Relevant bibliographies by topics / Anti-HER2 therapy

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

Academic literature on the topic 'Anti-HER2 therapy'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Anti-HER2 therapy"

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Pospíšková, Markéta, and Milan Kohoutek. "Breast cancer a chronic disease? The Anti-HER2 therapy." Klinická farmakologie a farmacie 30, no. 4 (December 1, 2016): 28–30. http://dx.doi.org/10.36290/far.2016.032.

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Nahleh, Zeina A., Elizabeth B. Elimimian, Leah C. Elson, Brian Hobbs, Wei Wei, and Cassann N. Blake. "Endocrine Therapy Plus Anti-HER2 Therapy as Adjuvant Systemic Therapy for Luminal HER2-Positive Breast Cancer: An Analysis of the National Cancer Database." Breast Cancer: Basic and Clinical Research 14 (January 2020): 117822342094569. http://dx.doi.org/10.1177/1178223420945694.

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Background: Guidelines regarding the usage of adjuvant systemic therapy in patients with small human epidermal growth factor receptor 2 (HER2)-positive and estrogen receptor/progesterone receptor–positive (luminal HER2 positive) tumors are nonspecific. Outcomes of chemotherapy followed by endocrine therapy (ET), with or without anti-HER2 therapy, vs ET alone (no chemotherapy) have not been widely studied in this disease subtype. We sought to examine the usage and outcomes of adjuvant systemic therapy (ET vs chemotherapy with or without trastuzumab) in stage I luminal HER2-positive breast cancer (BC), based on the large National Cancer Database. Methods: We conducted a retrospective analysis of patients with luminal HER2-positive stage I BC, diagnosed between 2010 and 2015, in the United States, using univariable and multivariable logistic regression analyses. The Kaplan-Meier method estimated overall survival (OS). Results: A total of 37 777 patients were included in the analysis; of these, n = 32 594 (86%) received adjuvant ET and n = 5183 (14%) received chemotherapy. Around 40% of all patients received anti-HER2 therapy (trastuzumab). Patients who received trastuzumab had a better 5-year OS (93.4% vs 92.0%, P = .0002) compared with those who did not. Patients who received anti-HER2 therapy plus ET had the best OS rate at 5 years (93.5%, confidence interval [CI]: 89.2%-98%, P < .0001) compared with those receiving anti-HER2 therapy plus chemotherapy (92.7%, CI: 89.4%-96.1%, P < .0001). Conclusions: Most patients in the United States, with stage I luminal HER2 positive BC, received ET, not chemotherapy but most of them do not receive anti-HER2 therapy resulting in inferior outcome. Future trials exploring the de-escalation of systemic adjuvant therapy for early-stage luminal HER2-positive BC to ET plus anti-HER2 therapy would be desirable.
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Babar, Tania, Christopher Blomberg, Eileen Hoffner, and Xinhua Yan. "Anti-HER2 Cancer Therapy and Cardiotoxicity." Current Pharmaceutical Design 20, no. 30 (August 31, 2014): 4911–19. http://dx.doi.org/10.2174/1381612820666140604145037.

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Lück, Hans-Joachim, Michael Untch, Christian Jackisch, Christoph Zielinski, and Rupert Bartsch. "Optimal Sequencing of Anti-HER2 Therapy." Breast Care 9, no. 2 (2014): 138. http://dx.doi.org/10.1159/000362300.

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Martínez-Jañez, Noelia, Ignacio Chacón, Ana de Juan, Luis Cruz-Merino, Sònia del Barco, Isaura Fernández, Paula García-Teijido, et al. "Anti-HER2 Therapy Beyond Second-Line for HER2- Positive Metastatic Breast Cancer: A Short Review and Recommendations for Several Clinical Scenarios from a Spanish Expert Panel." Breast Care 11, no. 2 (2016): 133–38. http://dx.doi.org/10.1159/000443601.

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Background: The aim of this project was to provide an expert opinion regarding anti-human epidermal growth factor receptor 2 (HER2) therapy beyond second-line treatment of metastatic breast cancer (mBC). Methods: A group of experts discussed specific issues concerning anti-HER2 therapy in late-line settings in mBC. Results: Trastuzumab emtansine (T-DM1) or dual HER2 blockade appeared to be good options for HER2-positive mBC after ≥ 2 HER2-targeted therapies. Once an objective response has been achieved with anti-HER2-containing therapy, the anti-HER2 agent can be continued until progression of the disease, unacceptable toxicity or patient decision. mBC treated with ≥ 3 consecutive lines of anti-HER therapy, ≥ 1 being a dual HER2 blockade and with early progression of disease during a fourth or later-line treatment, are clinically resistant to anti-HER therapy. For progression of metastasis in the brain after anti-HER2 therapy, lapatinib and chemotherapy appear to be a good alternative after best local treatment. Conclusions: Further clinical trials are needed to provide valuable knowledge about the best treatment options in the later settings of mBC.
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Crespo, James, Hongxia Sun, Jimin Wu, Qingqing Ding, Guilin Tang, Melissa Robinson, Hui Chen, Aysegul A. Sahin, and Bora Lim. "HER2 targeted therapy and outcome in HER2-equivocal cases after 2018 ASCO/CAP HER2 guideline modification." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14729-e14729. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14729.

