Relevant bibliographies by topics / Herceptin resistant breast cancer

Contents

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

Academic literature on the topic 'Herceptin resistant breast cancer'

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 'Herceptin resistant breast cancer.'

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 "Herceptin resistant breast cancer"

1

Buiga, Elson, Tabernero, and Schwartz. "Kinetic Modeling of DUSP Regulation in Herceptin-Resistant HER2-Positive Breast Cancer." Genes 10, no. 8 (July 26, 2019): 568. http://dx.doi.org/10.3390/genes10080568.

Full text
Abstract:
Background: HER2 (human epidermal growth factor 2)-positive breast cancer is an aggressive type of breast cancer characterized by the overexpression of the receptor-type protein tyrosine kinase HER2 or amplification of the HER2 gene. It is commonly treated by the drug trastuzumab (Herceptin), but resistance to its action frequently develops and limits its therapeutic benefit. Dual-specificity phosphatases (DUSPs) were previously highlighted as central regulators of HER2 signaling; therefore, understanding their role is crucial to designing new strategies to improve the efficacy of Herceptin treatment. We investigated whether inhibiting certain DUSPs re-sensitized Herceptin-resistant breast cancer cells to the drug. We built a series of kinetic models incorporating the key players of HER2 signaling pathways and simulating a range of inhibition intensities. The simulation results were compared to live tumor cells in culture, and showed good agreement with the experimental analyses. In particular, we observed that Herceptin-resistant DUSP16-silenced breast cancer cells became more responsive to the drug when treated for 72 h with Herceptin, showing a decrease in resistance, in agreement with the model predictions. Overall, we showed that the kinetic modeling of signaling pathways is able to generate predictions that assist experimental research in the identification of potential targets for cancer treatment.
APA, Harvard, Vancouver, ISO, and other styles
2

Choi, Michael Phillip, Alice P. Chung, Shikha Bose, Bingchen Han, Ying Qu, Xiao Zhang, Xiaojiang Cui, and Armando E. Giuliano. "The basal phenotype as a clinically relevant indicator of trastuzumab resistance in HER2+ breast cancer." Journal of Clinical Oncology 32, no. 26_suppl (September 10, 2014): 154. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.154.

Full text
Abstract:
154 Background: Trastuzumab (Herceptin) resistance remains a clinical challenge but the mechanism is not well understood. Recently, studies have identified a subset of Her2+ breast cancer called basal HER2 that expresses basal genes. We investigated the effect of basal gene expression on Herceptin response in HER2+ breast cancer cell lines and on prognosis in HER2+ breast cancer patients. Methods: Non-basal (BT474, SKBR3) and basal (HCC1569, HCC1954, JIMT-1) HER2+ cell lines were chosen based on basal cytokeratin expression. Cell proliferation was assessed after treatment with vehicle, Herceptin (H), Paclitaxel (P), H+P, Akt Inhibitor (AI), and H+AI. HER2 signaling was examined using immunoblotting of p-Akt and p-ERK. Because breast cancer stem cells (BCSC) are linked to basal breast tumors and treatment resistance, we assessed BCSC activity using mammosphere formation and aldehyde dehydrogenase (ALDH) positivity. Immunohistochemical staining of HER2+ breast cancers for basal markers CK5/6, CK14, and EGFR was correlated with clinicopathologic features and survival in 88 patients with Stage 1-3 HER2+ breast cancer treated with Herceptin. Results: Basal HER2 cells were resistant to Herceptin compared to non-basal HER2 cells but this resistance was overcome by Akt inhibition. Immunoblotting showed that non-basal HER2 cells had decreased p-Akt after Herceptin treatment which was not seen in basal HER2 cells. There was no difference in p-ERK levels after Herceptin therapy in all cell lines. Basal HER2 cells had increased mammosphere formation and ALDH positivity suggesting higher stem cell activity compared to non-basal HER2 cells. Of the HER2+ patients, 33/88 (37.5%) expressed at least one basal marker. Basal Her2 tumors were associated with higher grade (p = 0.04) and more ER/PR negativity (p < 0.01). CK14 expression correlated with worse overall survival by log-rank test (p = 0.02), while EGFR showed a similar trend (p = 0.06). Conclusions: Basal HER2 breast cancer cell lines have Herceptin resistance which may be due to constitutively active Akt signaling and increased stem cell activity. Clinically, basal marker expression predicts Herceptin resistance and worse outcomes in HER2+ breast cancer patients.
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Bin, Yuanzhong Wang, Susan E. Kane, and Shiuan Chen. "Improvement of sensitivity to tamoxifen in estrogen receptor-positive and Herceptin-resistant breast cancer cells." Journal of Molecular Endocrinology 41, no. 5 (September 3, 2008): 367–77. http://dx.doi.org/10.1677/jme-08-0026.

Full text
Abstract:
ERBB2 overexpression in estrogen receptor (ER)-positive breast cancer cells such as BT474 (BT) cells has been found to confer resistance to tamoxifen, and suppression of ERBB2 improves the antiproliferative effects of tamoxifen. In this study, the responsiveness to tamoxifen in the BT/HerR, Herceptin-resistant BT cell lines established through constant Herceptin exposure, was evaluated. Compared with BT cells, improvement of sensitivity to tamoxifen in BT/HerR was demonstrated by ER functional analysis and cell proliferation assay. Tamoxifen in the resistant cell line was found to inhibit 17β-estradiol-stimulating estrogen-responsive gene pS2 expression more effectively than in BT cells in real-time PCR assay. Western blot analysis showed that cross-phosphorylation between ER and downstream components of ERBB2 was attenuated in BT/HerR cells. ER redistribution from cytoplasm to nucleus could be found in these cells through immunofluorescence and confocal studies, and importantly, chromatin immunoprecipitation studies demonstrated that tamoxifen induced occupancy of the pS2 promoter by ER and nuclear receptor corepressor (NCOR1) instead of coactivator NCOA3 in these cells. Finally, combination of tamoxifen and Herceptin was found to improve the sensitivity of BT/HerR cells to Herceptin. Our results suggest that the ER genomic pathway in the ER-positive and Herceptin-resistant breast cancer cells may be reactivated, allowing tamoxifen therapy to be effective again, and a combination of tamoxifen and Herceptin can be a potential therapeutic strategy for ER-positive and Herceptin-resistant human breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
4

Lai, Hung-Wen, Su-Yu Chien, Shou-Jen Kuo, Ling-Ming Tseng, Hui-Yi Lin, Chin-Wen Chi, and Dar-Ren Chen. "The Potential Utility of Curcumin in the Treatment of HER-2-Overexpressed Breast Cancer: AnIn VitroandIn VivoComparison Study with Herceptin." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/486568.

