, human (EC 2.7.11.30)
Language	English
Publishing date	2017-07-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-06366-x
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Article ; Online: Efficient sortase-mediated N-terminal labeling of TEV protease cleaved recombinant proteins.

Sarpong, Kwabena / Bose, Ron

Analytical biochemistry

2017 Volume 521, Page(s) 55–58

Abstract: A major challenge in attaching fluorophores or other handles to proteins is the availability of a site-specific labeling strategy that provides stoichiometric modification without compromising protein integrity. We developed a simple approach that ... ...

Abstract	A major challenge in attaching fluorophores or other handles to proteins is the availability of a site-specific labeling strategy that provides stoichiometric modification without compromising protein integrity. We developed a simple approach that combines TEV protease cleavage, sortase modification and affinity purification to N-terminally label proteins. To achieve stoichiometrically-labeled protein, we included a short affinity tag in the fluorophore-containing peptide for post-labeling purification of the modified protein. This strategy can be easily applied to any recombinant protein with a TEV site and we demonstrate this on Epidermal Growth Factor Receptor (EGFR) and Membrane Scaffold Protein (MSP) constructs.
MeSH term(s)	Aminoacyltransferases/metabolism ; Bacterial Proteins/metabolism ; Chromatography, Affinity/methods ; Cysteine Endopeptidases/metabolism ; Cytoskeletal Proteins/chemistry ; Cytoskeletal Proteins/isolation & purification ; Cytoskeletal Proteins/metabolism ; Endopeptidases/metabolism ; Humans ; Membrane Proteins/chemistry ; Membrane Proteins/isolation & purification ; Membrane Proteins/metabolism ; Peptide Fragments/metabolism ; Receptor, Epidermal Growth Factor/chemistry ; Receptor, Epidermal Growth Factor/isolation & purification ; Receptor, Epidermal Growth Factor/metabolism ; Recombinant Fusion Proteins/chemistry ; Recombinant Fusion Proteins/isolation & purification ; Recombinant Fusion Proteins/metabolism ; Staphylococcus aureus/enzymology
Chemical Substances	Bacterial Proteins ; Cytoskeletal Proteins ; Membrane Proteins ; Peptide Fragments ; Recombinant Fusion Proteins ; erythrocyte membrane band 4.1 protein ; Aminoacyltransferases (EC 2.3.2.-) ; sortase A (EC 2.3.2.-) ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Endopeptidases (EC 3.4.-) ; TEV protease (EC 3.4.-) ; Cysteine Endopeptidases (EC 3.4.22.-)
Language	English
Publishing date	2017-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1110-1
ISSN	1096-0309 ; 0003-2697
ISSN (online)	1096-0309
ISSN	0003-2697
DOI	10.1016/j.ab.2017.01.008
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Article ; Online: Breast Cancer Mutations HER2V777L and PIK3CAH1047R Activate the p21-CDK4/6-Cyclin D1 Axis to Drive Tumorigenesis and Drug Resistance.

Cheng, Xiaoqing / Sun, Yirui / Highkin, Maureen / Vemalapally, Nagalaxmi / Jin, Xiaohua / Zhou, Brandon / Prior, Julie L / Tipton, Ashley R / Li, Shunqiang / Iliuk, Anton / Achilefu, Samuel / Hagemann, Ian S / Edwards, John R / Bose, Ron

Cancer research

2023 Volume 83, Issue 17, Page(s) 2839–2857

Abstract: In metastatic breast cancer, HER2-activating mutations frequently co-occur with mutations in PIK3CA, TP53, or CDH1. Of these co-occurring mutations, HER2 and PIK3CA are the most commonly comutated gene pair, with approximately 40% of HER2-mutated breast ... ...