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e14729 Background: The best targeted therapeutic approach for HER2-equivocal cases remains unclear. New ASCO/CAP HER2 guidelines are intended to decrease this ambiguity by combining immunohistochemistry and in situ hybridization to resolve equivocal cases as positive or negative. However, the benefit of anti-HER2 therapy in HER2-equivocal cases is unknown. Methods: We retrospectively reviewed patients who visited MD Anderson from April 2017 to March 2018 with equivocal HER2 results based on the 2013 ASCO/CAP guidelines. The population was divided into 2 cohorts according to biopsy origin (primary cohort: biopsy from breast or axilla; recurrent/metastatic cohort: biopsy from recurrent or metastatic site). HER2 status was redefined using the 2018 ASCO/CAP guidelines. OS and PFS were calculated (Kaplan-Meier method) based on redefined HER2 status and use of HER2 targeted therapy. Results: A total of 139 equivocal results were found. Primary cohort had 90 patients (33 received neoadjuvant and 57 adjuvant therapy). HER2 IHC results were 0 (6.6%), 1+ (37.7%), 2+ (50%), 3+ (1.1%), and no IHC (4.4%). 94% of HER2-equivocal results became HER2 negative. Only 5 patients received anti-HER2 therapy, all of them in the HER2-negative group. After median follow-up of 1.91 yrs, 3 deaths and 8 progressions had occurred. There was no statistically significant association between anti-HER2 therapy and OS (p = 0.67) or PFS (p = 0.49). The recurrence/metastatic cohort had 49 cases with equivocal results. HER2 IHC results were 0 (6.1%), 1+ (22.4%), 2+ (26.5%), and no IHC (44.9%). 55% of HER2-equivocal results became HER2 negative, and only 1 patient received anti-HER2 therapy. After median follow-up of 2.96 yrs, 15 deaths and 35 progressions had occurred. There was no statistically significant association between anti-HER2 therapy and OS (p = 0.61) or PFS (p = 0.78). Conclusions: Most HER2-equivocal results were redefined as HER2 negative using the new ASCO/CAP guidelines. Association between anti-HER2 therapy and OS or PFS according to the new HER2 status was not observed. Although this is a small sample with short follow-up, patients with HER2-equivocal breast cancers seem to have clinical behavior similar to HER2-negative breast cancer.
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Mehta, Sandhya, Jinlin Song, Melissa Pavilack, Jipan Xie, Xiaoyu Nie, Mohini Vembusubramanian, and Jackie Kwong. "Utilization of anti-HER2 regimens among HER2-positive metastatic breast cancer patients." Journal of Clinical Oncology 38, no. 29_suppl (October 10, 2020): 282. http://dx.doi.org/10.1200/jco.2020.38.29_suppl.282.

