Relevant bibliographies by topics / HER2/ErbB2

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'HER2/ErbB2'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'HER2/ErbB2.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "HER2/ErbB2"

1

Ding, Yunfeng, Yonghong Liu, Dong-Kee Lee та ін. "Cell lineage tracing links ERα loss in Erbb2-positive breast cancers to the arising of a highly aggressive breast cancer subtype". Proceedings of the National Academy of Sciences 118, № 21 (2021): e2100673118. http://dx.doi.org/10.1073/pnas.2100673118.

Full text
Abstract:
HER2-positive (HER2+) breast cancers (BrCs) contain approximately equal numbers of ERα+HER2+ and ERα−HER2+ cases. An enduring obstacle is the unclear cell lineage-related characteristics of these BrCs. Although ERα+HER2+ BrCs could lose ERα to become ERα−HER2+ BrCs, direct evidence is missing. To investigate ERα dependencies and their implications during BrC growth and metastasis, we generated ERαCreRFP-T mice that produce an RFP-marked ERα+ mammary gland epithelial cell (MGEC) lineage. RCAS virus-mediated expression of Erbb2, a rodent Her2 homolog, first produced comparable numbers of ERα+RFP
APA, Harvard, Vancouver, ISO, and other styles
2

Stein, Stacey, Jeremy Snider, Margaret Elizabeth McCusker, et al. "Association of real-world agreement between HER2 expression and ERBB2 amplification with trastuzumab therapy benefit in advanced gastric/esophageal (adv GE) cancer patients (pts)." Journal of Clinical Oncology 38, no. 4_suppl (2020): 310. http://dx.doi.org/10.1200/jco.2020.38.4_suppl.310.

Full text
Abstract:
310 Background: Trastuzumab (T) plus chemotherapy is standard of care for pts with HER2+ adv GE cancer. Selection for T relies on HER2+ result by immunohistochemistry (IHC) +/- in-situ hybridization (ISH); ERBB2 amplification by comprehensive genomic profiling (CGP) also predicts benefit. As CGP use increases, it is important to explore associations of IHC/ISH and CGP result agreement with clinical outcomes in pts with adv GE cancer. Methods: Pts with adv GE cancer were selected from the Flatiron Health-Foundation Medicine (FMI) clinico-genomic database (CGDB), a nationwide de-identified EHR-d
APA, Harvard, Vancouver, ISO, and other styles
3

Prat, Aleix, Tomás Pascual, Carmine De Angelis, et al. "HER2-Enriched Subtype and ERBB2 Expression in HER2-Positive Breast Cancer Treated with Dual HER2 Blockade." JNCI: Journal of the National Cancer Institute 112, no. 1 (2019): 46–54. http://dx.doi.org/10.1093/jnci/djz042.

Full text
Abstract:
Abstract Background Identification of HER2-positive breast cancers with high anti-HER2 sensitivity could help de-escalate chemotherapy. Here, we tested a clinically applicable RNA-based assay that combines ERBB2 and the HER2-enriched (HER2-E) intrinsic subtype in HER2-positive disease treated with dual HER2-blockade without chemotherapy. Methods A research-based PAM50 assay was applied in 422 HER2-positive tumors from five II–III clinical trials (SOLTI-PAMELA, TBCRC023, TBCRC006, PER-ELISA, EGF104090). In SOLTI-PAMELA, TBCRC023, TBCRC006, and PER-ELISA, all patients had early disease and were
APA, Harvard, Vancouver, ISO, and other styles
4

Kast, K., and W. Distler. "ErbB2 (HER2)-positives Mammakarzinom." Der Gynäkologe 43, no. 7 (2010): 574–78. http://dx.doi.org/10.1007/s00129-010-2529-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Aft, Rebecca, Chidananda Mudalagiriyappa, Sreeraj Pillai, Kathryn Trinkaus, Timothy Fleming, and Mark Watson. "Identification of patients at high risk of recurrent disease development by detection of HER2-positive disseminated tumor cells in bone marrow of patients with HER2-negative tumors." Journal of Clinical Oncology 31, no. 15_suppl (2013): 633. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.633.