Full text
Abstract:
HER-2 is an important oncoprotein overexpressed in about 15–25% of breast cancers. We hypothesized that the ability of curcumin to downregulate HER-2 oncoprotein and inhibit the signal transduction pathway of PI3K/Akt, MAPK, and NF-κB activation may be important in the treatment of HER-2-overexpressed breast cancer. To examine the effect of curcumin on breast cancer cells, MCF-7, MDA-MB-231, MCF-10A, BT-474, and SK-BR-3-hr (a herceptin resistant strain from SK-BR-3) cells were used forin vitroanalysis. Thein vivoeffect of curcumin on HER-2-overexpressed breast cancer was investigated with the HER-2-overexpressed BT-474 xenograft model. Cell growth, cell cycle change, the antimobility effect, signal transduction, and xenograft volume analysis between groups treated with herceptin and/or curcumin were tested. Curcumin decreased the cell growth of various breast cancer cell lines (MCF-7, MDA-MB-231, MCF-10A, BT-474, and SK-BR-3-hr). In Western blot analysis, the phosphorylation of Akt, MAPK, and expression of NF-κB were reduced in BT-474 cells, but not in SK-BR-3-hr cells, after treatment with herceptin. When treated with curcumin, the HER-2 oncoprotein, phosphorylation of Akt, MAPK and expression of NF-κB were decreased in both BT-474 and SK-BR-3-hr cells. In the BT-474 xenograft model, though not as much as herceptin, curcumin did effectively decrease the tumor size. The combination of curcumin with herceptin was not better than herceptin alone; however, the combination of taxol and curcumin had an antitumor effect comparable with taxol and herceptin. The results suggested that curcumin has potential as a treatment for HER-2-overexpressed breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
5

Crawford, Anatasha, and Rita Nahta. "Targeting Bcl-2 in Herceptin-Resistant Breast Cancer Cell Lines." Current Pharmacogenomics and Personalized Medicine 9, no. 3 (September 1, 2011): 184–90. http://dx.doi.org/10.2174/187569211796957584.

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

Kute, Timothy, Christopher M. Lack, Mark Willingham, Bimjhana Bishwokama, Holly Williams, Kathy Barrett, Tanita Mitchell, and James P. Vaughn. "Development of Herceptin resistance in breast cancer cells." Cytometry 57A, no. 2 (2004): 86–93. http://dx.doi.org/10.1002/cyto.a.10095.

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

Yuan, Yuan, Huanyao Gao, Yongxian Zhuang, Lixuan Wei, Jia Yu, Zhe Zhang, Lili Zhang, and Liewei Wang. "NDUFA4L2 promotes trastuzumab resistance in HER2-positive breast cancer." Therapeutic Advances in Medical Oncology 13 (January 2021): 175883592110278. http://dx.doi.org/10.1177/17588359211027836.

Full text
Abstract:
Background: Trastuzumab (Herceptin) is the key systemic therapy for HER2-positive breast cancer. However, the initial response rate is limited to approximately 50% in patients. Moreover, most patients, especially at an advanced stage, eventually develop acquired resistance. Understanding the mechanisms of trastuzumab resistance is crucial for achieving better treatment outcome in this group of patients. Methods: A trastuzumab-resistant (TR) cell line was developed using the BT474 HER2-positive breast cancer cell line. Whole-transcriptome expression array was performed and the TR-related gene NDUFA4L2 was identified by differential expression analysis between BT474 and BT474-TR. Mitochondrial localization of NDUFA4L2 was confirmed by immunofluorescence and western blotting using mitochondrial fractionation. Mitochondrial function and energy metabolism were evaluated using Seahorse, ATP production, and lactate production assays, and cellular reactive oxygen species (ROS) levels were determined using DCFDA. NDUFA4L2 expression in patients was evaluated by immunohistochemistry, and relapse-free survival was analyzed using the Kaplan–Meier method. Results: NDUFA4L2 was highly expressed in the TR HER2-positive breast cancer cell line. High expression level of NDUFA4L2 was associated with shorter relapse-free intervals in trastuzumab-treated HER2-positive breast cancer patients. Overexpression of NDUFA4L2 enhanced Warburg effects, enhanced aerobic glycolysis, reduced oxygen consumption, and lowered ROS production. Mechanistically, overexpression of NDUFA4L2 facilitated mitochondrial relocalization of HER2 and suppressed ROS production, thus rendering cancer cells more resistant to trastuzumab treatment. Conclusions: We identified NDUFA4L2 as a new biomarker and potential therapeutic target for TR HER2-positive breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
8

Eitler, Jiri, Natalie Wotschel, Nicole Miller, Laurent Boissel, Hans G. Klingemann, Winfried Wels, and Torsten Tonn. "Inability of granule polarization by NK cells defines tumor resistance and can be overcome by CAR or ADCC mediated targeting." Journal for ImmunoTherapy of Cancer 9, no. 1 (January 2021): e001334. http://dx.doi.org/10.1136/jitc-2020-001334.