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282 Background: HER2-positive (+) metastatic breast cancer (mBC) has a poor prognosis and many patients require multiple lines of HER2 targeted regimens. This study aims to examine the treatment sequencing of anti-HER2 regimens for HER2+ mBC among Medicare beneficiaries. Methods: A retrospective study was conducted using linked 1999-2016 Surveillance, Epidemiology, and End Results (SEER) cancer registries and Medicare claims. Adults patients who had mBC diagnosis, HER2+ status documented in SEER or claims of ≥1 anti-HER2 drug, continuous enrollment in Medicare from the date of mBC diagnosis until end of study period/death, and 2 anti-HER2 regimens with or without chemotherapy (Ch) or hormonal therapy (HT) were included. Discontinuation of anti-HER2 regimen was defined as the absence of claims for all anti-HER2 drugs for >60 days, or initiation of a different anti-HER2 drug. Re-initiation of the same regimen after >60 days was considered as a new regimen. The first two anti-HER2 regimens and subsequent therapies were summarized. Results: 804 patients with 2 anti-HER2 regimens were included. Trastuzumab (T) based regimen (defined as: T±Ch/HT; without other anti-HER2 drugs) was the most common 1st regimen (82%), followed by T+ pertuzumab (P) (14%) and lapatinib (L) (3%). For the 2nd regimen, T (52%) was most common, followed by T+P (18%), L (11%), trastuzumab emtansine (T-DM1) (11%) and T+L (7%). After a 2nd regimen, 578 (72%) initiated a subsequent therapy, with over half switching to non-targeted therapies [52%; HT alone (35%), Ch±HT (17%)] followed by T (17%), T-DM1 (12%) and T+P (7%). Among those with subsequent therapy, 2 T-based regimens followed by HT alone (21%) was the most common sequence. After the 1st regimen, 52% patients reused the same anti-HER2 drugs in the 2nd regimen, 21% added another anti-HER2 drug and 27% switched to a different anti-HER2 regimen. After the 2nd regimen, 14% reused anti-HER2 drugs and 6% added another anti-HER2 drug, 25% switched to a different anti-HER2 regimen; 15% reused anti-HER2 drugs from the 1st regimen. Conclusions: Trastuzumab based regimen was the mainstay of anti-HER2 drug regimens during the study timeframe. Despite availability of multiple anti-HER2 drugs, reuse of prior anti-HER2 drugs and switching to non-targeted therapies alone were common after using 2 anti-HER2 regimens. These findings underscore the unmet needs in later lines of therapy. Recently approved anti-HER2 agents may provide additional treatment options for pre-treated HER2+ metastatic breast cancer patients.
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Katayama, Ayaka, Islam M. Miligy, Sho Shiino, Michael S. Toss, Karim Eldib, Sasagu Kurozumi, Cecily M. Quinn, et al. "Predictors of pathological complete response to neoadjuvant treatment and changes to post-neoadjuvant HER2 status in HER2-positive invasive breast cancer." Modern Pathology 34, no. 7 (February 1, 2021): 1271–81. http://dx.doi.org/10.1038/s41379-021-00738-5.

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AbstractThe response of human epidermal growth factor receptor2 (HER2)- positive breast cancer (BC) patients to anti-HER2 targeted therapy is significant. However, the response is not uniform and a proportion of HER2-positive patients do not respond. This study aims to identify predictors of response in the neoadjuvant treatment and to assess the discordance rate of HER2 status between pre- and post-treatment specimens in HER2-positive BC patients. The study group comprised 500 BC patients treated with neoadjuvant chemotherapy (NACT) and/or neoadjuvant anti-HER2 therapy and surgery who had tumours that were 3+ or 2+ with HER2 immunohistochemistry (IHC). HER2 IHC 2+ tumours were classified into five groups by fluorescence in situ hybridisation (FISH) according to the 2018 ASCO/CAP guidelines of which Groups 1, 2 and 3 were considered HER2 amplified. Pathological complete response (pCR) was more frequent in HER2 IHC 3+ tumours than in HER2 IHC 2+/HER2 amplified tumours, when either in receipt of NACT alone (38% versus 13%; p = 0.22) or neoadjuvant anti-HER2 therapy (52% versus 20%; p < 0.001). Multivariate logistic regression analysis showed that HER2 IHC 3+ and histological grade 3 were independent predictors of pCR following neoadjuvant anti-HER2 therapy. In the HER2 IHC 2+/HER2 amplified tumours or ASCO/CAP FISH Group 1 alone, ER-negativity was an independent predictor of pCR following NACT and/or neoadjuvant anti-HER2 therapy. In the current study, 22% of HER2-positive tumours became HER2-negative by IHC and FISH following neoadjuvant treatment, the majority (74%) HER2 IHC 2+/HER2 amplified tumours. Repeat HER2 testing after neoadjuvant treatment should therefore be considered.
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Petráková, Katarína. "Residual disease after neoadjuvant systemic anti-HER2 therapy: the KATHERINE trial." Onkologie 14, no. 2 (June 2, 2020): 93–95. http://dx.doi.org/10.36290/xon.2020.017.

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Raghav, Kanwal, Jonathan M. Loree, Jeffrey S. Morris, Michael J. Overman, Ruoxi Yu, Funda Meric-Bernstam, David Menter, et al. "Validation of HER2 Amplification as a Predictive Biomarker for Anti–Epidermal Growth Factor Receptor Antibody Therapy in Metastatic Colorectal Cancer." JCO Precision Oncology, no. 3 (December 2019): 1–13. http://dx.doi.org/10.1200/po.18.00226.