Full text
Abstract:
633 Background: A subpopulation of patients with HER2-negative tumors benefit from HER2 therapy. HER2 expression can be discordant between primary tumors and metastases. We have examined the bone marrow (BM) of early stage breast cancer patients for HER2-expression by disseminated tumor cells (DTCs) and the association with disease recurrence. Methods: BM was collected from clinical stage II-III breast cancer prior to treatment between 2007-2011. Gene expression of ERBB2 was determined by multiplex PCR (Fluidigm Biomark [FB]). Positive expression was defined as at least 1.4 fold above a pool o
APA, Harvard, Vancouver, ISO, and other styles
6

Nami, Babak, Avrin Ghanaeian, Corbin Black, and Zhixiang Wang. "Epigenetic Silencing of HER2 Expression during Epithelial-Mesenchymal Transition Leads to Trastuzumab Resistance in Breast Cancer." Life 11, no. 9 (2021): 868. http://dx.doi.org/10.3390/life11090868.

Full text
Abstract:
HER2 receptor tyrosine kinase (encoded by the ERBB2 gene) is overexpressed in approximately 25% of all breast cancer tumors (HER2-positive breast cancers). Resistance to HER2-targeting therapies is partially due to the loss of HER2 expression in tumor cells during treatment. However, little is known about the exact mechanism of HER2 downregulation in HER2-positive tumor cells. Here, by analyzing publicly available genomic data we investigate the hypothesis that epithelial-mesenchymal transition (EMT) abrogates HER2 expression by epigenetic silencing of the ERBB2 gene as a mechanism of acquired
APA, Harvard, Vancouver, ISO, and other styles
7

Isharwal, Sumit, Hongying Huang, Gouri Nanjangud, et al. "Intratumoral heterogeneity of ERBB2/HER2 expression in micropapillary urothelial carcinoma." Journal of Clinical Oncology 35, no. 6_suppl (2017): 383. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.383.

Full text
Abstract:
383 Background: Micropapillary urothelial carcinoma (MPUC) is a rare but an aggressive variant of urothelial carcinoma. Histologically, most of these tumors are associated with variable amounts of “not otherwise specified (NOS)” urothelial carcinoma. MPUC has been shown to be associated with ERBB2/HER2 amplification and protein overexpression. However, the status and distribution of these findings within the different components of tumors containing both MP and NOS urothelial carcinoma have not been addressed. Methods: We identified 44 cases of MPUC that had tissue available for FISH and IHC a
APA, Harvard, Vancouver, ISO, and other styles
8

Hansen, Malene Bredahl, Maria Postol, Siri Tvingsholm, et al. "Identification of lysosome‐targeting drugs with anti‐inflammatory activity as potential invasion inhibitors of treatment resistant HER2 positive cancers." Cellular Oncology 44, no. 4 (2021): 805–20. http://dx.doi.org/10.1007/s13402-021-00603-2.

Full text
Abstract:
Abstract Purpose Most HER2 positive invasive cancers are either intrinsic non-responsive or develop resistance when treated with 1st line HER2 targeting drugs. Both 1st and 2nd line treatments of HER2 positive cancers are aimed at targeting the HER2 receptor directly, thereby strongly limiting the treatment options of HER2/ErbB2 inhibition resistant invasive cancers. Methods We used phenotypic high throughput microscopy screening to identify efficient inhibitors of ErbB2-induced invasion using 1st line HER2 inhibitor trastuzumab- and pertuzumab-resistant, p95-ErbB2 expressing breast cancer cel
APA, Harvard, Vancouver, ISO, and other styles
9

Shah, Ami N., Brian Finkelman, Lorenzo Gerratana, et al. "ERBB2 amplifications and mutations in 109 advanced breast cancer patients by next-generation sequencing." Journal of Clinical Oncology 38, no. 15_suppl (2020): 3565. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3565.

Full text
Abstract:
3565 Background: In advanced breast cancer (ABC) HER2 status is based on ASCO/CAP immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) criteria. Next generation sequencing (NGS) of tissue and blood can detect aberrations in ERBB2 such as copy number gain/amplifications (cng/amp) and mutations. Methods: We retrospectively identified patients (pts) seen at Northwestern University between 2015 and 2019 with ABC and an alteration in ERBB2 identified by tissue and/or circulating tumor DNA (ctDNA) NGS. We included pts with testing by Guardant360, TempusX, and/or FoundationOne pla
APA, Harvard, Vancouver, ISO, and other styles
10

Cocco, Emiliano, F. Javier Carmona, Pedram Razavi, et al. "Neratinib is effective in breast tumors bearing both amplification and mutation of ERBB2 (HER2)." Science Signaling 11, no. 551 (2018): eaat9773. http://dx.doi.org/10.1126/scisignal.aat9773.

