Relevant bibliographies by topics / Drug resistance in cancer cells

Academic literature on the topic 'Drug resistance in cancer cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Drug resistance in cancer cells.'

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 "Drug resistance in cancer cells"

1

Cho, Heyrim, and Doron Levy. "The impact of competition between cancer cells and healthy cells on optimal drug delivery." Mathematical Modelling of Natural Phenomena 15 (2020): 42. http://dx.doi.org/10.1051/mmnp/2019043.

Full text
Abstract:
Cell competition is recognized to be instrumental to the dynamics and structure of the tumor-host interface in invasive cancers. In mild competition scenarios, the healthy tissue and cancer cells can coexist. When the competition is aggressive, competitive cells, the so called super-competitors, expand by killing other cells. Novel chemotherapy drugs and molecularly targeted drugs are commonly administered as part of cancer therapy. Both types of drugs are susceptible to various mechanisms of drug resistance, obstructing or preventing a successful outcome. In this paper, we develop a cancer growth model that accounts for the competition between cancer cells and healthy cells. The model incorporates resistance to both chemotherapy and targeted drugs. In both cases, the level of drug resistance is assumed to be a continuous variable ranging from fully-sensitive to fully-resistant. Using our model we demonstrate that when the competition is moderate, therapies using both drugs are more effective compared with single drug therapies. However, when cancer cells are highly competitive, targeted drugs become more effective. The results of the study stress the importance of adjusting the therapy to the pre-treatment resistance levels. We conclude with a study of the spatiotemporal propagation of drug resistance in a competitive setting, verifying that the same conclusions hold in the spatially heterogeneous case.
APA, Harvard, Vancouver, ISO, and other styles
2

Zhao, Ziyi, Yong Mei, Ziyang Wang, and Weiling He. "The Effect of Oxidative Phosphorylation on Cancer Drug Resistance." Cancers 15, no. 1 (December 22, 2022): 62. http://dx.doi.org/10.3390/cancers15010062.

Full text
Abstract:
Recent studies have shown that oxidative phosphorylation (OXPHOS) is a target for the effective attenuation of cancer drug resistance. OXPHOS inhibitors can improve treatment responses to anticancer therapy in certain cancers, such as melanomas, lymphomas, colon cancers, leukemias and pancreatic ductal adenocarcinoma (PDAC). However, the effect of OXPHOS on cancer drug resistance is complex and associated with cell types in the tumor microenvironment (TME). Cancer cells universally promote OXPHOS activity through the activation of various signaling pathways, and this activity is required for resistance to cancer therapy. Resistant cancer cells are prevalent among cancer stem cells (CSCs), for which the main metabolic phenotype is increased OXPHOS. CSCs depend on OXPHOS to survive targeting by anticancer drugs and can be selectively eradicated by OXPHOS inhibitors. In contrast to that in cancer cells, mitochondrial OXPHOS is significantly downregulated in tumor-infiltrating T cells, impairing antitumor immunity. In this review, we summarize novel research showing the effect of OXPHOS on cancer drug resistance, thereby explaining how this metabolic process plays a dual role in cancer progression. We highlight the underlying mechanisms of metabolic reprogramming in cancer cells, as it is vital for discovering new drug targets.
APA, Harvard, Vancouver, ISO, and other styles
3

NM, Nandini. "Cancer Stem Cells and Drug Resistance." Acta Scientific Cancer Biology 4, no. 6 (May 27, 2020): 12–18. http://dx.doi.org/10.31080/ascb.2020.04.0228.

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

Marx, J. "Drug resistance of cancer cells probed." Science 234, no. 4778 (November 14, 1986): 818–20. http://dx.doi.org/10.1126/science.2877493.

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

Leary, Meghan, Sarah Heerboth, Karolina Lapinska, and Sibaji Sarkar. "Sensitization of Drug Resistant Cancer Cells: A Matter of Combination Therapy." Cancers 10, no. 12 (December 4, 2018): 483. http://dx.doi.org/10.3390/cancers10120483.

Full text
Abstract:
Cancer drug resistance is an enormous problem. It is responsible for most relapses in cancer patients following apparent remission after successful therapy. Understanding cancer relapse requires an understanding of the processes underlying cancer drug resistance. This article discusses the causes of cancer drug resistance, the current combination therapies, and the problems with the combination therapies. The rational design of combination therapy is warranted to improve the efficacy. These processes must be addressed by finding ways to sensitize the drug-resistant cancers cells to chemotherapy, and to prevent formation of drug resistant cancer cells. It is also necessary to prevent the formation of cancer progenitor cells by epigenetic mechanisms, as cancer progenitor cells are insensitive to standard therapies. In this article, we emphasize the role for the rational development of combination therapy, including epigenetic drugs, in achieving these goals.
APA, Harvard, Vancouver, ISO, and other styles
6

Wtorek, Karol, Angelika Długosz, and Anna Janecka. "Drug resistance in topoisomerase-targeting therapy." Postępy Higieny i Medycyny Doświadczalnej 72 (December 21, 2018): 1073–83. http://dx.doi.org/10.5604/01.3001.0012.8131.

Full text
Abstract:
Drug resistance is a well-known phenomenon that occurs when initially responsive to chemotherapy cancer cells become tolerant and elude further effectiveness of anticancer drugs. Based on their mechanism of action, anticancer drugs can be divided into cytotoxic-based agents and target-based agents. An important role among the therapeutics of the second group is played by drugs targeting topoisomerases, nuclear enzymes critical to DNA function and cell survival. These enzymes are cellular targets of several groups of anticancer agents which generate DNA damage in rapidly proliferating cancer cells. Drugs targeting topoisomerase I are mostly analogs of camtothecin, a natural compound isolated from the bark of a tree growing in China. Drugs targeting topoisomerase II are divided into poisons, such as anthracycline antibiotics, whose action is based on intercalation between DNA bases, and catalytic inhibitors that block topoisomerase II at different stages of the catalytic cycle. Unfortunately, chemotherapy is often limited by the induction of drug resistance. Identifying mechanisms that promote drug resistance is critical for the improvement of patient prognosis. Cancer drug resistance is a complex phenomenon that may be influenced by many factors. Here we discuss various mechanisms by which cancer cells can develop resistance to topoisomerase-directed drugs, which include enhanced drug efflux, mutations in topoisomerase genes, hypophosphorylation of topoisomerase II catalytic domain, activation of NF-κB transcription factor and drug inactivation. All these events may lead to the ineffective induction of cancer cell death. Attempts at circumventing drug resistance through the inhibition of cellular efflux pumps, use of silencing RNAs or inhibition of some important mechanisms, which can allow cancer cells to survive therapy, are also presented.
APA, Harvard, Vancouver, ISO, and other styles
7

Altamura, Concetta, Paola Gavazzo, Michael Pusch, and Jean-François Desaphy. "Ion Channel Involvement in Tumor Drug Resistance." Journal of Personalized Medicine 12, no. 2 (February 3, 2022): 210. http://dx.doi.org/10.3390/jpm12020210.

Full text
Abstract:
Over 90% of deaths in cancer patients are attributed to tumor drug resistance. Resistance to therapeutic agents can be due to an innate property of cancer cells or can be acquired during chemotherapy. In recent years, it has become increasingly clear that regulation of membrane ion channels is an important mechanism in the development of chemoresistance. Here, we review the contribution of ion channels in drug resistance of various types of cancers, evaluating their potential in clinical management. Several molecular mechanisms have been proposed, including evasion of apoptosis, cell cycle arrest, decreased drug accumulation in cancer cells, and activation of alternative escape pathways such as autophagy. Each of these mechanisms leads to a reduction of the therapeutic efficacy of administered drugs, causing more difficulty in cancer treatment. Thus, targeting ion channels might represent a good option for adjuvant therapies in order to counteract chemoresistance development.
APA, Harvard, Vancouver, ISO, and other styles
8

De Conti, Giulia, Matheus Henrique Dias, and René Bernards. "Fighting Drug Resistance through the Targeting of Drug-Tolerant Persister Cells." Cancers 13, no. 5 (March 5, 2021): 1118. http://dx.doi.org/10.3390/cancers13051118.

Full text
Abstract:
Designing specific therapies for drug-resistant cancers is arguably the ultimate challenge in cancer therapy. While much emphasis has been put on the study of genetic alterations that give rise to drug resistance, much less is known about the non-genetic adaptation mechanisms that operate during the early stages of drug resistance development. Drug-tolerant persister cells have been suggested to be key players in this process. These cells are thought to have undergone non-genetic adaptations that enable survival in the presence of a drug, from which full-blown resistant cells may emerge. Such initial adaptations often involve engagement of stress response programs to maintain cancer cell viability. In this review, we discuss the nature of drug-tolerant cancer phenotypes, as well as the non-genetic adaptations involved. We also discuss how malignant cells employ homeostatic stress response pathways to mitigate the intrinsic costs of such adaptations. Lastly, we discuss which vulnerabilities are introduced by these adaptations and how these might be exploited therapeutically.
APA, Harvard, Vancouver, ISO, and other styles
9

Puris, Elena, Gert Fricker, and Mikko Gynther. "The Role of Solute Carrier Transporters in Efficient Anticancer Drug Delivery and Therapy." Pharmaceutics 15, no. 2 (January 21, 2023): 364. http://dx.doi.org/10.3390/pharmaceutics15020364.

Full text
Abstract:
Transporter-mediated drug resistance is a major obstacle in anticancer drug delivery and a key reason for cancer drug therapy failure. Membrane solute carrier (SLC) transporters play a crucial role in the cellular uptake of drugs. The expression and function of the SLC transporters can be down-regulated in cancer cells, which limits the uptake of drugs into the tumor cells, resulting in the inefficiency of the drug therapy. In this review, we summarize the current understanding of low-SLC-transporter-expression-mediated drug resistance in different types of cancers. Recent advances in SLC-transporter-targeting strategies include the development of transporter-utilizing prodrugs and nanocarriers and the modulation of SLC transporter expression in cancer cells. These strategies will play an important role in the future development of anticancer drug therapies by enabling the efficient delivery of drugs into cancer cells.
APA, Harvard, Vancouver, ISO, and other styles
10

Valinezhad Sani, Fatemeh, Abbasali Palizban, Fatemeh Mosaffa, and Khadijeh Jamialahmadi. "Glucosamine attenuates drug resistance in Mitoxantrone-resistance breast cancer cells." Journal of Pharmacy and Pharmacology 73, no. 7 (April 22, 2021): 922–27. http://dx.doi.org/10.1093/jpp/rgaa032.

Full text
Abstract:
Abstract Objectives This study was aimed at investigating the cytotoxicity and multi-drug resistance (MDR) reversal effect of Glucosamine (GlcN) on resistant BCRP-overexpressing breast cancer MCF-7/MX cells. Methods After confirming the overexpression of BCRP, the cytotoxicity and MDR reversing potential of GlcN on MCF-7/MX mitoxantrone-resistant and MCF-7 sensitive breast cancer cells were assessed via MTT assay. The effects of GlcN on mitoxantrone accumulation were analyzed through flow cytometry. Finally, the expression of BCRP and Epithelial-Mesenchymal Transition (EMT)-related markers following the exposure to GlcN were assessed by real-time RT-PCR. Key findings This study showed that glucosamine had an inhibitory effect on the proliferation of human breast cancer cells. The respective IC50 values for MCF-7/MX cells following exposure to mitoxantrone (MX) in the presence of GlcN (0, 0.5 and 1 mm) for 72 h were 3.61 ± 0.21, 0.598 ± 0.041 and 0.284 ± 0.016 μm, respectively. Furthermore, GlcN reduced the expression of BCRP mRNA without any significant effect on EMT-related markers in breast cancer cells. Conclusions These results proposed that glucosamine as a natural sugar could down regulate the BCRP expression and increased MX cytotoxicity in breast cancer cells.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Drug resistance in cancer cells"

1

Stordal, Britta Kristina. "Regrowth resistance in platinum-drug resistant small cell lung cancer cells." Bill Walsh Cancer Research Laboratories, Royal North Shore Hospital and The University of Sydney, 2007. http://hdl.handle.net/2123/2467.

Full text
Abstract:
Doctor of Philosophy (PhD)
The H69CIS200 cisplatin-resistant and H69OX400 oxaliplatin-resistant cell lines developed as part of this study, are novel models of low-level platinum resistance. These resistant cell lines do not have common mechanisms of platinum resistance such as increased expression of glutathione or decreased platinum accumulation. Rather, these cell lines have alterations in their cell cycle allowing them to proliferate rapidly post drug treatment in a process known as ‘regrowth resistance’. This alteration in cell cycle control has come at the expense of DNA repair capacity. The resistant cell lines show a decrease in nucleotide excision repair and homologous recombination repair, the reverse of what is normally associated with platinum resistance. The alterations in these DNA repair pathways help signal the G1/S checkpoint to allow the cell cycle to progress despite the presence of DNA damage. The decrease in DNA repair capacity has also contributed to the development of chromosomal alterations in the resistant cell lines. Similarities in chromosomal change between the two platinum resistant cell lines have been attributed to inherent vulnerabilities in the parental H69 cells rather than part of the mechanism of resistance. The H69CIS200 and H69OX400 resistant cells are cross-resistant to both cisplatin and oxaliplatin. This demonstrates that oxaliplatin does not have increased activity in low-level cisplatin-resistant cancer. Oxaliplatin resistance also developed more rapidly than cisplatin resistance suggesting that oxaliplatin may be less effective than cisplatin in the treatment of SCLC. The resistant cell lines have also become hypersensitive to taxol but show no alterations in the expression, polymerisation or morphology of tubulin. Rather, the PI3K/Akt/mTOR pathway is involved in both platinum resistance and taxol sensitivity as both are reversed with rapamycin treatment. mTOR is also phosphorylated in the resistant cell lines indicating that platinum resistance is associated with an increase in activity of this pathway. The mechanism of regrowth resistance in the platinum-resistant H69CIS200 and H69OX400 cells is a combination of activation of PI3K/Akt/mTOR signalling and alterations in control of the G1/S cell cycle checkpoint. However, more work remains to determine which factors in these pathways are governing this novel mechanism of platinum resistance.
APA, Harvard, Vancouver, ISO, and other styles
2

Stordal, Britta. "Regrowth resistance in platinum-drug resistant small cell lung cancer cells." Connect to full text, 2006. http://hdl.handle.net/2123/2467.

Full text
Abstract:
Thesis (Ph. D.)--University of Sydney, 2007.
Title from title screen (viewed 10 June 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Medicine, Faculty of Medicine. Degree awarded 2007; thesis submitted 2006. Includes bibliographical references. Also available in print form.
APA, Harvard, Vancouver, ISO, and other styles
3

Richardson, Julie. "Ovarian cancer stem-like cells and drug resistance." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/8009/.

Full text
Abstract:
Ovarian cancer is characterised by late diagnosis, relatively poor survival and high recurrence due to the development of multidrug resistance (MDR – resistance to various types of drug). Cancer stem-like cells (CSCs) are thought to contribute to drug resistance due to the over-expression of ABC transporters which efflux chemotherapeutic drugs. Frequently overexpressed ABC transporters include Multidrug resistance protein 1 (MRP1), P-glycoprotein (Pgp) and Breast cancer resistance protein (BCRP). No definitive stem cell marker panel has been determined for ovarian CSC detection; investigation of multiple putative stem cell markers (CD133, CD24, CD44 and Aldehyde dehydrogenase (ALDH)) may prove beneficial to the identification of these cells. All three ABC transporters are heterogeneously expressed in the ovarian cancer cell lines studied. Functional MRP1 and Pgp activity was identified utilising the Calcein-AM assay. Stem cell markers CD133 and ALDH were undetectable by western blot (WB). However small populations of ALDH expressing cells were detected using the ALDEFLUOR™ assay. Low-level CD44 was observed by WB, and confirmed by IF. RT-qPCR and microarray analysis confirmed the gene expression of all three ABC transporters and stem cell markers. A potential CSC population of high Hoechst effluxing cells, called a side population (SP) was identified. However, the viability of the SP was greatly reduced. Chemotherapeutic resistance to carboplatin, paclitaxel and doxorubicin was determined in ovarian cancer cell lines. The ovarian cancer cell line 1847 supports CSC and MDR theories, showing greater colony and spheroid formation and is most resistant to chemotherapeutics. Heterogeneous ABC transporter and stem cell marker expression was confirmed in primary samples. IHC analysis confirmed marker expression was not correlated with patient survival. Correlations were observed between MRP1 and CD44 and ALDH, CD44 and Pgp, BCRP and ALDH expression. Cells derived from patient ascites were also capable of forming colonies and spheroids, indicative of CSC properties.
APA, Harvard, Vancouver, ISO, and other styles
4

Davidson, Scott M. "Analysis of prognostic and drug resistance markers in lung cancer." Connect to e-thesis, 2007. http://theses.gla.ac.uk/101/.

Full text
Abstract:
Thesis (M.D.) - University of Glasgow, 2007.
M.D. thesis submitted to the Centre for Oncology and Applied Pharmacology, Cancer Research UK Beatson Laboratories, University of Glasgow, 2007. Includes bibliographical references. Print version also available.
APA, Harvard, Vancouver, ISO, and other styles
5

Anthoney, David Alan. "Defective mismatch repair and cisplatin resistance in ovarian cancer cells." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363161.

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

Fung, Kwong-lam, and 馮廣林. "Chemoresistance induced by mesenchymal stromal cells on cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/205639.

Full text
Abstract:
Human mesenchymal stromal cells (hMSCs) are part of bone marrow micro-environment that supports hematopoiesis. However, hMSCs also enhance tumor progression and survival when they become part of the cancer micro-environment. I aimed to investigate the interaction between hMSCs and cancer cells during chemotherapy. Firstly, I studied the interaction between hMSCs and T-lineage acute lymphoblastic leukemia (T-ALL) cells under pegylated arginase I (BCT-100) treatment. Three T-ALL cell lines were sensitive to BCT-100 but not hMSCs. Conversely, hMSCs could partly protect all T-ALL cell lines from BCT-100 induced cell death under transwell co-culture condition. Concerning the possible mechanism, the intermediate metabolite L-ornithine could not rescue most T-ALL cells from BCT-100 treatment. But the downstream L-arginine precursor, L-citrulline could partly rescue all T-ALL cells from BCT-100 treatment. Ornithine transcarbamylase (OTC) converts L-ornithine into L-citrulline. OTC expression level in hMSCs remained relatively high during BCT-100 treatment but OTC expressions in T-ALL cell lines declined drastically. It suggested that hMSCs may protect T-ALL cells against BCT-100 treatment by having sustained OTC expression. Suppression of hMSCs by vincristine (VCR) disrupted the protective effect of hMSCs to most T-ALL cells during BCT-100 treatment. This suggests that by transiently suppressing hMSCs, we may abolish the protective effect of hMSCs to T-ALL cells during BCT-100 treatment. Then I studied the interaction between hMSCs and neuroblastoma under cisplatin treatment. Two neuroblastoma cell lines were used for both of them are cisplatin sensitive while hMSCs are cisplatin resistant. hMSCs could partly protect neuroblastoma cells from cisplatin induced cytotoxicity. On the other hand, exogenous IL-6 but not IL-8 could also partly rescue them from cisplatin induced cytotoxicity. IL-6 activated STAT3 phosphorylation dose-dependently and enhanced expression of detoxifying enzyme (glutathione S-transferase π, GST-π) in neuroblastoma. Such effect could be counteracted by anti-IL-6R neutralizing antibody tocilizumab (TCZ). However, TCZ failed to suppress hMSCs’ protection to neuroblastoma during cisplatin treatment. This suggests involvement of multiple factors. Up-regulation of serum GST-πin some hTertMSCs/neuroblastoma co-engrafted SCID mice compared to neuroblastoma engrafted mice provided a clue that GST-π might be a possible stromal-protection factor. Caffeic acid phenethyl ester (CAPE) is a known GST inhibitor after tyrosinase activation. Neuroblastoma cells expressed tyrosinase and CAPE enhanced cisplatin cytotoxicity on them, with or without hMSCs. Paradoxically, CAPE enhanced GST-πexpression with or without cisplatin treatment in neuroblastoma suggesting possible negative feedback to GST-π inhibition. However, such additive effect of CAPE to cisplatin cytotoxicity was not observed in vivo. Further delineation of the in vivo study design may help to verify the additive effect of CAPE to cisplatin cytotoxicity in vivo. Finally, I studied the effect of apoptotic cancer cells (AC) on the immune function of hMSCs. hMSCs could phagocytose apoptotic neuroblastoma cells with respective up-regulation of many immune-mediators including two highly-expressed cytokines IL-6 and IL-8. Up-regulation of these immune-mediators may enhance immune cells chemotaxis. Further detailed investigation on the effect of AC-engulfed hMSCs to other immune cells will help us to understand the dynamic interaction between cancer cells and stromal cells during chemotherapy.
published_or_final_version
Paediatrics and Adolescent Medicine
Doctoral
Doctor of Philosophy
APA, Harvard, Vancouver, ISO, and other styles
7

Strong, Rachael F. "A comparative proteomic analysis of mitochondrial proteins from drug susceptible and drug resistant human MCF-7 breast cancer cells." College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/2870.

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

Vlerken, Lilian Emilia van. "Modulation of multidrug resistance in cancer using polymer-blend nanoparticles : thesis /." Diss., View dissertation online, 2008. http://hdl.handle.net/2047/d10017355.

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

Windsor, James Brian. "Establishing a role for ecto-phosphatase in drug resistance /." Digital version accessible at:, 2000. http://wwwlib.umi.com/cr/utexas/main.

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

Timme, Cindy R. "Drug Resistance Mechanisms to Gamma-secretase Inhibitors in Human Colon Cancer Cells." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4954.

Full text
Abstract:
Colorectal cancer is the third leading cause of cancer-related mortality. Much progress has been achieved in combating this disease with surgical resection and chemotherapy in combination with targeted drugs. However, most metastatic patients develop drug resistance so new modalities of treatment are needed. Notch signaling plays a vital role in intestinal homeostasis, self-renewal, and cell fate decisions during post-development and is activated in colorectal adenocarcinomas. Under debate is its role in carcinomas and metastatic disease. In theory, blocking Notch activation using gamma-secretase inhibitors (GSIs) may show efficacy alone or in combination with chemotherapy in the treatment of colon cancer. In Chapter Three, we tested the capacity for GSIs to synergize with oxaliplatin in colon cancer cell lines and evaluated the underlying molecular mechanisms. GSI alone had no effect on colon cancer cell lines. Surprisingly, we show that GSIs blocked oxaliplatin-induced apoptosis through increased protein levels of the anti-apoptotic Bcl-2 proteins Mcl-1 and/or Bcl-xL. Restoration of apoptosis was achieved by blocking Mcl-1 and/or Bcl-xL with obatoclax (an anti-apoptotic Bcl-2 agonist) or siRNA. An unexpected result was the induction of cell death with the combination of GSI and obatoclax. In Chapter Four, we examined the mechanism of GSI + obatoclax-mediated cell death. We found that apoptosis played a minimal role. Rather, we identified blockage of cytoprotective autophagy played a causative role. Interestingly, we also saw autophagy induction in GSI-treated cells, which could explain the insensitivity of colon cancer cells to GSI. When autophagy was blocked in GSI-treated cells, cells became sensitive to GSI and cell death was elicited. The mechanism by which induction of autophagy occurs in GSI- treated cells is an area for further research. Overall, our work questions the validity of the use of GSIs in the treatment of colorectal cancers. We show that GSIs may block apoptosis and induce cytoprotective autophagy simultaneously, resulting in increased drug resistance and cellular survival. Whether these two cellular survival processes occurs in patients needs to be examined before GSIs can be utilized in a clinical setting. If so, these two hurdles must be overcome.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Drug resistance in cancer cells"

1

Dr, Mehta Kapil, and Siddik Zahid H, eds. Drug resistance in cancer cells. New York, NY: Springer, 2009.

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

Siddik, Zahid H., and Kapil Mehta, eds. Drug Resistance in Cancer Cells. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4.

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

N, Hait William, ed. Drug resistance. Boston: Kluwer Academic Publishers, 1996.

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

Multi-drug resistance in cancer. Totowa, N.J: Humana, 2010.

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

Verrite, Ethan G. Drug resistant neoplasms. New York: Nova Science Publishers, 2009.

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

F, Ozols Robert, ed. Drug resistance in cancer therapy. Boston: Kluwer Academic Publishers, 1989.

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

D, Tew Kenneth, and Woolley Paul V. 1939-, eds. Mechanisms of drug resistance in neoplastic cells. Orlando: Academic Press, 1987.

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

1949-, Bernal Samuel D., ed. Drug resistance in oncology. New York: M. Dekker, 1997.

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

Börje, Andersson, and Murray David Ph D, eds. Clinically relevant resistance in cancer chemotherapy. Boston: Kluwer Academic, 2002.

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

1952-, Teicher Beverly A., ed. Drug resistance in oncology. New York: Dekker, 1993.

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

Book chapters on the topic "Drug resistance in cancer cells"

1

Barbarotto, Elisa, and George A. Calin. "MicroRNAs and Drug Resistance." In Drug Resistance in Cancer Cells, 257–70. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_11.

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

Fan, Dominic, Sun-Jin Kim, Robert L. Langley, and Isaiah J. Fidler. "Metastasis and Drug Resistance." In Drug Resistance in Cancer Cells, 21–52. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_2.

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

Troester, Melissa A., Jason I. Herschkowitz, and Katherine A. Hoadley. "Molecular Signatures of Drug Resistance." In Drug Resistance in Cancer Cells, 271–94. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_12.

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

Chan, Marion M., and Dunne Fong. "Overcoming Drug Resistance by Phytochemicals." In Drug Resistance in Cancer Cells, 315–42. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_14.

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

Hodkinson, P. S., and Tariq Sethi. "Extracellular Matrix-Mediated Drug Resistance." In Drug Resistance in Cancer Cells, 115–35. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_6.

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

Ozpolat, Bulent. "Resistance to Differentiation Therapy." In Drug Resistance in Cancer Cells, 233–55. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_10.

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

Szakács, Gergely, Kenneth Kin Wah, Orsolya Polgár, Robert W. Robey, and Susan E. Bates. "Multidrug Resistance Mediated by MDR-ABC Transporters." In Drug Resistance in Cancer Cells, 1–20. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_1.

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

Charnley, Natalie, Catharine West, and Pat Price. "Assessment of Drug Resistance in Anticancer Therapy by Nuclear Imaging." In Drug Resistance in Cancer Cells, 295–313. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_13.

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

Yokoyama, Tomohisa, Yasuko Kondo, Oliver Bögler, and Seiji Kondo. "The Role of Autophagy and Apoptosis in the Drug Resistance of Cancer." In Drug Resistance in Cancer Cells, 53–71. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_3.

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

Baker, Stacey J., and E. Premkumar Reddy. "Mechanisms of Resistance to Targeted Tyrosine Kinase Inhibitors." In Drug Resistance in Cancer Cells, 73–93. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_4.

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

Conference papers on the topic "Drug resistance in cancer cells"

1

Khamenehfar, Avid, Ji Liu, Jia Cai, Michael Wong, Paul C. H. Li, Patrick Ling, and Pamela Russell. "Drug Accumulation Into Single Drug-Sensitive and Drug-Resistant Prostate Cancer Cells Conducted on the Single Cell Bioanalyzer." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-36166.

Full text
Abstract:
Multidrug resistance (MDR) occurs in prostate cancer, and this happens when the cancer cells resist chemotherapeutic drugs by pumping them out of the cells. MDR inhibitors such as cyclosporin A (CsA) can stop the pumping and enhance the drugs accumulated in the cells. The cellular drug accumulation is monitored using a microfluidic chip mounted on a single cell bioanalyzer. This equipment has been developed to measure accumulation of drugs such as doxorubicin (DOX) and fluorescently labeled paclitaxel (PTX) in single prostate cancer cells. The inhibition of drug efflux on the same prostate cell was examined in drug-sensitive and drug-resistant cells. Accumulation of these drug molecules was not found in the MDR cells, PC-3 RX-DT2R cells. Enhanced drug accumulation was observed only after treating the MDR cell in the presence of 5 μM of CsA as the MDR inhibitor. We envision this monitoring of the accumulation of fluorescent molecules (drug or fluorescent molecules), if conducted on single patient cancer cells, can provide information for clinical monitoring of patients undergoing chemotherapy in the future.
APA, Harvard, Vancouver, ISO, and other styles
2

Teo, Ka Yaw, and Bumsoo Han. "Freezing-Assisted Intracellular Drug Delivery to Multi-Drug Resistant Cancer Cells." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192373.

Full text
Abstract:
The efficacy of chemotherapy is significantly impaired by multi-drug resistance (MDR) of cancer cells. The mechanism of MDR is associated with the overexpression of certain ATP-binding cassette protein transporters in plasma membranes. These transporters actively keep intracellular drug concentration below the cell-killing threshold by extruding cytotoxic drugs. Various strategies to overcome MDR have been proposed and have shown promising results at the laboratory level. However, pharmacokinetic alteration of co-administered anticancer agents reduces their clinical effectiveness. This leads to increased toxicity and undesirable side effects at effective concentrations [1]. Hence, a clinically feasible strategy to overcome the phenomenon of MDR is highly desired.
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Yuchun, and Paul C. H. Li. "Real-Time Measurement of Chemotherapeutic Drug Transport in an Individual Cancer Cell Selected in a Microfluidic Biochip." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18112.

Full text
Abstract:
Multidrug resistance (MDR) is a significant obstacle to effective chemotherapy to many patients. Because of the overexpression of one membrane protein, P-glycoprotein (P-gp), there is an increased efflux of chemotherapeutic drug in the resistant cancer cells. The main research goal of MDR study is to get improved intracellular drug retention inside the cancer cells. So it is important to study the chemotherapeutic drug transport in the cancer cells. In this work, single leukemia CEM MDR cell has been isolated and captured by a microfluidic single-cell biochip for drug transport and retention study.
APA, Harvard, Vancouver, ISO, and other styles
4

Gründing, Anna, Beatriz Martinez-Delgado, Bin Liu, David Deluca, Sabine Wrenger, Tobias Welte, and Sabina Janciauskiene. "Lipid-related anti-cancer drug resistance of lung adenocarcinoma cells." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa1118.

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

Leu, Yu-Wei, Mei-Yu Pai, Chia-Chen Hsu, Kuan-Der Lee, Chih-Cheng Chen, Yao-Li Chen, Tim H. M. Huang, and Shu-Huei Hsiao. "Abstract 603: TargetedCasp8AP2methylation increased drug resistance in mesenchymal stem cell and cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-603.

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

Lichtenfels, Martina, Camila Alves Silva, Caroline Brunetto Farias, Alessandra Borba Anton Souza, and Antônio Luiz Frasson. "TIN VITRO BREAST CANCER CHEMORESISTANCE TEST." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1058.

