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Journal articles on the topic 'Resistance to therapies'

Author: Grafiati

Published: 16 November 2024

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1

Gupta, P. D. "Reducing drug resistance should be the aim of therapies." Clinical Research and Clinical Trials 3, no. 4 (April 30, 2021): 01–05. http://dx.doi.org/10.31579/2693-4779/028.

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Over the period, due to evolutionary constrains, gene mutations, changes in micro- and mega- environment gave a tool to bacteria to adopt for survival in the hostile environment. When they are exposed with broad spectrum antibiotics, they have adopted to live and become resistant to antibiotics. In this review many preventive and curative strategies has been described to avoid antibiotics. These lines of treatments would not give chances to microbes to become drug resistant. “Prevention is better than cure” adopting this strategy we have described immunochemicals and many herbal medicines which will prevent infections. Also given importance to maintain proper balance of microbiota in the gut by replacement of the lost (may be due to many reasons) species which are considered necessary for maintaining a balance in bacterial population.

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2

Bartolotti, Marco, Enrico Franceschi, Rosalba Poggi, Alicia Tosoni, Monica Di Battista, and Alba A. Brandes. "Resistance to antiangiogenic therapies." Future Oncology 10, no. 8 (June 2014): 1417–25. http://dx.doi.org/10.2217/fon.14.57.

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3

Prasad, Rajendra, Atanu Banerjee, and Abdul Haseeb Shah. "Resistance to antifungal therapies." Essays in Biochemistry 61, no. 1 (February 28, 2017): 157–66. http://dx.doi.org/10.1042/ebc20160067.

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The evolution of antifungal resistance among fungal pathogens has rendered the limited arsenal of antifungal drugs futile. Considering the recent rise in the number of nosocomial fungal infections in immunocompromised patients, the emerging clinical multidrug resistance (MDR) has become a matter of grave concern for medical professionals. Despite advances in therapeutic interventions, it has not yet been possible to devise convincing strategies to combat antifungal resistance. Comprehensive understanding of the molecular mechanisms of antifungal resistance is essential for identification of novel targets that do not promote or delay emergence of drug resistance. The present study discusses features and limitations of the currently available antifungals, mechanisms of antifungal resistance and highlights the emerging therapeutic strategies that could be deployed to combat MDR.

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4

Tejpar, Sabine, Hans Prenen, and Massimiliano Mazzone. "Overcoming Resistance to Antiangiogenic Therapies." Oncologist 17, no. 8 (July 6, 2012): 1039–50. http://dx.doi.org/10.1634/theoncologist.2012-0068.

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5

Sledge, George W. "Resistance to Anti-HER2 Therapies." Breast 20 (October 2011): S16. http://dx.doi.org/10.1016/j.breast.2011.08.014.

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6

Lawrence Drew, W. "Cytomegalovirus resistance to antiviral therapies." American Journal of Health-System Pharmacy 53, suppl_2 (April 1, 1996): S17—S23. http://dx.doi.org/10.1093/ajhp/53.8_suppl_2.s17.

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7

Thangavadivel, Shanmugapriya, and Jennifer A. Woyach. "Genomics of Resistance to Targeted Therapies." Hematology/Oncology Clinics of North America 35, no. 4 (August 2021): 715–24. http://dx.doi.org/10.1016/j.hoc.2021.03.004.

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8

Guièze, Romain. "Mechanisms of resistance to targeted therapies." Hématologie 26, S3 (September 2020): 20–26. http://dx.doi.org/10.1684/hma.2020.1564.

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9

Fong, Chun Yew, Omer Gilan, Enid Lam, Alan Rubin, Jessica Morison, George Giotopoulos, Kym Stanley, et al. "Modelling Resistance to Emerging Epigenetic Therapies." Blood 124, no. 21 (December 6, 2014): 3546. http://dx.doi.org/10.1182/blood.v124.21.3546.3546.