Full text
Abstract:
Mutations in ERBB2, the gene encoding epidermal growth factor receptor (EGFR) family member HER2, are common in and drive the growth of “HER2-negative” (not ERBB2 amplified) tumors but are rare in “HER2-positive” (ERBB2 amplified) breast cancer. We analyzed DNA-sequencing data from HER2-positive patients and used cell lines and a patient-derived xenograft model to test the consequence of HER2 mutations on the efficacy of anti-HER2 agents such as trastuzumab, lapatinib, and neratinib, an irreversible pan-EGFR inhibitor. HER2 mutations were present in ~7% of HER2-positive tumors, all of which we
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "HER2/ErbB2"

1

Lo, Vivian. "The Role of Periostin in HER2/ErbB2-induced Breast Cancer." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19909.

Full text
Abstract:
Periostin (Postn) is a secreted cell adhesion protein that shares a structural homology to the insect axon guidance protein fasciclin I (FAS1). Periostin interacts with multiple cell-surface receptors, most notably integrins, which activate signaling pathways to promote cancer cell survival, angiogenesis, invasion, and metastasis. Interestingly, periostin is frequently overexpressed in numerous human cancers, including breast, lung, colon, pancreatic, and ovarian cancer. Here, we investigated the role of periostin in HER2/ErbB2-induced mammary tumorigenesis. Although periostin is primarily exp
APA, Harvard, Vancouver, ISO, and other styles
2

Saito, Hiroko. "Rôle des protéines PDZ dans la fonction de ERBB2/HER2." Aix-Marseille 2, 2002. http://www.theses.fr/2002AIX22015.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Campesato, Luís Felipe Ingrássia. "Investigação do papel de SIGIRR/IL-1R8 no crosstalk entre células tumorais e o infiltrado leucocitário." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-05042016-140157/.

Full text
Abstract:
Células tumorais desenvolvem diversas estratégias para escapar da identificação e eliminação pelo sistema imune. Dessa forma, a investigação dos mecanismos envolvidos na comunicação celular no microambiente tumoral e na desregulação local do sistema imune é crítica para uma melhor compreensão da progressão da doença e para o desenvolvimento de alternativas terapêuticas mais eficazes. Nós aqui demonstramos que SIGIRR/IL-1R8, um importante regulador negativo de receptores de Interleucina-1 (ILRs) e receptores do tipo Toll (TLRs), apresenta expressão aumentada em uma linhagem celular epitelial ma
APA, Harvard, Vancouver, ISO, and other styles
4

Flowers, Margaret. "In Vitro and In Vivo Effects of Conjugated Linoleic Acid on Mammary Tumorigenesis." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/195806.

Full text
Abstract:
Conjugated linoleic acid (CLA) exhibits multiple biological and molecular activities that have made it the subject of considerable nutrition-related research. Numerous studies support broad acting anti-tumor effects including anti-inflammatory, anti-proliferation, and pro-apoptosis in a variety of model systems. CLA’s ability to influence multiple tumor promoting pathways, without toxicity, may prove valuable in the chemoprevention of breast cancer. The overall objective of this dissertation research was to investigate the potential of CLA in the chemoprevention of breast cancer in a subgroup
APA, Harvard, Vancouver, ISO, and other styles
5

Montanez-Wiscovich, Marjorie E. "Discerning the Role of LMO4 as a Global Modulator of G2/M Cell Cycle Progression and Centrosome Cycle in Breast Cancer Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1259899890.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Zuo, Tao. "FOXP3 is a novel X-linked breast cancer suppressor gene." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1150079443.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Streller, Felix [Verfasser], Matthias [Akademischer Betreuer] Dobbelstein, Dieter [Akademischer Betreuer] Kube, and Ramona [Akademischer Betreuer] Schulz. "Die Interaktion von ErbB2/Her2 mit Hitzeschockproteinen in Mammakarzinomzellen / Felix Streller. Gutachter: Matthias Dobbelstein ; Dieter Kube ; Ramona Schulz. Betreuer: Matthias Dobbelstein." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1071713213/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Djerbi-Bouillié, Rym. "Mécanismes de recrutement et d'activation du récepteur tyrosine kinase ErbB2/HER2 en réponse à l'infection par Neisseria meningitidis : de la méningite au cancer du sein." Paris 7, 2009. http://www.theses.fr/2009PA077166.