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Purpose HER2 amplification has been implicated in resistance to therapy with anti–epidermal growth factor receptor antibodies (anti-EGFRabs) in metastatic colorectal cancer (mCRC). The purpose of the study was to validate the predictive impact of HER2 amplification in mCRC. Patients and Methods We analyzed patients with RAS/BRAF wild-type mCRC across two distinct cohorts. In cohort 1 (n = 98), HER2 amplification was tested in tumor tissue using dual in situ hybridization ( HER2 amplification: HER2/CEP17 ratio, 2.0 or greater). Cohort 2 (n = 70) included 16 patients with HER2 amplification and 54 HER2 nonamplified controls identified by next-generation sequencing ( HER2 amplification: four or more copies) who had received prior anti-EGFRabs. The primary end point was progression-free survival (PFS) on treatment with anti-EGFRab therapy, which was estimated and compared using the Kaplan-Meier method and log-rank test. Results Median PFS in cohort 1 on anti-EGFRab–based therapy was significantly shorter in patients with HER2 amplification compared with HER2 nonamplified patients (2.8 v 8.1 months, respectively; hazard ratio [HR], 7.05; 95% CI, 3.4 to 14.9; P < .001). These findings were validated in cohort 2 (median PFS for HER2 amplified v nonamplified: 2.8 v 9.3 months, respectively; HR, 10.66; 95% CI, 4.5 to 25.1; P < .001). The median PFS on therapy without anti-EGFRabs was similar among HER2-amplified and nonamplified patients in both cohort 1 (9.7 v 11.1 months, respectively; HR, 1.01; 95% CI, 0.4 to 2.4; P = .97) and cohort 2 (9.6 v 11.3 months, respectively; HR, 1.21; 95% CI, 0.5 to 3.1; P = .66). In multivariable analyses, HER2 amplification emerged as a single independent predictor of poor PFS on anti-EGFRab therapy in both cohort 1 (HR, 6.48; 95% CI, 3.1 to 13.6; P < .001) and cohort 2 (HR, 10.1; 95% CI, 4.3 to 23.9; P < .001). Conclusion HER2 amplification in RAS/RAF wild-type mCRC seems to be a predictive biomarker for lack of efficacy of anti-EGFRab therapy. Screening patients with RAS/BRAF wild-type mCRC for HER2 amplification should be considered before anti-EGFRab treatment to guide therapy and to identify patients for early referral to clinical trials.
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Dissertations / Theses on the topic "Anti-HER2 therapy"

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VITALE, STEFANIA. "Role of endocrine therapy in combination with anti-HER2 therapy and CDK4/6 inhibitors in hormone receptor positive/HER2 positive breast cancer." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1073185.

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In clinical practice, patients with advanced ER+/HER2+ BC are treated with a combination of anti-HER2 and chemotherapy as first choice but it is clear that a proportion of these derive prolonged benefit from the combination of hormonal therapy (HT) and anti-HER2 therapy (AH2T). Preclinical evidence from cellular models of BC indicates that ER and HER2 pathways are strictly interdependent and that targeting both pathways in ER+/HER2+ BC might be an effective therapeutic strategy; few trials investigated this combination showing a significant, albeit modest, clinical improvement. CDK4/6 pathway acts downstream of both the ER and HER2 pathways. CDK4/6 inhibitors (PD)have shown synergistic activity with HT or AH2T but data on the combination of PD with both HT and AH2T in ER+/HER2+ BC are lacking. PD activity is dependent on an intact RB pathway; therefore we analyzed whether Cyclin D/Rb/E2F pathway might help discriminating the subgroup of ER+/HER2+ BC resistant to PD therapy. We developed a gene expression signature of Rb-loss-of-function, the RBsig, that included a final set of 87 genes that is predictive of resistance to PD in BC cell lines. An in-silico analisys on a meta-dataset of neoadjuvant trials has also shown a good performance of RBsig in prediction of a better response to neoadjuvant chemotherapy. These data suggest RBsig as a potential marker for identifying patients with differential benefit from chemotherapy or HT+PD, both in combination with AH2T.
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Hashimoto, Kenji. "Investigating a role of HER3 in anti-HER2 target therapy in breast cancer." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:39025871-f32f-4e38-bd14-c13dbc9301f6.

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Background HER2-positive breast cancer is a poor prognostic subgroup, even if treated with anti-HER2 directed therapy. Trastuzumab is an important HER2-targeting antibody but only limited patients respond to this drug, and acquired resistance is a common problem. HER3 has been shown to be a key candidate in mediating resistance to trastuzumab and other ErbB inhibitors. The aims of the project are to investigate the resistance mechanisms and the relevant biomarkers in relation to trastuzumab treatment and resistance in HER2-positive breast cancer, in particular, HER3 subcellular localisation and HER3 phosphorylation. Methods Effects of trastuzumab on HER3 subcellular localisation and HER3 phosphorylation in relation to MET receptor were studied using western blots, nuclear fractionation, confocal microscopy, and immunoprecipitation in a panel of HER2-positive cell lines, including SKBr3 and BT474 breast cancer cells in which trastuzumab resistance was induced by long-term drug exposure. Effects of drug and knockdown experiments were tested by cell viability and proliferation assays. HER3 and MET expression was assessed by immunohistochemistry in xenograft tumours and human tissue samples, and clinical impact was assessed in different cohorts of HER2-positive breast cancer patients. Results Acquired trastuzumab resistant SKBr3 cells showed an increase of nuclear HER3100kD, which was derived from C-terminus of HER3. Nuclear HER3100kD could be due to the proteolytic cleavage of HER3 since it was reduced by ADAM17 or gamma-secretase inhibitor. In a panel of HER2-positive cell lines and xenograft samples, nuclear HER3 was observed only in the resistant cells. In addition, nuclear HER3 was associated with poor progression-free and overall survivals in HER2-positive breast cancer patients. It was also found that HER3 phosphorylation was maintained in acquired trastuzumab resistant cells, which was contributed by the ligand independent interaction of MET and HER3. Higher MET expression was associated with better overall survival in HER2-positive, breast cancer patients who were not treated with trastuzumab. Conclusions Nuclear HER3 was found in trastuzumab resistant cells and appeared to result from HER3 proteolytic cleavage mediated by ADAM17 and gamma-secretase. Further studies are required to investigate its mechanism and to identify the HER3 cleavage sites. MET was a key factor in maintaining HER3 phosphorylation during trastuzumab resistance. Lastly, nuclear HER3 and MET could be two potential biomarkers in HER2-positive breast cancer.
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Guardia, Valenzuela Cristina 1990. "Cancer-associated fibroblasts and response to anti-HER2 monoclonal antibodies in breast cancer." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668327.

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El cáncer de mama HER2-positivo es un subtipo muy agresivo. El desarrollo de terapias anti-diana HER2, particularmente el anticuerpo monoclonal (Mab) trastuzumab, supuso una mejora significativa en el pronóstico de esta enfermedad. De manera más reciente, otro Mab llamado pertuzumab, ha mejorado todavía más la eficiencia de trastuzumab. Aún y así, no todas las pacientes se beneficiarán de esta combinación de mAbs. Una proporción de estas pacientes no se beneficiarán de estas terapias anti-HER2, y fallecerán a causa de la presencia o el desarrollo de mecanismos de resistencia. Los tumores consisten no únicamente de una población heterogénea de células tumorales; si no también del conocido como rnicroentorno tumoral (IME por sus siglas en inglés). En los últimos años, se ha evidenciado que los fibroblastos asociados al tumor (CAFs por sus siglas en inglés) (una población estroma! muy abundante dentro del TME), directamente promueven los procesos tutnorogénicos así cotno la resistencia a los fármacos. No obstante, al inicio de este proyecto de tesis doctoral, los estudios relativos sobre el papel de los CAFs en la resistencia a la terapia anti-HER2 eran escasos. En resumen, este proyecto de tesis doctoral evidencia el papel de los fibroblastos asociado al tumor en la resistencia a la terapia anti-HER2 a través de la secreción de factores solubles que promueven la activación de mecanismos moleculares que promueven la supervivencia tumoral así como la resistencia terapéutica.
HER2-positive breast cancer (BC) is an aggressive subtype of this disease. The development of anti-HER2 targeted therapies, particularly the monoclonal antibody (Mab) trastuzumab, significantly improved its otherwise poor prognosis. More recently, another Mab called pertuzumab, has further improved the efficacy of trastuzumab, yet no all patients benefit from the combination of the two Mabs. A proportion of HER2-breast cancer patients will not benefit from anti-HER2 agents, and will ultimately die as a consequence of innate or acquired drug resistance mechanisms. Tumours consist not only of heterogeneous populations of cancer cells, but also of the tumour microenvironment (TME). In recent years, increasing evidence has shown that cancer-associated fibroblasts (CAFs; an abundant stromal cell population within the TME), directly support tumorigenesis and promote therapy resistance. However, at the beginning of this PhD study, there was little published work on the role of CAFs on anti-HER2 targeted therapy resistance. The work presented in this doctoral thesis supported a role of CAFs in tumour resistance to anti-HER2 targeted therapies in HER2+ breast cancer through paracrine secretion of soluble molecules that ultimately will promote breast cancer survival and therapy resistance.
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Rieker, Marcel. "Targeted Combination Therapy: Discovery and Evaluation of Synergistic Anticancer Effects of Anti-HER2-Duocarmycin Antibody-Drug Conjugates Combined with ATR Inhibitors." Phd thesis, Shaker Verlag GmbH, 2020. https://tuprints.ulb.tu-darmstadt.de/8615/7/2019-06-13_PhD_thesis_Rieker.pdf.