Full text
Abstract:
BackgroundOn encountering a susceptible target, natural killer (NK) cells mediate cytotoxicity through highly regulated steps of directed degranulation. Cytotoxic granules converge at the microtubule organizing center and are polarized toward the immunological synapse (IS), followed by granule exocytosis. NK cell retargeting by chimeric antigen receptors (CARs) or mAbs represents a promising strategy for overcoming tumor cell resistance. However, little is known about the lytic granule dynamics of such retargeted NK cells toward NK-cell-resistant tumors.MethodsHere, we used spinning disk confocal microscopy for live-cell imaging to analyze granule-mediated NK cell cytotoxicity in ErbB2-targeted CAR-expressing NK-92 cells (NK-92/5.28.z) and high-affinity FcR transgenic NK-92 cells plus Herceptin toward ErbB2-positive breast cancer cells (MDA-MB-453), which are resistant to parental NK-92.ResultsUnmodified NK-92 cells cocultured with resistant cancer cells showed stable conjugate formation and granule clustering, but failed to polarize granules to the IS. In contrast, retargeting by CAR or FcR+Herceptin toward the MDA-MB-453 cells enabled granule polarization to the IS, resulting in highly effective cytotoxicity. We found that in NK-92 the phosphoinositide 3-kinase pathway was activated after contact with resistant MDA-MB-453, while phospholipase C-γ (PLCγ) and mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) were not activated. In contrast, retargeting by CAR or antibody-dependent cell-mediated cytotoxicity (ADCC) provided the missing PLCγ and MEK/ERK signals.ConclusionsThese observations suggest that NK cells can create conjugates with resistant cancer cells and respond by granule clustering, but the activation signals are insufficient to induce granule polarization and consequent release of lytic enzymes. Retargeting by CAR and/or the FcR/mAb (ADCC) axis provide the necessary signals, leading to granule polarization and thereby overcoming tumor cell resistance.Keywords: NK cells, NK-92, haNK, ADCC, Chimeric Antigen Receptor (CAR), breast cancer, cancer immunotherapy, live-cell imaging, granule polarization
APA, Harvard, Vancouver, ISO, and other styles
9

Lu, Jianguo, Jun Pu, Xiaozhao Lu, Haiyan Fu, Mengying Wei, and Guodong Yang. "β-Diketone modified trastuzumab: A next-generation of Herceptin for resistant breast cancer cells?" Medical Hypotheses 79, no. 5 (November 2012): 602–4. http://dx.doi.org/10.1016/j.mehy.2012.07.030.

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

Buiga, Petronela, Ari Elson, Lydia Tabernero, and Jean-Marc Schwartz. "Modelling the role of dual specificity phosphatases in herceptin resistant breast cancer cell lines." Computational Biology and Chemistry 80 (June 2019): 138–46. http://dx.doi.org/10.1016/j.compbiolchem.2019.03.018.

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

Dissertations / Theses on the topic "Herceptin resistant breast cancer"

1

Wimana, Léna. "ImmunoPet imaging using Zirconium-89 radiolabeled trastuzumab to explore resistance in HER2+/MUC4+ breast cancer." Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/221750.

Full text
Abstract:
Notre travail s’est focalisé sur l’utilisation du trastuzumab‐immunoPET afin d’étudier et deguider une approche nouvelle visant à surmonter la résistance au médicament trastuzumab,causée par la surexpression de MUC4 dans le cancer du sein.Pour ce faire, nous avons préparé et utilisé du 89Zr‐trastuzumab dans le but de suivresa capacité de liaison au récepteur HER2 ainsi que son accumulation dans des cellulescancéreuses mammaires. Ensuite, nous avons formulé l’hypothèse que des agentsmucolytiques, tels que la N‐Acétylcystéine (NAC), en démêlant les réseaux formés par lesmucines, permettent l’amélioration de la captation du radiotraceur in vitro et in vivo. Eneffet, l’addition du NAC a occasionné une accumulation significative de 89Zr‐trastuzumab,sans altération ni changement de l’affinité de liaison au récepteur. Ceci semble égalementproduire une meilleure sensibilité des imageries PET dans le modèle animal choisi.Dans une seconde étape, nous avons évalué, dans un modèle murin de cancer du seinrésistant au trastuzumab et surexprimant la MUC4, si cette captation accrue se traduit parun bénéfice thérapeutique en utilisant le NAC combiné au trastuzumab. Nous avons obtenuun effet inhibiteur qui réduit de moitié la croissance tumorale, comparable à celui observépour la tumeur mammaire sensible au trastuzumab (implantée dans le même animal).En conclusion, notre étude démontre l’efficacité de l’utilisation de traceurs PETsurtout à visée théranostique, comme c’est le cas du 89Zr‐trastuzumab, pour étudier etévaluer la résistance aux médicaments ciblés apparentés au radiotraceur lui‐même. Ellepropose l’utilisation du NAC pour améliorer l’accessibilité du récepteur pour le radiotraceurainsi que pour le médicament « froid » ouvrant, de ce fait, une perspective vers uneutilisation clinique chez un sous‐type de patientes atteintes d’un cancer du sein.
Doctorat en Sciences biomédicales et pharmaceutiques (Pharmacie)
info:eu-repo/semantics/nonPublished
APA, Harvard, Vancouver, ISO, and other styles
2

Kenicer, Juliet Elisabeth Margaret. "Investigation into taxane resistant breast cancer." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5915.