Abstract	In metastatic breast cancer, HER2-activating mutations frequently co-occur with mutations in PIK3CA, TP53, or CDH1. Of these co-occurring mutations, HER2 and PIK3CA are the most commonly comutated gene pair, with approximately 40% of HER2-mutated breast cancers also having activating mutations in PIK3CA. To study the effects of co-occurring HER2 and PIK3CA mutations, we generated genetically engineered mice with the HER2V777L; PIK3CAH1047R transgenes (HP mice) and studied the resulting breast cancers both in vivo as well as ex vivo using cancer organoids. HP breast cancers showed accelerated tumor formation in vivo and increased invasion and migration in in vitro assays. HP breast cancer cells were resistant to the pan-HER tyrosine kinase inhibitor, neratinib, but were effectively treated with neratinib plus the HER2-targeted antibody-drug conjugate trastuzumab deruxtecan. Proteomic and RNA-seq analysis of HP breast cancers identified increased gene expression of cyclin D1 and p21WAF1/Cip1 and changes in cell-cycle markers. Combining neratinib with CDK4/6 inhibitors was another effective strategy for treating HP breast cancers, with neratinib plus palbociclib showing a statistically significant reduction in development of mouse HP tumors as compared to either drug alone. The efficacy of both the neratinib plus trastuzumab deruxtecan and neratinib plus palbociclib combinations was validated using a human breast cancer patient-derived xenograft with very similar HER2 and PIK3CA mutations to the HP mice. Further, these two drug combinations effectively treated spontaneous lung metastasis in syngeneic mice transplanted with HP breast cancer organoids. This study provides valuable preclinical data to support the ongoing phase 1 clinical trials of these drug combinations in breast cancer. Significance: In HER2-mutated breast cancer, PIK3CA mutation activates p21-CDK4/6-cyclin D1 signaling to drive resistance to HER2-targeted therapies, which can be overcome using CDK4/6 inhibitors.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Transformation, Neoplastic ; Class I Phosphatidylinositol 3-Kinases/genetics ; Cyclin D1/genetics ; Cyclin-Dependent Kinase 4/genetics ; Drug Resistance, Neoplasm/genetics ; Mutation ; Proteomics ; Receptor, ErbB-2/metabolism
Chemical Substances	CDK4 protein, human (EC 2.7.11.22) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Cyclin D1 (136601-57-5) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Receptor, ErbB-2 (EC 2.7.10.1) ; PIK3CA protein, human (EC 2.7.1.137) ; ERBB2 protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-3558
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Article ; Online: Using multigene tests to select treatment for early-stage breast cancer.

Goncalves, Rodrigo / Bose, Ron

Journal of the National Comprehensive Cancer Network : JNCCN

2013 Volume 11, Issue 2, Page(s) 174–82; quiz 182

Abstract: Oncotype DX, PAM50, and MammaPrint are multigene tests that are being used clinically for early-stage breast cancer to predict recurrence risk and guide adjuvant chemotherapy decisions. These tests have been validated in multiple retrospective studies, ... ...

Abstract	Oncotype DX, PAM50, and MammaPrint are multigene tests that are being used clinically for early-stage breast cancer to predict recurrence risk and guide adjuvant chemotherapy decisions. These tests have been validated in multiple retrospective studies, and prospective clinical trials are in progress. The TAILORx trial uses the Oncotype DX recurrence score to assign estrogen receptor-positive (ER+), node-negative patients to chemotherapy plus hormonal therapy versus hormonal therapy alone. The RxPONDER (SWOG S1007) trial uses Oncotype DX in a similar approach but on node-positive patients, and it includes the PAM50 test as a secondary analysis. The MINDACT trial uses Mamma-Print and Adjuvant! Online for treatment arm assignments. MINDACT has very broad eligibility criteria and 2 secondary randomizations for selecting chemotherapy and hormonal therapy regimens. This article discusses how the latest results on cancer genome sequencing apply to early-stage breast cancer. Several hundred breast cancers have already undergone genome sequencing, and the somatic DNA changes found in the tumor, compared with the patient's normal DNA, have been identified. Higher rates of point mutations and chromosomal translocations are found in aromatase inhibitor-resistant ER+ cancers and in the basal-like and HER2-enriched breast cancer subtypes. Correlations of somatic mutations with neoadjuvant aromatase inhibitor response are discussed. Genome sequencing can potentially identify the molecular abnormalities that underlie the poor risk identified by multigene tests and provide potential new targets for therapy, but more clinical trials correlating clinical outcome and somatic DNA changes are needed.
MeSH term(s)	Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Clinical Trials as Topic ; Female ; Genetic Testing/methods ; Genome, Human ; Humans ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology ; Point Mutation ; Sequence Analysis, DNA/methods ; Translocation, Genetic
Language	English
Publishing date	2013-01-31
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2250759-0
ISSN	1540-1413 ; 1540-1405
ISSN (online)	1540-1413
ISSN	1540-1405
DOI	10.6004/jnccn.2013.0025
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Article ; Online: HER2 and APC Mutations Promote Altered Crypt-Villus Morphology and Marked Hyperplasia in the Intestinal Epithelium.