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While the global cancer burden is still high with 10 million people being diagnosed with cancer and 6 million cancer-related deaths yearly, academia and industry are developing more and more sophisticated therapies to combat cancer. One recent development are antibody-drug conjugates (ADCs) which consist of an antibody portion that mediates tumor selectivity and a highly cytotoxic drug designed to efficiently kill cancer cells. The majority of ADCs in clinical trials today carries payloads targeting the cytoskeleton. However, microtubule-targeting agents often lack clinical efficacy and thus, drugs with other mode of actions are in focus of current ADC research. With Mylotarg and Besponsa for example two ADCs carrying DNA damaging agents are already approved and SYD985 an ADC carrying the DNA-alkylating agent duocarmycin is currently showing promising results in a clinical phase III study. Although ADCs have shown promising anticancer effects and often come along with a broadened therapeutic window compared to conventional chemotherapy, there is still room for improvement regarding e.g. saftey aspects. Establishment of combination therapy for ADCs might pose a strategy for increasing efficacy, diminish side-effects and slow down resistance development especially because single agent therapy has seldom been curative. This work aimed at the discovery of a synergistic drug combination that might enhance the efficacy of duocarmycin-based ADCs like the clinically evaluated ADC SYD985. Therefore, 17 DNA-damage response inhibitors (DDRis), potentially involved in the repair of duocarmycin-induced lesions, were selected based on literature and tested in in vitro models. HCC-1954 and MDA-MB-468 cancer cells were treated with a combination of the selected DDRis and duocarmycin and the antiproliferative effects of the combination treatment were compared to the effects of the single agents alone. These experiments clearly demonstrated that inhibitors of the kinase ATR, which plays a central role in the response to replication stress, synergistically enhanced the cytotoxic effects of duocarmycin. This observation was additionally confirmed by treatment of ATR Knock-down cells with duocarmycin. Further drug combination experiments revealed the impact of structural features of different duocarmycins and ATR inhibtors on the synergism level. Besides studying the combinatorial effects of the small molecules alone, it was demonstrated that this combination effect could be translated to a targeted therapy approach like antibody-drug conjugates. Several duocarmycin based ADCs showed strong synergistic effects in combination with different ATR inhibitors in vitro as well as in vivo. rag2 mice bearing a HER2-expressing NCI-N87 tumor were treated with HER2-targeting duocarmycin-ADC and two different ATR inhibitors. The ATR inhibitors monotreatment showed very mild tumor growth inhibition while the treatment with the ADC at concentrations below the maximum effective dose led to a partial tumor response. The combination treatment, however, resulted in very strong anti-tumor effects while being well tolerated. The present study demonstrates the superiority of combining the targeted delivery of duocarmycin to the tumor using an anti-HER2-duocarmycin ADC with systemic application of ATR inhibitors over the treatment with the drugs as single agents. This might support endeavors of evaluating such combinations in a clinical setting.
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Oechsle, Crystal Mae. "The Use and Enhancement of Anti-Cancer Vaccine Therapy with Low-Toxicity Drugs for the Treatment of HER2 Positive Breast Cancer." Kent State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1561121654968093.

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Rieker, Marcel [Verfasser]. "Targeted Combination Therapy: Discovery and Evaluation of Synergistic Anticancer Effects of Anti-HER2-Duocarmycin Antibody-Drug Conjugates Combined with ATR Inhibitors / Marcel Rieker." Düren : Shaker, 2019. http://d-nb.info/1198600004/34.

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Rieker, Marcel [Verfasser], Harald [Akademischer Betreuer] Kolmar, and Felix [Akademischer Betreuer] Hausch. "Targeted Combination Therapy: Discovery and Evaluation of Synergistic Anticancer Effects of Anti-HER2-Duocarmycin Antibody-Drug Conjugates Combined with ATR Inhibitors / Marcel Rieker ; Harald Kolmar, Felix Hausch." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2020. http://d-nb.info/1202922872/34.

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Guisier, Florian. "Contribution à l'identification de marqueurs de la réponse des carcinomes bronchiques non à petites cellules aux immunothérapies Anti-PD1 immunotherapy for NSCLC with actionable oncogenic driver mutations Janus or Hydra : the many faces of T helper cells in the human tumour microenvironment A rationale for surgical debulking to improve anti-PD1 therapy outcome in non small cell lung cancer Efficacy and safety of anti-PD-1 immunotherapy in pretreated NSCLC patients with BRAF, HER2 or MET mutation or RET-translocation. GFPC 01-2018." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR148.