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Abstract The BET inhibitors are first-in-class, epigenetic targeted therapies that deliver a new therapeutic paradigm by directly targeting protein-protein interactions at chromatin. Early clinical trials have shown significant promise, especially in AML, suggesting that these compounds are likely to form an important component of future anti-cancer regimens. Therapeutic resistance is an inevitable consequence of most cancer therapies, therefore the evaluation of resistance mechanisms is of utmost importance in order to optimize the clinical utility of this novel class of drugs. Using primary murine stem and progenitor cells immortalized with MLL-AF9, we have developed a novel approach to generate over 20 clones stably resistant to the prototypical BET inhibitor, IBET. Resistance has been established at >IC90 of the parental cell line. In parallel, we have maintained matched vehicle treated clones in addition to the parental cell line. Resistant clones maintain their clonogenic capacity in IBET and are also impervious to IBET induced cell-cycle arrest and apoptosis. Resistance to IBET confers cross-resistance to other chemically distinct BET inhibitors such as JQ1 and also resistance to genetic knockdown of BET proteins. Moreover, resistance is stably maintained across subsequent cell generations in the absence of ongoing selective pressure. Resistance is not mediated through increased drug efflux or metabolism but is demonstrated to emerge from the leukemia stem cell (LSC) compartment. Resistant clones display an immature phenotype (c-kithi/Gr1-/CD11b-) and functionally, exhibit increased clonogenic capacity in vitro and markedly shorter disease latency following primary syngeneic transplantation (Figure A, B and C). Importantly, resistant clones maintain their resistance to IBET therapy in vivo. We will present data gleaned from exome capture sequencing, ChIP-seq and RNA-seq, to demonstrate the underlying molecular mechanisms of resistance to epigenetic therapies, including genetic changes, molecular events at chromatin and the upregulation of compensatory pathways that will inform future combination therapies to obviate and/or overcome BET inhibitor resistance. In summary, we have utilized a primary murine model of MLL leukemia to derive over 20 individual clones that are resistant to BET inhibition. Our data is consistent with resistance emerging from the LSC population. This data will allow us to develop rational drug combinations to overcome resistance and enhance the therapeutic efficacy of emerging epigenetic therapies. Furthermore, our data provides novel insights into the biology of AML and provides an unprecedented opportunity to study leukemia stem cells and develop therapeutic strategies to eradicate them. Figure 1 Figure 1. Disclosures Lugo: GlaxoSmithKline: Employment. Jeffrey:GlaxoSmithKline: Employment. Gregory:GlaxoSmithKline: Employment. Prinjha:GlaxoSmithKline: Employment.

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10

Smith, Sinéad M., Colm O’Morain, and Deirdre McNamara. "Helicobacter pylori resistance to current therapies." Current Opinion in Gastroenterology 35, no. 1 (January 2019): 6–13. http://dx.doi.org/10.1097/mog.0000000000000497.

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11

Olson, Oakley C., and Johanna A. Joyce. "Microenvironment-mediated resistance to anticancer therapies." Cell Research 23, no. 2 (September 4, 2012): 179–81. http://dx.doi.org/10.1038/cr.2012.123.

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12

Fischbach, Michael A. "Combination therapies for combating antimicrobial resistance." Current Opinion in Microbiology 14, no. 5 (October 2011): 519–23. http://dx.doi.org/10.1016/j.mib.2011.08.003.

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13

Debela, Negeri, and Solome Nekahiwot. "Sepsis, Antimicrobial Resistance, and Alternative Therapies." American Journal of Health Research 12, no. 1 (March 7, 2024): 8–18. http://dx.doi.org/10.11648/j.ajhr.20241201.12.

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Sepsis, a life-threatening condition caused by the body's excessive response to an infection, has emerged as a global health menace. Around 20% of all global deaths are attributable to sepsis. Conversely, the presence of antimicrobial resistance (AMR) poses a significant peril to the health system. AMR constitutes an escalating pandemic that we must not disregard, as the absence of effective antibiotics would compromise the treatment of even commonplace bacterial infections. Therefore, the increasing prevalence of AMR further adds complexity to the management and outcomes of individuals with sepsis. AMR plays a contributory role in aggravating the consequences of sepsis, ranging from prolonged hospitalization to mortality. The World Health Organization (WHO) has prioritized AMR as a major concern necessitating immediate action to prevent dire consequences in the future. Though, One Health approach, infection prevention, rational use of antibiotics, strengthening surveillance systems, as well as research and development, are crucial strategies in combating antimicrobial resistance, alternative therapies, such as phage therapy and immunotherapeutics, are being explored for the management of AMR infections. Advances in these therapies show promise in addressing the challenges posed by antibiotic resistance in treating sepsis. In this critical assessment, we succinctly delineate the existing challenges of AMR in managing sepsis cases, and we provide an overview of the advancements in treating sepsis through alternative therapeutic modalities.

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14

köroğlu, Mehmet, nilgün akalın, selçuk Sezikli, yıldız okuturlar, and özlem harmankaya. "Impacts of Dialysis Replacement Therapies on Insulin Resistance and Assessment of Atherosclerotic Parameters." Turkish Nephrology Dialysis Transplantation 25, no. 01 (January 22, 2016): 59–64. http://dx.doi.org/10.5262/tndt.2016.1001.06.

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15

Drouin, Eric. "Helicobacter pylori: Novel Therapies." Canadian Journal of Gastroenterology 13, no. 7 (1999): 581–83. http://dx.doi.org/10.1155/1999/485237.

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The ideal therapy forHelicobacter pyloriwould cure the infection without resulting in the development of antibiotic resistance. Current therapies have variable cure rates; the reasons for treatment failure include bacterial resistance and poor compliance. Some antibiotics, such as furazolidone, may be affordable agents to treat this infection worldwide. New proton pump inhibitors, such as rabeprazole, can potentiate antibiotics. Nutriceuticals and probiotics demonstrate interesting in vitro activity againstH pylori. Children rarely have symptoms to this infection and, therefore, are a suitable group in which to assess different nonaggressive therapies.

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16

Hrustanovic, Gorjan, Bianca J. Lee, and Trever G. Bivona. "Mechanisms of resistance to EGFR targeted therapies." Cancer Biology & Therapy 14, no. 4 (April 2013): 304–14. http://dx.doi.org/10.4161/cbt.23627.

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17

Zhao, Xianda, Dechen Wangmo, Matthew Robertson, and Subbaya Subramanian. "Acquired Resistance to Immune Checkpoint Blockade Therapies." Cancers 12, no. 5 (May 5, 2020): 1161. http://dx.doi.org/10.3390/cancers12051161.

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Immune checkpoint blockade therapy (ICBT) has revolutionized the treatment and management of numerous cancers, yet a substantial proportion of patients who initially respond to ICBT subsequently develop resistance. Comprehensive genomic analysis of samples from recent clinical trials and pre-clinical investigation in mouse models of cancer provide insight into how tumors evade ICBT after an initial response to treatment. Here, we summarize our current knowledge on the development of acquired ICBT resistance, by examining the mechanisms related to tumor-intrinsic properties, T-cell function, and tumor-immune cell interactions. We discuss current and future management of ICBT resistance, and consider crucial questions remaining in this field of acquired resistance to immune checkpoint blockade therapies.

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18

Wang, Zhixiang. "Drug Resistance and Novel Therapies in Cancers." Cancers 12, no. 10 (October 12, 2020): 2929. http://dx.doi.org/10.3390/cancers12102929.

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19

Patel, Meet, Adam Eckburg, Shahina Gantiwala, Zachary Hart, Joshua Dein, Katie Lam, and Neelu Puri. "Resistance to Molecularly Targeted Therapies in Melanoma." Cancers 13, no. 5 (March 5, 2021): 1115. http://dx.doi.org/10.3390/cancers13051115.