Full text
Abstract:
ErbB2 est un récepteur tyrosine kinase jouant un rôle crucial dans la morphogenèse et l'oncogenèse. Dépourvu de ligand soluble propre ce récepteur orphelin ne peut être physiologiquement activé que par hétérodimérisation avec les autres membres de sa famille (famille de l'EGFR) en réponse à la liaison de leurs ligands spécifiques. L'activation anormale ligand indépendante d'ErbB2 est néanmoins observée dans un grand nombre de tumeurs mammaires et ovariennes suite à sa surexpression ou à des mutations oncogènes et est associée à un mauvais pronostique clinique, soulevant la question de la régul
APA, Harvard, Vancouver, ISO, and other styles
9

Landis, Melissa D. "Elucidating Molecular Mechanisms of ERBB2/Neu-Induced Mammary Tumorigenesis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1134662885.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Streller, Felix. "Die Interaktion von ErbB2/Her2 mit Hitzeschockproteinen in Mammakarzinomzellen." Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0015-A382-7.

Full text
Abstract:
Her2-positiver Brustkrebs, der Subtyp des Mammakarzinoms, bei dem eine Überexpression des epidermalen Wachstumsfaktor-Rezeptors-2 (ErbB2/Her2) vorliegt, hat für die betroffenen Frauen eine besonders schlechte Prognose. Eine positive Korrelation zwischen der ErbB2-Expression in Brusttumoren und der Expression des Makrophagen-Migration-inhibierenden Faktors (MIF), einem inzwischen gut bekannten tumorfördernden Protein, konnte bereits gezeigt werden. Ferner konnte gezeigt werden, dass MIF durch das Hitzeschockprotein 90 (Hsp90) in einem Mausmodell des Her2-positiven Brustkrebses stabilisiert wird
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "HER2/ErbB2"

1

Todorović-Raković, Nataša. "TGF-β and HER2/ErbB2 and Breast Cancer Progression". У Transforming Growth Factor-β in Cancer Therapy, Volume II. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-293-9_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ardanza-Trevijano, Sergio, Georgina Gonzalez, Tyler Borrman, Juan Luis Garcia, and Javier Arsuaga. "Topological Analysis of Amplicon Structure in Comparative Genomic Hybridization (CGH) Data: An Application to ERBB2/HER2/NEU Amplified Tumors." In Computational Topology in Image Context. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39441-1_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Jodlowski, Tomasz, and K. H. Ramesh. "Molecular Pathway and Fluorescence In Situ Hybridization Testing of ERBB2 (HER2) Gene Amplification in Invasive Ductal Carcinoma of Breast." In Molecular Diagnostics in Cancer Patients. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-5877-7_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

"Fish for ERBB2 (HER2) Gene Amplifications." In Diagnostic Pathology: Molecular Oncology. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-37678-5.50043-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

"Anti-HER2/c-erbB2 Monoclonal Antibody." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_100209.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Yamamoto, Tadashi, Makoto Saito, Kentaro Kumazawa, et al. "ErbB2/HER2: Its Contribution to Basic Cancer Biology and the Development of Molecular Targeted Therapy." In Breast Cancer - Carcinogenesis, Cell Growth and Signalling Pathways. InTech, 2011. http://dx.doi.org/10.5772/21965.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Koleckova, Marketa, Katherine Vomackova, and Zdenek Kolar. "Molecular Prognostic and Predictive Markers in Triple - Negative Breast Cancer." In Breast Cancer [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97282.

Full text
Abstract:
Triple-negative breast cancer (TNBC) is defined as a molecular subtype of breast cancer that lacks expression of hormone receptors (oestrogen and progesterone receptor) and HER2/neu/ErbB2 protein. It accounts for 15–20% of all invasive breast cancers. The occurrence of TNBC is often associated with younger age at the time of diagnosis and pre-menopausal status, early onset of menarche, higher body mass index (BMI) in the pre-menopausal period, race and ethnicity (African, Hispanic) and the presence of germline mutation in the BRCA1/2 genes or somatic mutation in the TP53 or PTEN genes. TNBCs are specific in its aggressive biological behaviour, shorter interval to disease progression and more frequent relapse within five years (19 to 40 months). The most of TNBCs are represented by high-grade invasive carcinomas of no special type (NST) with high proliferation index measured by Ki-67 nuclear expression, followed by metaplastic carcinomas, secretory carcinomas, and adenoid cystic carcinomas. Genetical and morphological heterogeneity inside TNBC is responsible for the higher frequency of primary and secondary resistance to systemic therapy. The scope of this chapter is to summarise the potential therapeutic agents involved in regulation of cell proliferation, migration, angiogenesis, apoptosis, gene expression and DNA damage or immune response. The insight into this issue is essential for the setting of the optimal chemotherapy regimen and targeted therapeutic strategy.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "HER2/ErbB2"

1

"PAMAM Dendrimers as anti-HER2 Positive Breast Cancer Treatment." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0176.