Full text
Abstract:
One group of chemotherapeutics that are used successfully to treat breast cancer, alone or in combination with other agents, are the taxanes; paclitaxel and docetaxel. They act by interfering with the spindle microtubule dynamics of the cell causing cell cycle arrest. However, the complexities underlying the mechanism of action are yet to be fully elucidated. Arguably, one of the most significant problems with taxanes is chemoresistance. Unfortunately, some patients are intrinsically resistant to taxanes and others acquire resistance to taxanes as treatment advances. This problem is exacerbated by a lack of understanding of the mechanisms underlying taxane resistance. Isogenic breast cancer cell lines that were taxane resistant were generated to use as an experimental model. Paclitaxel resistant (PACR) MDA-MB-231, paclitaxel resistant ZR75-1 and docetaxel resistant (DOCR) ZR75-1 cell lines were successfully generated by incrementally increasing taxane dose in respective native cell lines in vitro. An extensive characterisation of each of the resistant cell lines was conducted, focussing primarily on the 25nM resistant cells which were determined to be the most clinically relevant dose of taxane. A suboptimal dose of 5nM, a “superoptimal” dose of 50nM and the native, taxane sensitive cells was included. Dose response cell count experiments were performed that confirmed taxane resistant cells had been generated. It was shown that MDA-MB-231 native cells were more sensitive to paclitaxel than the ZR75-1 native cells, suggesting that ZR75-1 cells may already have low level inherent resistance. The MDA-MB-231 25nM PACR cells were tested to determine whether they retained PACR when maintained in media containing no paclitaxel. MDA-MB-231 25nM PACR cells were maintained in a taxane free environment for six months and then rechallenged with taxane. When rechallenged, the PACR cells previously maintained in the absence of paclitaxel mirrored the pattern of growth of corresponding PACR cells that had been maintained in the presence of paclitaxel. This proved that in the absence of paclitaxel, PACR cells did not revert to parent phenotype. This meant that experiments could be designed to grow cell lines as xenografts in mice, (in the absence of paclitaxel) & bring in vitro experiments into an in vivo setting. Effects of taxane treatment on both native and resistant cells were analysed using flow cytometry. Paclitaxel treatment exerted G2/M block in native MDA-MB-231 cells but when PACR cells were treated with the same dose of paclitaxel no G2/M block was observed, suggesting that PACR cells had developed a mechanism for escaping G2/M block. ZR75-1 native lines were also investigated and we established that treatment with paclitaxel also exerted a G2/M block in these lines. In future studies this process will be repeated to investigate the effect of taxane treatment on the ZR75-1 PACR and DOCR lines. CD 1 nude mice were injected with cells from all five cell lines to grow xenografts, unfortunately MDA-MB-231 PACR cells failed to grow so they could not be used for further xenograft experiments. PACR, DOCR and Native ZR75-1 cells did successfully grow as xenografts in mice and confirmed that all 3 groups showed very similar growth patterns. A cross resistance experiment was conducted and it was determined that the DOCR xenografts maintained a taxane resistant phenotype to docetaxel, and not paclitaxel and the PACR xenografts may be perpetuate the paclitaxel resistant phenotype in xenografts and that there may be cross resistance to docetaxel in the paclitaxel resistant xenografts. This is the first time that taxane resistant cell lines grown in this way have been established as xenografts in mice. These cross resistance experiments represent novel findings and merit further investigation. Extensive genomic and transcriptomic analyses were carried out on the cell lines to help identify potential taxane resistance markers. aCGH experiments were carried out to compliment the illumina experiments. The first set of experiments used DNA from pooled whole female blood as ref sample and DNA from each of the native and taxane resistant cell lines as test samples. The second set of experiments used DNA from native cells as a ref sample and DNA from their respective taxane resistant cells as a test, which allowed areas of loss or gain to be tracked in the genome as resistance increased. In the MDA-MB-231 cell lines the following areas of loss extended with increasing resistance: 1p36.13-q44, 6p25.3-q12, 8p, 10p, 19q, X Chr and the following areas of gain 2p25.3-23.3, 3p24.3-q13.3, 4p16.1-q12, 5q14.3-q31.1, 8q21.13-24.3, 11q15.1-q25, centromeric 12, and centromeric 14. In the ZR75-1 PACR and DOCR cell lines the areas of loss extended with increasing resistance in the following regions: 7q, 12p and 16q. For gene expression analysis RNA was extracted from the MDA-MB-231 cell lines, labelled and hybridised them to illumina human ref 8 vs. 2 chips. Data showed a progressive increase in mRNA dysregulation as paclitaxel resistance increased. Eleven genes were dysregulated across all resistance levels in the PACR MDA-MB-231 cells when compared to the relative cell lines; RGS16, CLDN1, IL7R, P&PP1R14C, COBL, TRPV4, TSPAN8, CD33, NLRP2, P13, and PAGE5. The experiment was repeated using MDA-MB-231 PACR, ZR75-1 PACR and DOCR cells and resulting data was analysed to determine genes commonly dysregulated across resistance levels, between MDA-MB-231 PACR and ZR75-1 PACR and between ZR75-1 PACR and DOCR cell lines. An extensive literature search was conducted and established four genes of interest in the context of our genomic and transcriptomic experiments including AURKA, Mdr-1, Stathmin and YY1. The novel biomarkers identified in the illumina experiments were validated with complimentary qPCR gene expression experiments looking at expression levels of the eleven commonly dysregulated genes identified and a panel of 19 other genes with significantly increased or decreased expression as resistance increased including AURKA, Mdr-1, Stathmin and YY1. Western blots were performed with lysates from the cell lines using a standard panel of predictive breast cancer markers and AURKA, Mdr-1, Stathmin and YY1. Combining the data from the genomic study, the gene expression profile, qPCR and Western blotting it was established that Mdr-1 had increased expression in the taxane resistant ZR75-1 lines and YY1 had increased expression in the MDA-MB-231 PACR line. Material from the LAPATAX trial was used to observe any transcriptomic changes occurring in tumours following treatment with docetaxel and to compare them to changes identified in our in vitro and xenograft models, this allowed the final step to be taken into a translational environment. LAPATAX (EORTC 10054) is a phase I-II study of Lapatanib and Docetaxel as neoadjuvant treatment for HER-2 +ve locally advanced/inflammatory or large operable breast cancer. Tumour material from eighteen core biopsies pre and post treatment was obtained, the mRNA was extracted, labelled and hybridised to the illumina array. This allowed the changes in gene expression pre and post docetaxel treatment to be tracked. The gene expression data from the LAPATAX trial was combined with gene expression data from our cell line panel and identified two novel putative markers of taxane resistance DUSP1 and FOS. Although sample size is small this has provided extremely valuable evidence directly from the clinic. These two novel putative biomarkers are extremely intriguing and certainly merit further investigation, ideally using additional taxane treated breast tumour tissue. Ultimately, an isogenic in vitro model of taxane resistance was developed in two different cell lines and with two different taxanes within one cell line. The cell lines were characterised and the effect of the taxanes on the cell cycle was determined in the native and taxane resistant lines. Selected cell lines were grown as xenografts in mice and performed successful cross resistance studies upon them. A large transcriptomic and genomic analysis was conducted and has identified a panel of potential taxane resistance markers and areas of loss and gain in the genome perpetuated by increasing taxane resistance. This analysis was validated using qPCR and Western blotting. This allowed a panel of novel taxane resistance markers to be identified. In future studies it is hoped that these targets will be knocked down with shRNA to observe if the taxane resistant cell lines revert to the parental phenotype. In vitro studies will be conducted to find agents that may be used to reduce expression of these markers and restore sensitivity to taxanes and consequently restore the efficacy of these drugs in a clinical setting. As far as the author is aware this is the first time that isogenic taxane resistant cell lines have been generated and investigated in this way.
APA, Harvard, Vancouver, ISO, and other styles
3

Micallef, Rachel Antonia. "Wnt signalling in endocrine resistant breast cancer." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/41274/.