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Malignant melanoma is the most aggressive type of skin cancer with invasive growth patterns. In 2021, 106,110 patients are projected to be diagnosed with melanoma, out of which 7180 are expected to die. Traditional methods like surgery, radiation therapy, and chemotherapy are not effective in the treatment of metastatic and advanced melanoma. Recent approaches to treat melanoma have focused on biomarkers that play significant roles in cell growth, proliferation, migration, and survival. Several FDA-approved molecular targeted therapies such as tyrosine kinase inhibitors (TKIs) have been developed against genetic biomarkers whose overexpression is implicated in tumorigenesis. The use of targeted therapies as an alternative or supplement to immunotherapy has revolutionized the management of metastatic melanoma. Although this treatment strategy is more efficacious and less toxic in comparison to traditional therapies, targeted therapies are less effective after prolonged treatment due to acquired resistance caused by mutations and activation of alternative mechanisms in melanoma tumors. Recent studies focus on understanding the mechanisms of acquired resistance to these current therapies. Further research is needed for the development of better approaches to improve prognosis in melanoma patients. In this article, various melanoma biomarkers including BRAF, MEK, RAS, c-KIT, VEGFR, c-MET and PI3K are described, and their potential mechanisms for drug resistance are discussed.

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20

&NA;. "Potential therapies for biofilm-based antibacterial resistance." Inpharma Weekly &NA;, no. 1297 (July 2001): 2. http://dx.doi.org/10.2165/00128413-200112970-00002.

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21

Garber, Ken. "Melanoma combination therapies ward off tumor resistance." Nature Biotechnology 31, no. 8 (August 2013): 666–67. http://dx.doi.org/10.1038/nbt0813-666b.

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22

Redmond, Keara L., Anastasia Papafili, Mark Lawler, and Sandra Van Schaeybroeck. "Overcoming Resistance to Targeted Therapies in Cancer." Seminars in Oncology 42, no. 6 (December 2015): 896–908. http://dx.doi.org/10.1053/j.seminoncol.2015.09.028.

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23

Lo, Roger. "Evolution of resistance to MAPK-targeted therapies." Journal of Translational Medicine 13, Suppl 1 (2015): K2. http://dx.doi.org/10.1186/1479-5876-13-s1-k2.

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24

Sundar, Shyam, Jaya Chakravarty, and Lalit P. Meena. "Leishmaniasis: treatment, drug resistance and emerging therapies." Expert Opinion on Orphan Drugs 7, no. 1 (December 5, 2018): 1–10. http://dx.doi.org/10.1080/21678707.2019.1552853.

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25

Lin, Jessica J., and Alice T. Shaw. "Resisting Resistance: Targeted Therapies in Lung Cancer." Trends in Cancer 2, no. 7 (July 2016): 350–64. http://dx.doi.org/10.1016/j.trecan.2016.05.010.

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26

Kelsey, Rebecca. "Genomic drivers of resistance to AR therapies." Nature Reviews Urology 15, no. 4 (February 13, 2018): 202. http://dx.doi.org/10.1038/nrurol.2018.18.

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27

Dagogo-Jack, Ibiayi, and Alice T. Shaw. "Tumour heterogeneity and resistance to cancer therapies." Nature Reviews Clinical Oncology 15, no. 2 (November 8, 2017): 81–94. http://dx.doi.org/10.1038/nrclinonc.2017.166.

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28

Tay, Andy. "Upgrading Phage Therapies to Crush Antimicrobial Resistance." Genetic Engineering & Biotechnology News 43, no. 11 (November 1, 2023): 24–26. http://dx.doi.org/10.1089/gen.43.11.10.

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29

Giuliano, Sandy, and Gilles Pagès. "Mechanisms of resistance to anti-angiogenesis therapies." Biochimie 95, no. 6 (June 2013): 1110–19. http://dx.doi.org/10.1016/j.biochi.2013.03.002.

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30

V Riley, Thomas. "Old therapies, new science." Microbiology Australia 23, no. 5 (2002): 18. http://dx.doi.org/10.1071/ma02518.

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With the emergence of antibiotic resistance as a major public health problem and the apparent decline in pharmaceutical company drive to produce new antimicrobials, there has been an increase in interest in revisiting remedies and agents once popular before the advent of the antibiotic era.

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31

Zanardi, R., F. Attanasio, C. De Cesare, V. Fazio, and C. Colombo. "Resistance or pseudo-resistance?" European Psychiatry 65, S1 (June 2022): S370—S371. http://dx.doi.org/10.1192/j.eurpsy.2022.941.

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Introduction Treatment-Resistant Depression continues to represent a great challenge for clinicians. Objectives We investigated patients with history of resistance, assessing prognostic factors, response to treatments, and remission over time. Methods We recruited 202 unipolar and bipolar depressed inpatients. According to anamnestic backgrounds, patients were assigned to: A) Non-resistant : responders, with no characteristics of resistance in the current episode. B) Resistant: resistant to two antidepressant trials of adequate doses and duration. C) Pseudo-resistant : non-responders, not classifiable as Resistant because of inadequate trials. During hospitalization, patients were treated by clinical judgment, following a rehabilitation program. Results Table 1 Non-resistant (111) Resistant (54) Pseudo-resistant (35) p-value Age 59.1±11.9 63.0±12.6 57.0±11.3 0.036* Episodes of illness 3.8±2.1 4.0±1.9 3.0±1.8 0.036* Personality disorders 27.0% 18.9% 48.6% 0.009** Therapies: 0.014** SSRI 62.4% 40.4% 69.7% SNRI 19.8% 42.3% 15.1% TCA 17.8% 17.3% 15.1% Augmentation 24.3% 38.9% 17.1% 0.05** Remission 76.5% 59.5% 81.2% CvsB:0.045** CvsA:0.587** On the day of admission, non-responders were 44.5% of the sample, but 39.3% of them did not meet the Resistant criteria, defining the Pseudo-resistant group. Pseudo-resistant differed from others by younger age, fewer illness episodes, higher rate of personality disorders, and different therapies during hospitalization [Fig.1,2,3]. Pseudo-resistant remission rate, significantly greater than Resistant one, was comparable to Non-resistant [Tab.1]. *Kruskal-Wallis Test **Chi-Squared Test Conclusions This study outlines a new group of depressed patients that, apparently drug-resistant, displays the same outcome as responders when treated with first-line drugs during hospitalization, certainly taking benefit from the psychoeducational program. Quick recognition of these patients could be crucial to giving optimal care. Disclosure No significant relationships.

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32

Lovly, Christine M., Puneeth Iyengar, and Justin F. Gainor. "Managing Resistance to EFGR- and ALK-Targeted Therapies." American Society of Clinical Oncology Educational Book, no. 37 (May 2017): 607–18. http://dx.doi.org/10.1200/edbk_176251.

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Targeted therapies have transformed the management of non–small cell lung cancer (NSCLC) and placed an increased emphasis on stratifying patients on the basis of genetic alterations in oncogenic drivers. To date, the best characterized molecular targets in NSCLC are the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK). Despite steady advances in targeted therapies within these molecular subsets, however, acquired resistance to therapy is near universal. Recent preclinical models and translational efforts have provided critical insights into the molecular mechanisms of resistance to EGFR and ALK inhibitors. In this review, we present a framework for understanding resistance to targeted therapies. We also provide overviews of the molecular mechanisms of resistance and strategies to overcome resistance among EGFR-mutant and ALK-rearranged lung cancers. To date, these strategies have centered on the development of novel next-generation inhibitors, rationale combinations, and use of local ablative therapies, such as radiotherapy.