Full text
Abstract:
Background: Poly (amidoamine) dendrimers (PAMAMs) are widely used in drug delivery systems and gene transfection as drug carriers. They also exert several biological effects like modulating gene expression, particularly EGFR (ErbB1) signaling pathway, which raises the question of whether these polymers can also inhibit the phosphorylation of HER2 (ErbB2) in breast cancer. However, this area hasn’t been investigated before. Methods: In this study, we evaluated the anticancer effects of different generations and surface chemistries of PAMAMs on HER2 positive breast cancer cells (SkBr3 and ZR-75
APA, Harvard, Vancouver, ISO, and other styles
2

Yamaji, D., GW Robinson, WJ Muller, and L. Hennighausen. "Deletion of STAT5 prevents HER2/Neu/ErbB2-induced mammary tumor development." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-3045.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Zhang, Concong, Kurt Schönfeld, Michael Burger, et al. "Abstract 3967: ErbB2/HER2-specific natural killer cells for adoptive immunotherapy of glioblastoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3967.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ding, Yan, Zixing Liu, Shruti Desai, et al. "Abstract 3025: Receptor tyrosine kinase ErbB2/HER2 translocates into mitochondria and regulates cellular metabolism." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3025.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Strasberg- Rieber, Mary, and Manuel Rieber. "Abstract 1107: Mutant p53 increases epithelial mesenchymal transition, estrogen receptor alpha and erbB2/Her2/neu." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1107.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kho, Dhonghyo. "Abstract 1079: Identification of autocrine motility factor (AMF) receptor, HER2 (ErbB2) in breast cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1079.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Wellberg, Elizabeth A., Angelo D'Allessandro, Andrew S. Lewis, et al. "Abstract PR03: GLUT1 is required for induction of mammary tumorigenesis by activated ErbB2/HER2/Neu." In Abstracts: AACR Special Conference: Advances in Breast Cancer; October 17-20, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.advbc15-pr03.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wang, Kai, Jeff S. Ross, Laurie M. Gay, et al. "Abstract B122: A high frequency of activating extracellular domain ERBB2 (HER2) mutation in micropapillary urothelial carcinoma." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b122.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Runkle, Edwin Aaron, Peter Young, Yasuhiro Nagai, Hiromichi Tsuchiya, Hongtao Zhang, and Mark I. Greene. "Abstract 1390: Interferon-gamma potentiates the targeted phenotypic reversion of erbb2/her2/neu transformed human tumor cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1390.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Tacha, D., J. Alba Dominguez, J. Gutierrez Bernal, et al. "A Multi-Method Analysis of c-erbB2/HER2 in FFPE Tissue: Correlation of a Novel and Rapid In Situ Hybridization Procedure, HER2 CISH and IHC." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6009.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "HER2/ErbB2"

1

Parmar, Hema R., and Gerald Cunha. Mammary Stromal Effects on Epithelial Differentiation and Expression of ESX and ErbB2 (HER2/neu). Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada411506.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Parmar, hema R., and Gerald Cunha. Mammary Stromal Effects on Epithelial Differentiation and Expression of ESX and ErbB2 (HER2/neu). Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada421067.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Long, Weiwen, and Tamika Duplessis. ErbB4 Overexpression as an Antagonist of ErbB2/HER2/Neu Induced Human Breast Cancer Cell Proliferation. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada464063.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Recio, Juan F., and Vsevolod Katritch. Antigene Strategy in Breast Cancer Therapy: Rationales for Direct Targeting of erbB2/Her2 DNA with Polyamides. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada415582.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Katritch, Vsevolod Y. Antigene Strategy in Breast Cancer Therapy: Rationales for Direct Targeting of erbB2/Her2 DNA with Polyamides. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada403668.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'HER2/ErbB2' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography