Relevant bibliographies by topics / Cancer drug resistance, tumor metabolism

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  2. Dissertations / Theses
  3. Books
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  5. Conference papers
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Academic literature on the topic 'Cancer drug resistance, tumor metabolism'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Cancer drug resistance, tumor metabolism"

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Yoo, Hee-Chan, and Jung-Min Han. "Amino Acid Metabolism in Cancer Drug Resistance." Cells 11, no. 1 (January 2, 2022): 140. http://dx.doi.org/10.3390/cells11010140.

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Despite the numerous investigations on resistance mechanisms, drug resistance in cancer therapies still limits favorable outcomes in cancer patients. The complexities of the inherent characteristics of tumors, such as tumor heterogeneity and the complicated interaction within the tumor microenvironment, still hinder efforts to overcome drug resistance in cancer cells, requiring innovative approaches. In this review, we describe recent studies offering evidence for the essential roles of amino acid metabolism in driving drug resistance in cancer cells. Amino acids support cancer cells in counteracting therapies by maintaining redox homeostasis, sustaining biosynthetic processes, regulating epigenetic modification, and providing metabolic intermediates for energy generation. In addition, amino acid metabolism impacts anticancer immune responses, creating an immunosuppressive or immunoeffective microenvironment. A comprehensive understanding of amino acid metabolism as it relates to therapeutic resistance mechanisms will improve anticancer therapeutic strategies.
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Chen, Xun, Shangwu Chen, and Dongsheng Yu. "Metabolic Reprogramming of Chemoresistant Cancer Cells and the Potential Significance of Metabolic Regulation in the Reversal of Cancer Chemoresistance." Metabolites 10, no. 7 (July 16, 2020): 289. http://dx.doi.org/10.3390/metabo10070289.

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Metabolic reprogramming is one of the hallmarks of tumors. Alterations of cellular metabolism not only contribute to tumor development, but also mediate the resistance of tumor cells to antitumor drugs. The metabolic response of tumor cells to various chemotherapy drugs can be analyzed by metabolomics. Although cancer cells have experienced metabolic reprogramming, the metabolism of drug resistant cancer cells has been further modified. Metabolic adaptations of drug resistant cells to chemotherapeutics involve redox, lipid metabolism, bioenergetics, glycolysis, polyamine synthesis and so on. The proposed metabolic mechanisms of drug resistance include the increase of glucose and glutamine demand, active pathways of glutaminolysis and glycolysis, promotion of NADPH from the pentose phosphate pathway, adaptive mitochondrial reprogramming, activation of fatty acid oxidation, and up-regulation of ornithine decarboxylase for polyamine production. Several genes are associated with metabolic reprogramming and drug resistance. Intervening regulatory points described above or targeting key genes in several important metabolic pathways may restore cell sensitivity to chemotherapy. This paper reviews the metabolic changes of tumor cells during the development of chemoresistance and discusses the potential of reversing chemoresistance by metabolic regulation.
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Tiek, Deanna, and Shi-Yuan Cheng. "DNA damage and metabolic mechanisms of cancer drug resistance." Cancer Drug Resistance 5, no. 2 (2022): 368–79. http://dx.doi.org/10.20517/cdr.2021.148.

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Cancer drug resistance is one of the main barriers to overcome to ensure durable treatment responses. While many pivotal advances have been made in first combination therapies, then targeted therapies, and now broadening out to immunomodulatory drugs or metabolic targeting compounds, drug resistance is still ultimately universally fatal. In this brief review, we will discuss different strategies that have been used to fight drug resistance from synthetic lethality to tumor microenvironment modulation, focusing on the DNA damage response and tumor metabolism both within tumor cells and their surrounding microenvironment. In this way, with a better understanding of both targetable mutations in combination with the metabolism, smarter drugs may be designed to combat cancer drug resistance.
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Varghese, Elizabeth, Samson Mathews Samuel, Alena Líšková, Marek Samec, Peter Kubatka, and Dietrich Büsselberg. "Targeting Glucose Metabolism to Overcome Resistance to Anticancer Chemotherapy in Breast Cancer." Cancers 12, no. 8 (August 12, 2020): 2252. http://dx.doi.org/10.3390/cancers12082252.