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33

Marchandet, Louise, Morgane Lallier, Céline Charrier, Marc Baud’huin, Benjamin Ory, and François Lamoureux. "Mechanisms of Resistance to Conventional Therapies for Osteosarcoma." Cancers 13, no. 4 (February 8, 2021): 683. http://dx.doi.org/10.3390/cancers13040683.

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Osteosarcoma (OS) is the most common primary bone tumor, mainly occurring in children and adolescents. Current standard therapy includes tumor resection associated with multidrug chemotherapy. However, patient survival has not evolved for the past decades. Since the 1970s, the 5-year survival rate is around 75% for patients with localized OS but dramatically drops to 20% for bad responders to chemotherapy or patients with metastases. Resistance is one of the biological processes at the origin of therapeutic failure. Therefore, it is necessary to better understand and decipher molecular mechanisms of resistance to conventional chemotherapy in order to develop new strategies and to adapt treatments for patients, thus improving the survival rate. This review will describe most of the molecular mechanisms involved in OS chemoresistance, such as a decrease in intracellular accumulation of drugs, inactivation of drugs, improved DNA repair, modulations of signaling pathways, resistance linked to autophagy, disruption in genes expression linked to the cell cycle, or even implication of the micro-environment. We will also give an overview of potential therapeutic strategies to circumvent resistance development.

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34

He, Boxue, Zhenyu Zhao, Qidong Cai, Yuqian Zhang, Pengfei Zhang, Shuai Shi, Hui Xie, et al. "miRNA-based biomarkers, therapies, and resistance in Cancer." International Journal of Biological Sciences 16, no. 14 (2020): 2628–47. http://dx.doi.org/10.7150/ijbs.47203.

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35

Lackner, Mark R., Timothy R. Wilson, and Jeff Settleman. "Mechanisms of acquired resistance to targeted cancer therapies." Future Oncology 8, no. 8 (August 2012): 999–1014. http://dx.doi.org/10.2217/fon.12.86.

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36

Jeught, Kevin Van der, Han-Chen Xu, Yu-Jing Li, Xiong-Bin Lu, and Guang Ji. "Drug resistance and new therapies in colorectal cancer." World Journal of Gastroenterology 24, no. 34 (September 14, 2018): 3834–48. http://dx.doi.org/10.3748/wjg.v24.i34.3834.

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37

Conway, Brian, and Bluma G. Brenner. "Can simplified antiretroviral drug combination therapies resist resistance?" AIDS 36, no. 11 (September 1, 2022): 1597–98. http://dx.doi.org/10.1097/qad.0000000000003308.

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38

Ward, Kurt E., David A. Fidock, and Jessica L. Bridgford. "Plasmodium falciparum resistance to artemisinin-based combination therapies." Current Opinion in Microbiology 69 (October 2022): 102193. http://dx.doi.org/10.1016/j.mib.2022.102193.

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39

Amer, Neveen. "Resistance to Targeted Therapies Against Adult Brain Cancers." Saudi Medical Journal 40, no. 11 (November 5, 2019): 1179. http://dx.doi.org/10.15537/smj.2019.11.24609.

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40

Baird, J. Kevin. "Resistance to Therapies for Infection by Plasmodium vivax." Clinical Microbiology Reviews 22, no. 3 (July 2009): 508–34. http://dx.doi.org/10.1128/cmr.00008-09.

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SUMMARY The gravity of the threat posed by vivax malaria to public health has been poorly appreciated. The widely held misperception of Plasmodium vivax as being relatively infrequent, benign, and easily treated explains its nearly complete neglect across the range of biological and clinical research. Recent evidence suggests a far higher and more-severe disease burden imposed by increasingly drug-resistant parasites. The two frontline therapies against vivax malaria, chloroquine and primaquine, may be failing. Despite 60 years of nearly continuous use of these drugs, their respective mechanisms of activity, resistance, and toxicity remain unknown. Although standardized means of assessing therapeutic efficacy against blood and liver stages have not been developed, this review examines the provisional in vivo, ex vivo, and animal model systems for doing so. The rationale, design, and interpretation of clinical trials of therapies for vivax malaria are discussed in the context of the nuance and ambiguity imposed by the hypnozoite. Fielding new drug therapies against real-world vivax malaria may require a reworking of the strategic framework of drug development, namely, the conception, testing, and evaluation of sets of drugs designed for the cure of both blood and liver asexual stages as well as the sexual blood stages within a single therapeutic regimen.