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L’immunothérapie par anti-PD1/PD L1 a bouleversé la prise en charge du cancer bronchique non à petites cellules (CBNPC) depuis 2015, offrant notamment la perspective d’un contrôle prolongé de la maladie métastatique. Néanmoins la majorité des patients ne tire pas de bénéfice de ces traitements. Il est donc indispensable d’identifier des biomarqueurs permettant de mieux Sélectionner les patients pour l’immunothérapie. A partir d’un modèle murin de CBNPC, nous avons établi le rôle du volume tumoral comme facteur prédictif de la réponse à un traitement par anti-PD1. La mesure du volume tumoral métabolique sur les données du PET scan préthérapeutique d’une cohorte de 48 patients porteurs d’un CBNPC métastatique et traités par Nivolumab a permis de confirmer ce rôle. Dans notre modèle murin, une chirurgie de cytoréduction permettait d’améliorer l’efficacité du traitement par anti-PD1. Dans une seconde étude, nous avons analysé l’efficacité des traitements par anti-PD1/PD-L1 dans le CBNPC avec mutation BRAF, MET ou HER2 ou translocation RET. Ces altérations oncogéniques sont autant de biomarqueurs permettant de proposer un traitement par thérapie ciblée, mais l’efficacité des anti-PD1/PD-L1 dans ces sous-groupes est mal connue. Des études antérieures suggèrent que cette efficacité est réduite. Nous avons mené une étude multicentrique nationale, réunissant 107 patients de 21 centres. : 26 BRAF-V600, 18 BRAF-nonV600, 30 MET, 23 HER2, 9 RET. Les taux de réponse aux anti-PD1/PD-L1 étaient de 26%, 33%, 27%, 38% et 38%, respectivement, soit des taux similaires à ceux de la population générale de CBNPC. Nos résultats incitent à poursuivre les études dans ces sous-groupes de patients puisque certains d’entre eux tirent un bénéfice prolongé des anti-PD1/PD-L1
Since 2015, anti-PD1/PD-L1 immunotherapy has emerged as a standard of care for non-small cell lung cancer (NSCLC), demonstrating a higher rate of long-term control of stage IV disease. Nonetheless, most patients do not derive benefit from these drugs. Reliable biomarkers are needed to better select patients for immunotherapy. Studying a mouse model of NSCLC, we identified tumor volume as a predictive marker of response to anti-PD1 therapy. We confirmed this role in a cohort of 48 NSCLC patients treated with Nivolumab, in whom metabolic tumor volume was assessed on pretherapeutic PET-scan. Moreover, in our mouse model, debulking surgery enhanced the efficacy of anti-PD1 treatment. In a second study, we analysed the efficacy of anti-PD1/PD-L1 treatment in NSCLC patients with BRAF, MET or HER2 mutations or RET translocation. These subgroups of patients were overlooked in clinical trials and previous studies suggest they are not good candidates for immunotherapy. We collected data from 107 patients in 21 centers : -26 BRAF-V600, 18 BRAF-nonV600, 30 MET, 23 HER2, 9 RET. Response rates to anti-PD1/PD-L1 treatment were 26%, 33%, 27%, 38% and 38%, respectively. These are close to the ones observed in unselected NSCLC patients. Our results emphasize the need for more studies in these patients, since some of them derive durable benefit from anti-PD1/PD-L1 treatment
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Book chapters on the topic "Anti-HER2 therapy"

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Barrios, Carlos, and Alessandra Morelle. "Anti-HER2 Adjuvant Therapy." In Breast Diseases, 497–508. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-13636-9_60.

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Tower, Amelia, Ruta D. Rao, Kalliopi P. Siziopikou, Melody A. Cobleigh, and Thomas B. Julian. "Anti-HER2/neu Therapy in DCIS." In Ductal Carcinoma In Situ and Microinvasive/Borderline Breast Cancer, 99–108. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2035-8_10.

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Theile, Dirk, Gal Lenz, Jamil A. Momand, and Susan E. Kane. "Resistance to HER2-Targeted Therapy." In Resistance to Targeted Anti-Cancer Therapeutics, 35–88. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70142-4_2.

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Nahta, Rita. "Novel Therapies to Overcome HER2 Therapy Resistance in Breast Cancer." In Resistance to Targeted Anti-Cancer Therapeutics, 191–221. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21477-7_7.

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Crook, Tim, Su Li, and Peter Harper. "Medical management of breast cancer." In Oxford Textbook of Medicine, edited by Tim Eisen, 505–8. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0051.

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Abstract:
Most patients with breast cancer are offered surgery, the main options being modified radical mastectomy, with or without immediate or delayed breast reconstruction, or breast-conserving surgery. All patients treated surgically for early breast cancer should be considered for risk-reducing neoadjuvant (before surgery) or adjuvant (after surgery) treatments. Adjuvant radiotherapy should be considered for all patients who have undergone breast-conserving surgery. Adjuvant medical therapies include (1) endocrine therapy—should be given to all oestrogen-receptor positive patients (premenopausal—tamoxifen; postmenopausal—aromatase inhibitors); (2) anti-HER2 targeted therapy (e.g. trastuzumab) in cancers that overexpress the HER2 oncogene; (3) chemotherapy—selection is informed by clinic-pathological parameters and increasingly by molecular genetic platforms such as Oncotype DX; patients with oestrogen-receptor negative, node-positive disease should receive regimens containing sequential anthracyclines and taxanes. Regimens for neoadjuvant treatment are similar to those used in the adjuvant setting.
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"Molecularly-Targeted Therapeutic Strategies for Breast Cancer Focusing on HER2-Targeted Therapy, mTOR Inhibitor and Antiangiogenic Therapy." In Frontiers in Anti-Cancer Drug Discovery, Volume 4, edited by Teruhiko Fujii, Keisuke Miwa, Tomoyuki Ushijima, Mototsugu Matsunaga, Masaru Fukahori, Kotaro Yuge, Uhi Toh, et al., 157–228. BENTHAM SCIENCE PUBLISHERS, 2014. http://dx.doi.org/10.2174/978160859225114040006.