Murray, Elisa / Cheng, Xiaoqing / Krishna, Anagha / Jin, Xiaohua / Ohara, Takahiro E / Stappenbeck, Thaddeus S / Bose, Ron

Cellular and molecular gastroenterology and hepatology

2021 Volume 12, Issue 3, Page(s) 1105–1120

Abstract: Background and aims: The Cancer Genome Atlas (TCGA) project has identified HER2 mutations or amplification in 7% of colon cancers. In addition to HER2 mutations, colon cancer patients also possess co-occurring mutations in genes such as APC. Here, we ... ...

Abstract	Background and aims: The Cancer Genome Atlas (TCGA) project has identified HER2 mutations or amplification in 7% of colon cancers. In addition to HER2 mutations, colon cancer patients also possess co-occurring mutations in genes such as APC. Here, we investigated the role of HER2 and APC mutations on the crypt-villus architecture of the intestinal epithelium, localization of secretory cells, and expression of intestinal stem cell markers. Methods: We generated a HER2 transgenic mouse (HER2 Results: HER2 Conclusions: We established an epithelial intrinsic role for HER2
MeSH term(s)	Adenomatous Polyposis Coli Protein/genetics ; Animals ; Gene Editing ; Hyperplasia ; Intestinal Mucosa/chemistry ; Intestinal Mucosa/pathology ; Matrix Metalloproteinase 7/metabolism ; Mice ; Mice, Transgenic ; Mucin-2/metabolism ; Mutation ; Receptor, ErbB-2/genetics
Chemical Substances	Adenomatous Polyposis Coli Protein ; Muc2 protein, mouse ; Mucin-2 ; adenomatous polyposis coli protein, mouse ; Erbb2 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Matrix Metalloproteinase 7 (EC 3.4.24.23)
Language	English
Publishing date	2021-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2021.04.012
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Article: Prognostic and Predictive Biomarkers of Endocrine Responsiveness for Estrogen Receptor Positive Breast Cancer.

Ma, Cynthia X / Bose, Ron / Ellis, Matthew J

Advances in experimental medicine and biology

2016 Volume 882, Page(s) 125–154

Abstract: The estrogen-dependent nature of breast cancer is the fundamental basis for endocrine therapy. The presence of estrogen receptor (ER), the therapeutic target of endocrine therapy, is a prerequisite for this therapeutic approach. However, estrogen- ... ...

Abstract	The estrogen-dependent nature of breast cancer is the fundamental basis for endocrine therapy. The presence of estrogen receptor (ER), the therapeutic target of endocrine therapy, is a prerequisite for this therapeutic approach. However, estrogen-independent growth often exists de novo at diagnosis or develops during the course of endocrine therapy. Therefore ER alone is insufficient in predicting endocrine therapy efficacy. Several RNA-based multigene assays are now available in clinical practice to assess distant recurrence risk, with majority of these assays evaluated in patients treated with 5 years of adjuvant endocrine therapy. While MammaPrint and Oncotype Dx are most predictive of recurrence risk within the first 5 years of diagnosis, Prosigna, Breast Cancer Index (BCI), and EndoPredict Clin have also demonstrated utility in predicting late recurrence. In addition, PAM50, or Prosigna, provides further biological insights by classifying breast cancers into intrinsic molecular subtypes. Additional strategies are under investigation in prospective clinical trials to differentiate endocrine sensitive and resistant tumors and include on-treatment Ki-67 and Preoperative Endocrine Prognostic Index (PEPI) score in the setting of neoadjuvant endocrine therapy. These biomarkers have become important tools in clinical practice for the identification of low risk patients for whom chemotherapy could be avoided. However, there is much work ahead toward the development of a molecular classification that informs the biology and novel therapeutic targets in high-risk disease as chemotherapy has only modest benefit in this population. The recognition of somatic mutations and their relationship to endocrine therapy responsiveness opens important opportunities toward this goal.
MeSH term(s)	Animals ; Antineoplastic Agents, Hormonal/therapeutic use ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/mortality ; Breast Neoplasms/pathology ; Chemotherapy, Adjuvant ; DNA Mutational Analysis ; Disease Progression ; Disease-Free Survival ; Female ; Gene Expression Profiling ; Humans ; Mutation ; Neoadjuvant Therapy ; Neoplasm Recurrence, Local ; Neoplasms, Hormone-Dependent/drug therapy ; Neoplasms, Hormone-Dependent/genetics ; Neoplasms, Hormone-Dependent/metabolism ; Neoplasms, Hormone-Dependent/mortality ; Neoplasms, Hormone-Dependent/pathology ; Predictive Value of Tests ; Receptors, Estrogen/drug effects ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Risk Assessment ; Risk Factors ; Signal Transduction/drug effects ; Time Factors ; Treatment Outcome
Chemical Substances	Antineoplastic Agents, Hormonal ; Biomarkers, Tumor ; Receptors, Estrogen
Language	English
Publishing date	2016-02-17
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-22909-6_5
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Article ; Online: Unsupervised detection of cancer driver mutations with parsimony-guided learning.