Full text
Abstract:
Introduction: Tumor resistance is the main cause of treatment failure leading to cancer progression and is classified into intrinsic and acquired resistance. Intrinsic resistance is related to a preexisting condition and acquired resistance is induced by a drug. Some methods are already available worldwide to assess drug resistance, however, in Brazil no in vitro chemoresistance test for cancer is validated for clinic use. Objectives: The aim of our study was to validate the in vitro chemoresistance test Chemobiogram for the drugs used in breast cancer (BC) treatment. An incomplete response to neoadjuvant treatment was used to validate the results at a short-term follow-up and treatment after primary BC will be used to validate the test in a long-term follow-up. Methods: Patients with invasive breast cancer were included in this initial report. Fresh tumor samples were collected during surgery and subsequently dissociated to obtain tumor cells. The tumor cells were cultured in a 96 well plate with the several drugs used for BC treatment, including cytotoxic, hormonal, antiHER2, and target therapies, and after 72 hours, cell viability was evaluated. The test result is defined based on cell viability as low (60%) resistance. The test result is compared to the patient`s response to the treatment. Results: To validate the dissociation and BC primary culture techniques we collected samples from six patients with in situ and invasive tumors. These samples were not tested in Chemobiogram. Samples from five BC patients undergoing neoadjuvant treatment and from three patients with primary BC were tested in the Chemobiogram. Of the five patients who underwent neoadjuvant treatment, two performed hormone therapy and three underwent chemotherapy. Four patients presented incomplete response to the treatment and one patient who underwent neoadjuvant chemotherapy presented disease progression during treatment. The chemoresistance test was able to demonstrate medium to high resistance for the drugs used in the neoadjuvant treatments (acquired resistance). The three patients with primary BC were diagnosed with Luminal tumors-HER2 negative. In the chemoresistance test all samples presented medium to high resistance to anti-HER2 drugs (intrinsic resistance) and low to medium resistance to cytotoxic drugs. These patients will be followed in the long term to compare patient outcomes with the test results. Conclusions: The primary culture of breast tumors was efficiently established and the preliminary result of the chemoresistance test was in accordance with the outcomes from five patients who underwent neoadjuvant treatment. This preliminary finding showed the capacity of the Chemobriogram to demonstrate drug resistance in accordance with the clinic and highlighted the importance of the in vitro chemoresistance test to avoid the use of inefficient drugs, improving and personalizing breast cancer treatment.
APA, Harvard, Vancouver, ISO, and other styles
7

Mittal, M., K. Singh, and G. Chaudhuri. "Mechanisms of SLUG-Induced Drug Resistance Development in Breast Cancer Cells." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1128.

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

Kulsum, Safeena, Sindhu VG, Ramanan Somasundara Pandian, Debashish Das, Binay Panda, Wesley Hicks, Mukund Seshadri, Moni Abraham Kuriakose, and Amritha Suresh. "Abstract A08: Cancer stem cell-like cells in drug resistance of head and neck squamous cell carcinoma." In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-a08.

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

Muthu, M., and A. Nordstrom. "PO-249 GLUL knockdown induces drug resistance in non-small cell lung cancer cells." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.282.

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

Luty, M., K. Piwowarczyk, T. Wróbel, D. Ryszawy, A. Łabędź-MasŁowska, M. Rak, Z. Madeja, and J. Czyż. "PO-235 Fenofibrate overcomes the drug-resistance of human prostate cancer cells." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.269.

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

Reports on the topic "Drug resistance in cancer cells"

1

Fong, E. J., H. Gemeda, N. Hum, M. Simon, and T. J. Ognibene. Catching Villains: Finding single cells responsible for cancer drug resistance and metastasis. Office of Scientific and Technical Information (OSTI), October 2019. http://dx.doi.org/10.2172/1571745.

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

Lekostaj, Jacqueline K. The Role of ABC Proteins in Drug Resistant Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada485613.

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

Pleeter, Perri, and Jacqueline K. Lekostaj. The Role of ABC Proteins in Drug Resistant Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada504701.

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

Lekostaj, Jacqueline K. The Role of ABC Proteins in Drug-Resistant Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470298.

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

Shen, Youqing, Maciej Radosz, and William J. Murdoch. Breast Cancer-Targeted Nuclear Drug Delivery Overcoming Drug Resistance for Breast Cancer Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada559246.

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

Hiscott, John. Oncolytic Virotherapy Targeting Lung Cancer Drug Resistance. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada589848.

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

Sikic, Branimir I. Paclitaxel (Taxol) Resistance in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 1996. http://dx.doi.org/10.21236/ada326396.

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

Wang, Zhaoyi, Hao Deng, XinTian Zhang, and GuanGuan Li. Breast Cancer Stem Cells in Antiestrogen Resistance. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada566767.

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

Wang, Zhaoyi, Hao Deng, and MingXi Guo. Breast Cancer Stem Cells in Antiestrogen Resistance. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada586468.

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

Sikic, Branimir I. Paclitaxel (Taxol) Resistance in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada392688.

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