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41

Newman, Cory F. "Overcoming Resistance and Other Roadblocks in Cognitive Therapies." Contemporary Psychology: A Journal of Reviews 35, no. 9 (September 1990): 897–98. http://dx.doi.org/10.1037/029057.

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42

Lovly, Christine M., Puneeth Iyengar, and Justin F. Gainor. "Managing Resistance to EFGR- and ALK-Targeted Therapies." American Society of Clinical Oncology Educational Book 37 (2017): 607–18. http://dx.doi.org/10.14694/edbk_176251.

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43

Rimawi, Mothaffar F., Carmine De Angelis, and Rachel Schiff. "Resistance to Anti-HER2 Therapies in Breast Cancer." American Society of Clinical Oncology Educational Book, no. 35 (May 2015): e157-e164. http://dx.doi.org/10.14694/edbook_am.2015.35.e157.

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HER2 is amplified or overexpressed in 20% to 25% of breast cancers. HER2 is a redundant, robust, and powerful signaling pathway that represents an attractive therapeutic target. Anti-HER2 therapy in the clinic has resulted in significant improvements in patient outcomes and, in recent years, combinations of anti-HER2 therapies have been explored and carry great promise. However, treatment resistance remains a problem. Resistance can be mediated, among others, by pathway redundancy, reactivation, or the utilization of escape pathways. Understanding mechanisms of resistance can lead to better therapeutic strategies to overcome resistance and optimize outcomes.

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44

Hrvatin, Vanessa. "Combating antibiotic resistance: New drugs or alternative therapies?" Canadian Medical Association Journal 189, no. 37 (September 17, 2017): E1199. http://dx.doi.org/10.1503/cmaj.109-5469.

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45

Iwanami, Akio, Webster K. Cavenee, and Paul S. Mischel. "Arsenic reverses glioblastoma resistance to mTOR-targeted therapies." Cell Cycle 12, no. 10 (May 15, 2013): 1473–74. http://dx.doi.org/10.4161/cc.24747.

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46

Wood, Kris C. "Mapping the Pathways of Resistance to Targeted Therapies." Cancer Research 75, no. 20 (September 21, 2015): 4247–51. http://dx.doi.org/10.1158/0008-5472.can-15-1248.

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47

Hopper-Borge, Elizabeth A., Rochelle E. Nasto, Vladimir Ratushny, Louis M. Weiner, Erica A. Golemis, and Igor Astsaturov. "Mechanisms of tumor resistance to EGFR-targeted therapies." Expert Opinion on Therapeutic Targets 13, no. 3 (March 2009): 339–62. http://dx.doi.org/10.1517/14712590902735795.

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48

Navarro, Pilar, Neus Martínez-Bosch, Ada G. Blidner, and Gabriel A. Rabinovich. "Impact of Galectins in Resistance to Anticancer Therapies." Clinical Cancer Research 26, no. 23 (July 24, 2020): 6086–101. http://dx.doi.org/10.1158/1078-0432.ccr-18-3870.

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49

Tuma, Rabiya S. "How to overcome resistance to molecular targeted therapies." Oncology Times UK 8, no. 12 (December 2011): 8. http://dx.doi.org/10.1097/01.otu.0000410186.16930.82.

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50

Burdach, Stefan. "Molecular Precision Chemotherapy: Overcoming Resistance to Targeted Therapies?" Clinical Cancer Research 20, no. 5 (February 17, 2014): 1064–66. http://dx.doi.org/10.1158/1078-0432.ccr-13-3194.

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