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Breast cancer (BC) is the most prevalent cancer in women. BC is heterogeneous, with distinct phenotypical and morphological characteristics. These are based on their gene expression profiles, which divide BC into different subtypes, among which the triple-negative breast cancer (TNBC) subtype is the most aggressive one. The growing interest in tumor metabolism emphasizes the role of altered glucose metabolism in driving cancer progression, response to cancer treatment, and its distinct role in therapy resistance. Alterations in glucose metabolism are characterized by increased uptake of glucose, hyperactivated glycolysis, decreased oxidative phosphorylation (OXPHOS) component, and the accumulation of lactate. These deviations are attributed to the upregulation of key glycolytic enzymes and transporters of the glucose metabolic pathway. Key glycolytic enzymes such as hexokinase, lactate dehydrogenase, and enolase are upregulated, thereby conferring resistance towards drugs such as cisplatin, paclitaxel, tamoxifen, and doxorubicin. Besides, drug efflux and detoxification are two energy-dependent mechanisms contributing to resistance. The emergence of resistance to chemotherapy can occur at an early or later stage of the treatment, thus limiting the success and outcome of the therapy. Therefore, understanding the aberrant glucose metabolism in tumors and its link in conferring therapy resistance is essential. Using combinatory treatment with metabolic inhibitors, for example, 2-deoxy-D-glucose (2-DG) and metformin, showed promising results in countering therapy resistance. Newer drug designs such as drugs conjugated to sugars or peptides that utilize the enhanced expression of tumor cell glucose transporters offer selective and efficient drug delivery to cancer cells with less toxicity to healthy cells. Last but not least, naturally occurring compounds of plants defined as phytochemicals manifest a promising approach for the eradication of cancer cells via suppression of essential enzymes or other compartments associated with glycolysis. Their benefits for human health open new opportunities in therapeutic intervention, either alone or in combination with chemotherapeutic drugs. Importantly, phytochemicals as efficacious instruments of anticancer therapy can suppress events leading to chemoresistance of cancer cells. Here, we review the current knowledge of altered glucose metabolism in contributing to resistance to classical anticancer drugs in BC treatment and various ways to target the aberrant metabolism that will serve as a promising strategy for chemosensitizing tumors and overcoming resistance in BC.
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Alfarouk, Khalid O. "Tumor metabolism, cancer cell transporters, and microenvironmental resistance." Journal of Enzyme Inhibition and Medicinal Chemistry 31, no. 6 (February 10, 2016): 859–66. http://dx.doi.org/10.3109/14756366.2016.1140753.

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Roy, Sukanya, Subhashree Kumaravel, Ankith Sharma, Camille L. Duran, Kayla J. Bayless, and Sanjukta Chakraborty. "Hypoxic tumor microenvironment: Implications for cancer therapy." Experimental Biology and Medicine 245, no. 13 (June 27, 2020): 1073–86. http://dx.doi.org/10.1177/1535370220934038.

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Hypoxia or low oxygen concentration in tumor microenvironment has widespread effects ranging from altered angiogenesis and lymphangiogenesis, tumor metabolism, growth, and therapeutic resistance in different cancer types. A large number of these effects are mediated by the transcription factor hypoxia inducible factor 1⍺ (HIF-1⍺) which is activated by hypoxia. HIF1⍺ induces glycolytic genes and reduces mitochondrial respiration rate in hypoxic tumoral regions through modulation of various cells in tumor microenvironment like cancer-associated fibroblasts. Immune evasion driven by HIF-1⍺ further contributes to enhanced survival of cancer cells. By altering drug target expression, metabolic regulation, and oxygen consumption, hypoxia leads to enhanced growth and survival of cancer cells. Tumor cells in hypoxic conditions thus attain aggressive phenotypes and become resistant to chemo- and radio- therapies resulting in higher mortality. While a number of new therapeutic strategies have succeeded in targeting hypoxia, a significant improvement of these needs a more detailed understanding of the various effects and molecular mechanisms regulated by hypoxia and its effects on modulation of the tumor vasculature. This review focuses on the chief hypoxia-driven molecular mechanisms and their impact on therapeutic resistance in tumors that drive an aggressive phenotype. Impact statement Hypoxia contributes to tumor aggressiveness and promotes growth of many solid tumors that are often resistant to conventional therapies. In order to achieve successful therapeutic strategies targeting different cancer types, it is necessary to understand the molecular mechanisms and signaling pathways that are induced by hypoxia. Aberrant tumor vasculature and alterations in cellular metabolism and drug resistance due to hypoxia further confound this problem. This review focuses on the implications of hypoxia in an inflammatory TME and its impact on the signaling and metabolic pathways regulating growth and progression of cancer, along with changes in lymphangiogenic and angiogenic mechanisms. Finally, the overarching role of hypoxia in mediating therapeutic resistance in cancers is discussed.
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Moiseenko, Fedor V., Nikita Volkov, Alexey Bogdanov, Michael Dubina, and Vladimir Moiseyenko. "Resistance mechanisms to drug therapy in breast cancer and other solid tumors: An opinion." F1000Research 6 (March 17, 2017): 288. http://dx.doi.org/10.12688/f1000research.10992.1.

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Cancer is an important contributor to mortality worldwide. Breast cancer is the most common solid tumor in women. Despite numerous drug combinations and regimens, all patients with advanced breast cancer, similarly to other solid tumors, inevitably develop resistance to treatment. Identified mechanisms of resistance could be classified into intra- and extracellular mechanisms. Intracellular mechanisms include drug metabolism and efflux, target modulations and damage restoration. Extracellular mechanisms might be attributed to the crosstalk between tumor cells and environmental factors. However, current knowledge concerning resistance mechanisms cannot completely explain the phenomenon of multi-drug resistance, which occurs in the vast majority of patients treated with chemotherapy. In this opinion article, we investigate the role of these factors in the development of drug-resistance.
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Qian, Yanrong, Reetobrata Basu, Joseph Terry, Samuel Casey Mathes, Nathan Arnett, Cole Smith, Isaac Mendez-Gibson, et al. "Antagonism of Growth Hormone Receptor Suppresses Cancer Growth and Drug Resistance in Mice." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A1011—A1012. http://dx.doi.org/10.1210/jendso/bvab048.2069.

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Abstract Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) play important roles in different stages of progression and drug resistance in many types of cancers, including breast, colon, endometrial, liver cancer and melanoma. GH receptor (GHR) is highly expressed in melanoma and promotes cancer proliferation and multidrug efflux pumps mediated drug resistance. Knockdown of GHR in melanoma cells significantly increased their drug sensitivity in vitro. Thus, a GHR antagonist could become a therapeutic molecule in suppressing melanoma cancer growth and sensitizing the tumor to chemotherapy in vivo. Here, we used GHR antagonist (GHA) transgenic mice which constitutively express a GHA to specifically suppress GH/IGF-1 axis. We found have circulating IGF-1 level was significantly lowered in these mice as a result of GHR antagonism. Furthermore, the sera from the mice could inhibit the growth of melanoma cells in culture. Recombinant GHA produced in our laboratory was able to suppress the phosphorylation of STAT5, a well-established marker of GH action, and the phosphorylation of MAPK, a critical signaling component of cell growth. The GHA mice were intradermally inoculated with mouse melanoma cells (B16-F10) or subcutaneously inoculated with mouse liver cancer cells (Hepa1-6) to generate syngeneic mouse tumor models. We observed that tumor size and tumor weight were markedly reduced and that phosphorylation of STAT5 and MAPK was suppressed in the livers from these mice. In parallel, the activation of GH signaling and the expression level of various types of multidrug efflux pumps were reduced in these tumors. To test the effect of GHA on drug synergy, the GHA mice or WT controls with liver cancer cells were treated with sorafenib or vehicle. Sorafenib is an FDA-approved tyrosine kinase inhibitor, widely used to treat advanced hepatocarcinoma, but has a reduced efficacy in application due to the multidrug efflux pump ABCG2. In vitro, recombinant bovine GH increased the IC50 of sorafenib and the expression of ABCG2. In vivo, GHA mice treated with sorafenib had the smallest tumors compared with WT mice, or in mice treated with sorafenib or GHA alone. Furthermore, ABCG2 mRNA levels were also suppressed in the liver tumors from GHA mice. All these findings from functional and mechanistic investigations confirm that a GHA or Pegvisomant is effective in cancer treatment in vivo and may be a novel therapeutic strategy or molecule to suppress the tumor growth and to sensitize different types of cancers to anti-cancer therapies. Acknowledgments: This work was supported by the State of Ohio’s Eminent Scholar Program that includes a gift from Milton and Lawrence Goll to J.K.; NIH-R01AG059779, the AMVETS, Edison Biotechnology Institute and Diabetes Institute at Ohio University; OURC funding and Baker Fund to Y.Q.; the PURF Fund and the John J. Kopchick Molecular Cell Biology Undergraduate Student Fund to N.A and J.T.
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Wen, Gui-Min, Xiao-Yan Xu, and Pu Xia. "Metabolism in Cancer Stem Cells: Targets for Clinical Treatment." Cells 11, no. 23 (November 26, 2022): 3790. http://dx.doi.org/10.3390/cells11233790.

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Cancer stem cells (CSCs) have high tumorigenicity, high metastasis and high resistance to treatment. They are the key factors for the growth, metastasis and drug resistance of malignant tumors, and are also the important reason for the occurrence and recurrence of tumors. Metabolic reprogramming refers to the metabolic changes that occur when tumor cells provide sufficient energy and nutrients for themselves. Metabolic reprogramming plays an important role in regulating the growth and activity of cancer cells and cancer stem cells. In addition, the immune cells or stromal cells in the tumor microenvironment (TME) will change due to the metabolic reprogramming of cancer cells. Summarizing the characteristics and molecular mechanisms of metabolic reprogramming of cancer stem cells will provide new ideas for the comprehensive treatment of malignant tumors. In this review, we summarized the changes of the main metabolic pathways in cancer cells and cancer stem cells.
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Bhardwaj, Vikas, and Jun He. "Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer." International Journal of Molecular Sciences 21, no. 10 (May 12, 2020): 3412. http://dx.doi.org/10.3390/ijms21103412.

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The metabolic abnormality observed in tumors is characterized by the dependence of cancer cells on glycolysis for their energy requirements. Cancer cells also exhibit a high level of reactive oxygen species (ROS), largely due to the alteration of cellular bioenergetics. A highly coordinated interplay between tumor energetics and ROS generates a powerful phenotype that provides the tumor cells with proliferative, antiapoptotic, and overall aggressive characteristics. In this review article, we summarize the literature on how ROS impacts energy metabolism by regulating key metabolic enzymes and how metabolic pathways e.g., glycolysis, PPP, and the TCA cycle reciprocally affect the generation and maintenance of ROS homeostasis. Lastly, we discuss how metabolic adaptation in cancer influences the tumor’s response to chemotherapeutic drugs. Though attempts of targeting tumor energetics have shown promising preclinical outcomes, the clinical benefits are yet to be fully achieved. A better understanding of the interaction between metabolic abnormalities and involvement of ROS under the chemo-induced stress will help develop new strategies and personalized approaches to improve the therapeutic efficiency in cancer patients.
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Dissertations / Theses on the topic "Cancer drug resistance, tumor metabolism"

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E, Pranzini. "Metabolic reprogramming of colorectal cancer cells resistant to 5-FU." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1095546.

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Metabolic rearrangements are essential to satisfy the different needs of cancer cells during tumorigenesis. Recent studies highlighted a role for such metabolic reprogramming in adaptation to therapies and chemo-resistance development. 5-fluorouracil (5-FU) is an antimetabolite drug widely used as a first-line treatment for colorectal cancer. Despite several advantages of 5-FU, its clinical application is still greatly limited, due to the acquisition of drug resistance. In the first part of this thesis, we illustrate the role of micro RNAs (miRNAs) in reprogramming colon cancer cells toward a resistant phenotype as well as their involvement in the response of resistant cells to acute treatment with 5-FU. We performed a global gene expression profile for the entire miRNA genome, and we found a change in the expression of four miRNAs following acute treatment with 5-FU in cells resistant to this drug. Among them, we focused on miR-210-3p, previously described as a key regulator of DNA damage repair mechanisms and mitochondrial metabolism. Here we show that miR-210-3p downregulation enables resistant cells to counteract the toxic effect of the drug increasing the expression of RAD-52 protein, involved in DNA damage repair. Moreover, miR-210-3p downregulation enhances mitochondrial oxidative metabolism, increasing the expression levels of succinate dehydrogenase subunits D, decreasing intracellular succinate levels and inhibiting HIF-1α expression. These results suggest that miR-210-3p downregulation following 5-FU treatment sustains DNA damage repair and metabolic adaptation to counteract drug treatment, thus supporting the resistant phenotype. In the second part of this thesis, we reveal important adaptations in serine and one-carbon metabolism associated with the acquisition of 5-FU resistance in colorectal cancer cells. 5-FU resistant cells showed an increase in both serine up-take from extracellular medium and de novo serine synthesis pathway. Together with increased serine availability, dynamic labeling experiment after 13C-serine incubation underlined a different utilization of serine-derived carbons in resistant cells with a sustained flux into the mitochondrial compartment supporting increased purine nucleotides synthesis. Accordingly, we found a strong decrease in the expression of the cytosolic isoform of the enzyme serine hydroxy-methyltransferase (SHMT1) and a concomitant increase in the expression of the mitochondrial isoform (SHMT2) in 5-FU resistant cells compared to parental cells, confirming the shift toward mitochondrial one-carbon branch activity. Accordingly, higher expression levels of the mitochondrial serine transporter SFXN1 have been observed in resistant cells with respect to the sensitive ones. Silencing SHMT2 in 5-FU resistant cells increases the efficacy of the treatment with 5-FU against resistant cells confirming the importance of the reported adaptation in the acquisition of resistance to 5-FU. In conclusion, the data shown in this thesis underline different adaptations related to both miRNAs expression and nutrient metabolism carried out by 5-FU resistant cells. This reprogramming supports the response of 5-FU resistant cells to overcome the toxic effect of the drug. The identification of such alterations opens the possibility of new therapeutic approaches to tackle resistant cells and overcome colon cancer relapse.
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Shahi, Thakuri Pradip. "MODELING ANTI-CANCER DRUG RESISTANCE USING TUMOR SPHEROIDS." University of Akron / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=akron1574725861735168.

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Kala, Shashwati. "Role of ginsenoside Rb1 and its metabolite compound K in attenuating chemoresistance and tumour-initiating properties of ovarian cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207178.

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Chau, Wing-ka, and 周穎嘉. "Characterization of ovarian tumor-initiating cells and mechanisms of chemoresistance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197834.