Full text
Abstract:
Wnt signalling components are reported to be deregulated in breast cancer but the contribution of this pathway in endocrine resistance is less clearly defined. Endocrine resistance is an important clinical challenge affecting up to a quarter of all breast cancer patients and is associated with a poorer clinical prognosis. This project focussed on exploring the role of Wnt signalling in endocrine resistant breast cancer cell models. Wnt pathway elements were deregulated in the acquired tamoxifen resistant cell line (Tam-R) compared to tamoxifen sensitive parental cells (MCF-7), with changes supportive of Wnt signalling activation in this tamoxifen resistant model apparent from Affymetrix HGU-133A gene microarray data and Western blot analysis. In contrast, Wnt signalling appeared to be suppressed based on Affymetrix data for MCF-7 cells treated with oestradiol for 10 days, with equivocal changes in MCF-7 cells treated with tamoxifen for 10 days or a faslodex resistant cell model (Fas-R). Excitingly, Tam-R cells were also more sensitive than MCF-7 cells to pharmacological manipulation of Wnt signalling. While Wnt activation using Wnt3a and LiCl did not affect cell growth or migration, inhibition of Wnt signalling usingIWP2, PNU 74654 and iCRT14 suppressed Tam-R cell growth and migration. There is mounting evidence of cross talk between Wnt and EGFR signalling in breast cancer, and EGFR activity is upregulated in Tam-R cells. The project’s findings tentatively supported cross-talk between the two signalling pathways in this model. Thus, targeting of the Wnt pathway alongside EGFR blockade was superior in suppressing cell growth and migration in Tam-R cells. The effect appeared to be more pronounced when Wnt signalling was inhibited at the nuclear level using iCRT14. Collectively, these data suggest that Wnt signalling may play an important role in tamoxifen resistance where it may offer an opportunity for more effective therapeutic intervention to control relapse and associated tumour aggressiveness.
APA, Harvard, Vancouver, ISO, and other styles
4

Palomeras, Sònia. "DNA methylome in HER2-positive resistant breast cancer." Doctoral thesis, Universitat de Girona, 2019. http://hdl.handle.net/10803/667582.

Full text
Abstract:
The major clinical problem for HER2+ breast cancer target therapies is the acquisition of resistance. The DNA methylation status of the promoter gene region has been described as a common epigenetic alteration for transcriptional repression in human malignancies as breast cancer. The purpose of this thesis was to evaluate how the DNA methylation was involved in trastuzumab and lapatinib resistance in HER2+ breast cancer. We identify the epigenetic silencing of the TGFBI gene in trastuzumab resistance HER2+ breast cancer cell model and in post-treatment samples of patients treated with neoadjuvant anthracycline-taxane-based chemotherapy plus trastuzumab. Furthermore, the in vitro analysis revealed that the TGFBI reexpression induced greater sensitivity to trastuzumab in our resistant model, probably through its integrin-binding domains (EPDIM, NKDIL, YH and RGD). These results provide a basis for further studies to validate the hypermethylation status of TGFBI gene as monitoring biomarkers of trastuzumab resistance in HER2 breast cancer patients.
L'adquisició de resistència a les teràpies actuals és el principal problema del càncer de mama HER2+. L’estat de metilació de l’ADN a la regió promotora s’ha descrit com una alteració epigenètica associada a la repressió transcripcional de gens involucrats en diferents càncers, com el càncer de mama. L’objectiu d’aquesta tesi doctoral ha estat avaluar la implicació de la metilació en càncer de mama HER2+ resistent a trastuzumab i lapatinib. S’ha identificat el silenciament epigenètic de TGFBI en el model cel·lular resistent a trastuzumab així com en mostres humanes posttractament, tractades amb quimioteràpia neoadjuvant més trastuzumab. L’anàlisi funcional in vitro va revelar com la re-expressió de TGFBI induïa a una major sensibilitat al tractament en el model resistent, probablement a través dels seus dominis d’interacció amb integrines. Aquests resultats són la base per futurs estudis de validació de TGFBI com a possible biomarcador de resistència en càncer de mama HER2+.
APA, Harvard, Vancouver, ISO, and other styles
5

Drayton, Ross. "Drug sensitivity and apoptosis in tamoxifen resistant breast cancer." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55694/.

Full text
Abstract:
Tamoxifen has long been used in the treatment of hormone responsive breast cancer. However, tumours frequently develop resistance within 2-5 years of treatment, characterised by the return of tumour growth. The epidermal growth factor receptor EGFR is an important contributing factor in allowing formerly tamoxifen sensitive tumours to grow in the presence of tamoxifen. High levels of EGFR in many tumours correlate with a poor prognosis and an increased resistance to cytotoxic drugs. It was the initial aim of this study to ascertain whether the increased EGFR signalling associated with tamoxifen resistance results in a phenotype more resistant to cytotoxic drugs, and to study the underlying mechanisms that may cause this. Rather than observing the expected increase in resistance to cytotoxic drugs upon the development of tamoxifen resistance, a greatly increased sensitivity to the radiomimetic drug bleomycin was observed. Inhibition of EGFR in either the tamoxifen sensitive or resistant cells had very little effect on bleomycin sensitivity, The rate of uptake of various drugs was measured, and found to be identical between tamoxifen sensitive cells and their tamoxifen resistant derivatives. Microarray analysis of mRNA levels of drug efflux proteins also showed no significant decrease in drug efflux pump gene expression, with two efflux pump genes MRP3 and MRP4 showing increased expression. Tamoxifen resistant cells displayed greatly increased sensitivity to the apoptosis inducer camptothecin, and showed a significant increase in the levels of activated caspases present. Immunocytochemistry revealed a significant downregulation of the anti-apoptotic protein bcl-2.. Sensitivity to bleomycin was also measured and was found to inversely correlate to bcl-2 status. Finally bcl-2 levels were modulated using oestrogens and antioestrogens, and with an siRNA directed against the oestrogen receptor. The effect on bleomycin sensitivity was examined. Reduction of bcl-2 expression by either method had no effect on bleomycin sensitivity
APA, Harvard, Vancouver, ISO, and other styles
6

Baruah, Bedanta Prakash. "Exploring the role of CD44 in tamoxifen resistant breast cancer." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/53654/.