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Conference papers on the topic "Anti-HER2 therapy"

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Metzger-Filho, O., S. Mandrekar, S. Loibl, E. Ciruelos, L. Gianni, E. Lim, K. Miller, et al. "Abstract OT3-05-07: PATINA: A randomized open label phase III trial to evaluate the efficacy and safety of palbociclib + anti HER2 therapy + endocrine therapy vs anti HER2 therapy + endocrine therapy after induction treatment for hormone receptor positive, HER2 positive metastatic breast cancer." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-ot3-05-07.

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Arima, Yoshimi, Mari Hosonaga, and Hideyuki Saya. "Abstract 3331: CD24 promotes HER2 signaling pathways and CD24 inhibition sensitizes anti-HER2 therapy in breast cancer." 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.am2014-3331.

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Liu, Yunhua, Xiaoming He, Xiongbin Lu, and Xinna Zhang. "Abstract 3803: Targeting 17q23 amplicon to overcome the resistance to anti-HER2 therapy in HER2+ breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3803.

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Liu, Yunhua, Xiaoming He, Xiongbin Lu, and Xinna Zhang. "Abstract 3803: Targeting 17q23 amplicon to overcome the resistance to anti-HER2 therapy in HER2+ breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3803.

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Qin, You, Hannah E. Dobson, Frank I. Comer, Alfred E. Chang, Max S. Wicha, and Qiao Li. "Abstract 514: Specific anti-HER2 host immunity conferred by HER2-targeted antibody drug conjugate therapy and checkpoint blockade." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-514.

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Borrero-García, Luis Daniel, Brian Vidal, and Suranganie Dharmawardhane. "Abstract 1824: Mechanisms of resistance to anti-EGFR/HER2 therapy in breast cancer." 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.am2018-1824.

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Im, S.-A., Y.-J. Bang, D.-Y. Oh, G. Giaccone, T. Bauer, J. Nordstrom, H. Li, et al. "Abstract P6-18-11: Long-term responders to single-agent margetuximab, an Fc-modified anti-HER2 monoclonal antibody, in metastatic HER2+ breast cancer patients with prior anti-HER2 therapy." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p6-18-11.

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Sethunath, Vidyalakshmi, Huizhong Hu, Carmine DeAngelis, Jamunarani Veeraraghavan, Lanfang Qin, Martin Shea, Tamika Mitchell, et al. "Abstract 4757: Targeting the mevalonate pathway in HER2+breast cancer to overcome resistance and enhance anti-HER2 therapy efficacy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4757.

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Sethunath, Vidyalakshmi, Huizhong Hu, Carmine DeAngelis, Jamunarani Veeraraghavan, Lanfang Qin, Martin Shea, Tamika Mitchell, et al. "Abstract 4757: Targeting the mevalonate pathway in HER2+breast cancer to overcome resistance and enhance anti-HER2 therapy efficacy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4757.

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Jiang, Z., L. Li, Y. Liu, T. Wang, S. Zhang, Y. Yuan, L. Bian, Q. Liu, and F. Qi. "Abstract OT1-1-04: HER2 status of circulating tumor cells in HER2-positive metastatic breast cancer patients: A valuable biomarker in anti-HER2 therapy." 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-ot1-1-04.

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Reports on the topic "Anti-HER2 therapy"

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Strube, Randall. Anti-HER2/Toxin Expressing Lymphocytes for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, May 2001. http://dx.doi.org/10.21236/ada395157.

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Strobe, Randall. Anti-HER2/Toxin Expressing Lymphocytes for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, May 2000. http://dx.doi.org/10.21236/ada393070.

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Guo, Kevin, Rebecca Hawkins, and Bonnie Wu. Engineering a Cell-Penetrating Anti-HER2 Monoclonal Antibody for Efficient Delivery of Gold Nanoparticles into Cancer Cells To Enhance X-Ray Cancer Radiation Therapy. Journal of Young Investigators, February 2020. http://dx.doi.org/10.22186/jyi.38.2.13-22.

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