Kumar, Runjun D / Swamidass, S Joshua / Bose, Ron

Nature genetics

2016 Volume 48, Issue 10, Page(s) 1288–1294

Abstract: Methods are needed to reliably prioritize biologically active driver mutations over inactive passengers in high-throughput sequencing cancer data sets. We present ParsSNP, an unsupervised functional impact predictor that is guided by parsimony. ParsSNP ... ...

Abstract	Methods are needed to reliably prioritize biologically active driver mutations over inactive passengers in high-throughput sequencing cancer data sets. We present ParsSNP, an unsupervised functional impact predictor that is guided by parsimony. ParsSNP uses an expectation-maximization framework to find mutations that explain tumor incidence broadly, without using predefined training labels that can introduce biases. We compare ParsSNP to five existing tools (CanDrA, CHASM, FATHMM Cancer, TransFIC, and Condel) across five distinct benchmarks. ParsSNP outperformed the existing tools in 24 of 25 comparisons. To investigate the real-world benefit of these improvements, we applied ParsSNP to an independent data set of 30 patients with diffuse-type gastric cancer. ParsSNP identified many known and likely driver mutations that other methods did not detect, including truncation mutations in known tumor suppressors and the recurrent driver substitution RHOA p.Tyr42Cys. In conclusion, ParsSNP uses an innovative, parsimony-based approach to prioritize cancer driver mutations and provides dramatic improvements over existing methods.
MeSH term(s)	Algorithms ; Data Collection/methods ; Humans ; Machine Learning ; Models, Genetic ; Mutation ; Neoplasms/genetics ; Polymorphism, Single Nucleotide ; Stomach Neoplasms/genetics
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Comparative Study ; Evaluation Studies ; Journal Article
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/ng.3658
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Article ; Online: MyPathway Human Epidermal Growth Factor Receptor 2 Basket Study: Pertuzumab + Trastuzumab Treatment of a Tissue-Agnostic Cohort of Patients With Human Epidermal Growth Factor Receptor 2-Altered Advanced Solid Tumors.

Sweeney, Christopher J / Hainsworth, John D / Bose, Ron / Burris, Howard A / Kurzrock, Razelle / Swanton, Charles / Friedman, Claire F / Spigel, David R / Szado, Tania / Schulze, Katja / Price, Richard / Malato, Julia / Lo, Amy A / Levy, Jonathan / Wang, Yong / Yu, Wei / Meric-Bernstam, Funda

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2023 Volume 42, Issue 3, Page(s) 258–265

Abstract: Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. Clinical Trial ... ...

Abstract	Clinical trials frequently include multiple end points that mature at different times. The initial report, typically based on the primary end point, may be published when key planned co-primary or secondary analyses are not yet available. Clinical Trial Updates provide an opportunity to disseminate additional results from studies, published in
MeSH term(s)	Adult ; Humans ; Trastuzumab/adverse effects ; Proto-Oncogene Proteins p21(ras)/metabolism ; Receptor, ErbB-2/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Antibodies, Monoclonal, Humanized
Chemical Substances	ERBB2 protein, human (EC 2.7.10.1) ; pertuzumab (K16AIQ8CTM) ; Trastuzumab (P188ANX8CK) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Antibodies, Monoclonal, Humanized
Language	English
Publishing date	2023-10-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
DOI	10.1200/JCO.22.02636
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