Full text
Abstract:
Resistance to endocrine therapy in breast cancer is associated with poor prognosis. Cell models of acquired tamoxifen resistance have implicated altered growth factor receptor signalling, especially the ErbB family of receptor tyrosine kinases, in development of the accompanying aggressive phenotype. Microarray analysis of an in vitro wtMCF-7 based model of acquired tamoxifen resistance (‘Tam-R’) identified upregulation of CD44, a transmembrane glycoprotein, known to interact with ErbB receptors and influence breast cancer progression. We investigated the hypothesis that CD44 overexpression in Tam-R cells can modulate ErbB activity and promote an adverse phenotype. CD44 gene overexpression was validated by RT-PCR and its protein expression determined by Western blotting and immunocytochemistry. CD44 contribution to intracellular signalling and phenotype of Tam-R cells (migration, invasion and growth), both endogenous and in response to hyaluronan (HA), was determined using Western blotting, immunocytochemistry and functional assays including wound healing, Boyden chamber migration, Matrigel™ invasion and growth assays in the presence or absence of siRNA-mediated CD44 knockdown. Interactions between CD44 and ErbB receptors were investigated using immunofluorescence and immunoprecipitation. CD44 was overexpressed at gene and protein level in Tam-R versus wtMCF-7 cells and whilst this did not influence the endogenous phenotype of Tam-R cells, it enhanced their sensitivity to HA as evidenced by HA-induced MAPK, EGFR and HER2 activation and increased migration. HA-induced migration was attenuated following treatment with the MAPK inhibitor PD098059, gefitinib as well as trastuzumab. CD44 was found to associate with HER2 and HER3 at the cell surface whilst HA stimulation appeared to modulate ErbB dimerisation patterns. Our data suggest that CD44 overexpression sensitises tamoxifen-resistant cells to HA thereby modulating ErbB dimerisation and enhancing migration. These observations may have importance in vivo where the tumour microenvironment can provide a rich source of HA to promote the progression of tamoxifen-resistant tumours.
APA, Harvard, Vancouver, ISO, and other styles
7

Crawford, Anatasha Carissa. "BCL-2 family function in antiestrogen-resistant breast cancer cells." Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/463256217/viewonline.

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

Hare, Stephen. "The development and characterisation of everolimus resistant breast cancer cells." Thesis, Brunel University, 2018. http://bura.brunel.ac.uk/handle/2438/17466.

Full text
Abstract:
The mTOR inhibitor and rapalogue everolimus was approved use in 2012, in HR+, HER-2-, post-menopausal patients, who had previously failed aromatase inhibitor treatment. mTOR pathway activation has been associated with resistance to breast cancer therapies, but how cells may become resistant to mTOR therapies themselves in breast cancer is currently not well explored, due to the relative recentness of everolimus approval. Drug resistance across all areas of cancer research is a major clinical issue, often leading to the spread of a patient's cancer. This project set out to create in vitro breast cancer models that were resistant to everolimus, and thus explore any changes that had developed in these models, help determine the mechanisms behind resistance and discover drugs/drug combinations that could overcome resistance. Cell lines T47D and MDA-MB-361 were subsequently developed into everolimus resistant lines (EveR) over the course of 4-6 months using an on/off exposure routine. The exact mechanism behind the everolimus resistance was not fully determined but EveR cells did show multiple intriguing characteristics. An increase in dormancy and stem-cell like phenotype was noted, as revealed by a decrease in cell cycle progression and an increase in increase ALDH activity. mTORC2 components and signalling was up-regulated although siRNA down-regulation of PKCα did not decrease everolimus resistance, suggesting other mTORC2 targets may be involved. The rapalogue 'receptor', FKBP12, was up-regulated which was accompanied by an increased growth inhibition by the rapalogue, temsirolimus, possible due to temsirolimus lower binding affinity for FKBP12 compared to everolimus. No resistance to the dual mTOR/PI3K inhibitor BEZ-235 was observed, in line with similar published work. The combination of vitamin D/calcitriol and everolimus had no added effect compared to everolimus alone, in parental cells, but the addition of 1μM calcitriol did drastically lower EveR cell resistance to everolimus. Future work focusing on the exact nature of calcitriol's interaction with the mTOR pathway is required to advance calcitriols role as a breast cancer therapeutic. Research with everolimus resistant breast cancer patients has not yet been published on, but the work presented here aims to help guide such studies, when they are carried out in the future.
APA, Harvard, Vancouver, ISO, and other styles
9

Rajalekshmi, Devi Sarika. "Development of Novel anti-estrogens for endocrine resistant Breast Cancer." Thesis, Virginia Tech, 2016. http://hdl.handle.net/10919/81275.

Full text
Abstract:
ER+ breast cancer raises a significant diagnostic challenge since resistance invariably develops to the current endocrine therapies. 70% of breast cancers are ER+, which results from the overexpression of estrogen receptor. ER mediates strong anti-inflammatory signaling in ER+ tissues. Once activated with estradiol (E2), ER inhibits inflammatory gene expression via protein-protein interactions that block NF-kappa B transcriptional activity. Importantly, NF-kappa B is a primary mediator of resistance in many cancers, including breast cancer. All current endocrine suppressive treatments block this palliative signaling pathway, along with the desired proliferative pathway. Thus, there is a significant unmet clinical need for novel endocrine treatments for breast cancer that can ameliorate patient outcome in resistant populations, be less prone to resistance development, retain anti-inflammatory action, and cause fewer side effects. Following the hypothesis driven approach, the work described here introduces structural analogs of an innovative ligand scaffold, 5,6-bis-(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hept-5-ene-2-sulfonic acid phenyl ester, termed OBHS, which reduces gene activation through ligand-induced shifts in helices 8 and 11, thereby indirectly modulating helix 12 of ER (hence, indirect antagonists). This new class of ligands with a bicyclic hydrophobic core retains strong anti-inflammatory effects while dialing out the proliferative effects of E2 (similar to Selective Estrogen Receptor Modulators, SERMS), and could potentially replace the current endocrine therapies of breast cancer. In this work, we carried out rational design and syntheses of two series of OBHS analogs, namely OBHS-A (for acetamido derivatives), and OBHS-P (for propargyl derivatives), while we explored a synthetic methodology for a third series of OBHS compounds. Many analogs from the OBHS-A series exhibited high binding affinity. For example, the exo diastereomer of 2.11a, 2.11b, 2.11c, 2.11d, and 2.11e exhibited Relative Binding Affinities (RBAs) of 22.6%, 10.5%, 19.5%, 12.1%, and 14.4%, respectively. As observed before, endo OBHS compounds exhibited lower binding affinities than exo compounds. The RBA values with acetamide, and isobutyramide (i.e. short hydrophobic chains) were very comparable to each other. However, unexpectedly the propionamide compound showed lower binding affinity than butyramide. Nevertheless, we consider OBHS analogs with RBA values greater than 1% (Kd = 20 nM) to be very potent. This data is only the first step in a battery of assays that will be conducted eventually on these compounds. In particular, our emphasis is in ascertaining and improving the NF-kappa B mediated anti-inflammatory property, where these compounds have shown promising activity in conjunction with their anti-proliferative activity.
Master of Science
APA, Harvard, Vancouver, ISO, and other styles
10

Geter, Phillip A. "Translational Reprogramming by eIF4E in Tamoxifen-Resistant ER+ Breast Cancer." Thesis, New York University, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10604789.

Full text
Abstract:

The majority of breast cancers express the estrogen receptor (ER+) and are treated with anti-estrogen therapies, particularly the inhibitor tamoxifen. However, many women treated with tamoxifen develop resistance, leading to metastatic disease, which is responsible for the majority of breast cancer deaths. Using small molecule inhibitors, phospho-mimetic proteins, tamoxifen sensitive and resistant breast cancer cells, a patient derived tamoxifen-resistant xenograft model, and genome-wide transcription and translation studies, we show that tamoxifen resistance is mediated by selective mRNA translational reprogramming. Tamoxifen resistant translation is mediated by increased expression of translation factor eIF4E, increased mTOR activity to promote eIF4E availability, and increased MNK activity to promote eIF4E Ser209 phosphorylation. Tamoxifen re-sensitization is restored only by reducing eIF4E expression or mTOR activity and blocking MNK1-directed eIF4E phosphorylation. Of the translationally upregulated mRNAs specific to tamoxifen resistant cells, we show that Runx2, which encodes a regulator of ER signaling that antagonizes estrogen responses and promotes breast cancer metastasis, significantly increases tamoxifen resistance and restores sensitivity when silenced. Moreover, tamoxifen resistant but not sensitive patient ER+ breast cancer specimens demonstrate strongly increased levels of mTOR and MNK activity and eIF4E protein. eIF4E levels, availability and phosphorylation therefore promote tamoxifen resistance in ER+ breast cancer through translatome reprogramming.

APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Herceptin resistant breast cancer"

1

1960-, Bernstein Amy, ed. Her-2: The making of herceptin, a revolutionary treatment for breast cancer. New York: Random House, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Bourgeault, Geoffrey A. Energy metabolism of wild type MCF-7 human breast cancer cells and its adriamyacin resistant derivative. Sudbury, Ont: Laurentian University, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Chadderton, Antony Robert. Valspodar restores paclitaxel induced apoptosis in the adriamycin resistant human breast cancer cell line MCF7/adr*. Sudbury, Ont: Laurentian University, School of Graduates Studies, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Pearce, Andrews G. The generation and characterization of a radiation resistant model system to study radioresistance in human breast cancer cells. Sudbury, Ont: Laurentian University, Chemistry and Biochemistry Department, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Gannon, Brian Robert. The role of camp-dependent protein kinase in the expression and function of p-glycoprotein and other molecules implicated in drug resistance in adriamycin-resistant MCF-7 human breast cancer cells. Sudbury, Ont: Laurentian University, Chemistry and Biochemistry Department, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bazell, Robert. Her-2: The Making of Herceptin, a Revolutionary Treatment for Breast Cancer. Random House, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bazell, Robert. Her-2: The Making of Herceptin, a Revolutionary Treatment for Breast Cancer. Random House, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Bazell, Robert. Her-2: The Making of Herceptin, a Revolutionary Treatment for Breast Cancer. Diane Pub Co, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Khayat, D. Optimising the Role of Herceptin in Breast Cancer (Supplement Issue: Oncology 2001, 2). S Karger Pub, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Wong, Ho-Lun. A study of nanoparticle drug carrier for treatment of multidrug-resistant breast cancer with loco-regional involvement. 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Herceptin resistant breast cancer"

1

Pegram, Mark D., Gottfried Konecny, and Dennis J. Slamon. "The Molecular and Cellular Biology of HER2/neu Gene Amplification/Overexpression and the Clinical Development of Herceptin (Trastuzumab) Therapy for Breast Cancer." In Advances in Breast Cancer Management, 57–75. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4757-3147-7_4.

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

Chowdhury, Ruhe, and Paul Ellis. "Trastuzumab (Herceptin®) and Ado-Trastuzumab Emtansine (Kadcyla®): Treatments for HER2-Positive Breast Cancer." In Handbook of Therapeutic Antibodies, 2041–68. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2014. http://dx.doi.org/10.1002/9783527682423.ch72.

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

Akekawatchai, Chareeporn, Sittiruk Roytrakul, Narumon Phaonakrop, Janthima Jaresitthikunchai, and Sarawut Jitrapakdee. "Proteomic Analysis of the Anoikis-Resistant Human Breast Cancer Cell Lines." In Methods in Molecular Biology, 185–93. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0471-7_11.

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

Chan, C. M. W., and M. Dowsett. "Oestrogen Receptor Expression Mutants and Variants in Tamoxifen-Resistant Breast Cancer." In Molecular Basis of Sex Hormone Receptor Function, 203–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03689-1_11.

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

Clarke, Robert, Todd Skaar, Fabio Leonessa, Brenda Brankin, Mattie James, Nils Brünner, and Marc E. Lippman. "Acquisition of an Antiestrogen-Resistant Phenotype in Breast Cancer: Role of Cellular and Molecular Mechanisms." In Drug Resistance, 263–83. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_11.

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

Khayat, D., Ch Borel, M. Weil, G. Auclerc, E. Vuillemin, and Cl Jacquillat. "Results of Cisplatin (CDDP)/Etoposide (VP16)/5-FU and alternatively Adriamycin or Mitomycin C (PEFAM) combination in primary resistant breast cancer and in heavily pre-treated metastatic breast cancer." In Proceedings of the 3rd International Congress on Neo-Adjuvant Chemotherapy, 136–45. Paris: Springer Paris, 1991. http://dx.doi.org/10.1007/978-2-8178-0782-9_34.

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

Ahmad, Rozaina, Noor Haida Mohd Kaus, and Shahrul Hamid. "Synthesis and Characterization of PLGA-PEG Thymoquinone Nanoparticles and Its Cytotoxicity Effects in Tamoxifen-Resistant Breast Cancer Cells." In Advances in Experimental Medicine and Biology, 65–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/5584_2018_302.

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

Carella, A. M., E. Lerma, A. Dejana, M. T. Corsetti, L. Celesti, F. Benvenuto, O. Figari, et al. "Autograft Followed by Allograft Without Myeloablative Conditioning Regimen: A New Approach for Resistant Hematologic Neoplasia and Breast Cancer." In Transplantation in Hematology and Oncology, 211–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59592-9_24.

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

Finn, Richard S., and Dennis J. Slamon. "Monoclonal antibody therapy for breast cancer: Herceptin." In Cancer Chemotherapy and Biological Response Modifiers Annual, 223–33. Elsevier, 2003. http://dx.doi.org/10.1016/s0921-4410(03)21010-3.

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

Rosa, Daniela D., and Gordon C. Jayson. "Herceptin in the Adjuvant Treatment of Breast Cancer." In Ethics, Law and Society, 257–59. Routledge, 2017. http://dx.doi.org/10.4324/9781315094311-25.

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

Conference papers on the topic "Herceptin resistant breast cancer"

1

Mehta, Rajeshwari, Fatouma Alimirah, Akash Gupta, Amit Kalra, and Rajendra Mehta. "Abstract 3812: Deguelin as a novel therapeutic agent for Herceptin resistant breast cancers." 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.am2012-3812.

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

Rivas, Martín A., Mercedes Tkach, Wendy Béguelin, Cecilia J. Proietti, María C. Díaz Flaqué, Esteban Maronna, Isabel Frahm, Eduardo H. Charreau, Patricia V. Elizalde, and Roxana Schillaci. "Abstract 611: Etanercept as a new tool for treatment of Herceptin-resistant breast cancer induced by tumor necrosis factor alpha." 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.am10-611.

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

Rehman, Sumaiyah K., Wen-Chien Huang, and Dihua Yu. "Abstract 4033: MiR-21 upregulation in breast cancer cells leads to PTEN loss and Herceptin resistance." 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.am10-4033.

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

Chaudhary, Pankaj, Lee Daniel Gibbs, and Jamboor K. Vishwanatha. "Abstract 1677: Annexin A2 antibody inhibits the progression of triple-negative and herceptin-resistant breast cancer by blocking epidermal growth factor receptor functions." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1677.

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

Sims, JD, M. Taguaim, C. Hanson, X. Cui, and LK Medina-Kauwe. "Abstract P5-08-08: A human epidermal growth factor receptor 3 (HER3)-binding nanoparticle targets and kills Herceptin®-resistant human epidermal growth factor receptor 2 (HER2)-positive breast cancer." In Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-p5-08-08.

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

He, Zhimin. "Abstract 5888: Disruption of FOXO3a-miRNAs mediated feedback inhibition of IGF2-IRS1 signaling contributes to Herceptin resistance in HER2 positive breast cancer cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5888.

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

Alami, N., Y. Sun, P. De, AM Benmassaoud, Y. Wang, and B. Leyland-Jones. "Combination effects of herceptin, pertuzumab and bevacizumab in a HER2-overexpressing breast cancer xenograft model." 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-4058.

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

Wadehra, Madhuri, Meagan Kiyohara, Christen Dillard, Negin Ashki, and Christie Qin. "Abstract 654: PG-101 in combination with docetaxel or Herceptin improves breast cancer survival." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-654.

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

Abouzeid, Abraham H., Niravkumar R. Patel, Ilya M. Rachman, Sean Senn, and Vladimir P. Torchilin. "Nanotechnology-based treatment for chemotherapy-resistant breast cancer." In SPIE NanoScience + Engineering, edited by Hooman Mohseni, Massoud H. Agahi, and Manijeh Razeghi. SPIE, 2014. http://dx.doi.org/10.1117/12.2064660.

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

Ma, Yongxian, Anju Preet, Changyan Hu, Akshay Kumar, James Ma, York Tomita, and Eliot M. Rosen. "Abstract 5574: Development of novel breast cancer therapeutics for anti-estrogen resistant breast cancer." 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.am2013-5574.

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

Reports on the topic "Herceptin resistant breast cancer"

1

Carraway, Kermit L. MUC4 Abrogation of Herceptin Responsiveness in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada397158.

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

Williams, Kristin P. Epigenetic Control of Tamoxifen-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada581650.

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

Williams, Kristin P. Epigenetic Control of Tamoxifen-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2014. http://dx.doi.org/10.21236/ada601260.

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

Mercola, Daniel A. Novel Array-Based Target Identification for Synergistic Sensitization of Breast Cancer to Herceptin. Fort Belvoir, VA: Defense Technical Information Center, May 2010. http://dx.doi.org/10.21236/ada631278.

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

Mercola, Daniel. Novel Array-Based Target Identification for Synergistic Sensitization of Breast Cancer to Herceptin. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada620074.

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

Lee, Yong J. Why are breast cancer stem cells resistant to radiation? Fort Belvoir, VA: Defense Technical Information Center, March 2013. http://dx.doi.org/10.21236/ada577634.

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

Graham, Justine D. Role of Nuclear Receptor Coregulators in Hormone Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada403446.

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

Graham, Justine D., and Kathryn B. Horwitz. Role of Nuclear Receptor Coregulators in Hormone Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada390669.

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

Scheinberg, David, and George Sgouros. Radiolabeled Herceptin to Increase Treatment Efficacy in Breast Cancer Patients with Low Tumor HER-2/neu Expression. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada438437.

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

Sgouros, George. Radiolabeled Herceptin to Increase Treatment Efficacy in Breast Cancer Patients With Low Tumor HER-2/neu Expression. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396561.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Herceptin resistant breast cancer' for particular source types:
Journal articles Dissertations / Theses
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