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Chemoresistance remains a major clinical obstacle to effective management of ovarian cancer. Cancer stem cells (or tumor-initiating cells, TICs) have been discovered recently, and have played a pivotal role in changing the view of cancer development; however, the molecular mechanisms by which these cells escape conventional therapies remain elusive. In this study, TICs were isolated from ovarian cancer cells as tumor spheres with specific stem properties under TIC-selective conditions. Unlike non-TICs, TICs strongly express stem cell factor (SCF) and c-Kit. Blocking SCF-c-Kit by SCF neutralizing antibodies, c-Kit small interfering RNA (siRNA) or imatinib (Gleevec), a clinical drug that inhibits c-Kit signaling, significantly inhibited TIC proliferation. Although cisplatin and paclitaxel killed the non-TICs, they did not eliminate TICs. Importantly, the combination of cisplatin/paclitaxel with c-Kit siRNA or imatinib inhibited the growth of both non-TICs and TICs. Similar results were obtained when patient-derived TICs were used. The findings also indicate that tumor-predisposing microenvironment, such as hypoxia, may promote ovarian TICs through upregulating c-Kit expression. Furthermore, I have showed that c-Kit expression induced activation of Phosphatidylinositol 3-kinases (PI3K)/Akt, -catenin, and ATP-binding cassette G2, which could be reversed by treatment with the PI3K/Akt inhibitor or -catenin siRNA. I further studied potential gene expression in TICs using cDNA and microRNA (miRNA) microarrays. The result from these microarrays provided a general profile in gene expression of TICs compared with the bulk tumor cells. In particular, let-7a, b, and c were shown to be downregulated in TICs compared to bulk tumor cells, suggesting that their loss may contribute to ovarian cancer development. Together, this study reveals a previously undescribed therapeutic effect of SCF-c-Kit signaling blockade to prevent ovarian cancer progression by eliminating TICs and the altered genes or miRNAs may represent possible molecular targets.
published_or_final_version
Biological Sciences
Master
Master of Philosophy
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Kim, Gloria J. "Cancer nanotechnology engineering multifunctional nanostructures for targeting tumor cells and vasculatures /." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/22610.

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Thesis (Ph. D.)--Biomedical Engineering, Georgia Institute of Technology, 2007.
Committee Chair: Nie, Shuming; Committee Member: Lyon, L. Andrew; Committee Member: McIntire, Larry V.; Committee Member: Murthy, Niren; Committee Member: Prausnitz, Mark R.
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Rajabi, Fatemeh. "Role of the xenoreceptor PXR (NR1I2) in colon cancer stem cells drug resistance and tumor relapse." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT027.

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La récidive tumorale est l'un des principaux obstacles à surmonter à l'avenir pour améliorer la survie globale des patients atteints de cancer du côlon (CCR). Les échecs thérapeutiques observés chez les patients sont compatibles avec une accumulation de cellules souches cancéreuses (CSCs) résistantes aux médicaments. Dans cette étude, nous démontrons que le récepteur nucléaire PXR (NR1I2) agit comme un régulateur important de la chimiorésistance des CSCs coliques et de leur capacité à initier la rechute tumorale après traitement. Nous avons d'abord montré que l'expression de PXR augmente avec celle de certains marqueurs des CSCs dans des cellules cancéreuses de patients CCR traitées par chimiothérapies. Nous avons constaté que PXR est préférentiellement exprimé dans les CSCs coliques et qu'il contribue à l'enrichissement des CSCs après chimiothérapies in vitro et in vivo. Par des approches de transcriptomiques, nous avons observé qu'au sein des CSCs coliques, PXR contrôle l'expression d'un large réseau de gènes marqueurs des CSCs coliques, ainsi que des gènes impliqués dans la résistance aux médicaments ou à l'apoptose, ou impliqués dans la dissémination métastatique. Enfin, l'inhibition de PXR par interférence à ARN diminue la survie et auto-renouvèlement des cellules souches cancéreuses du côlon in vitro, ainsi que leur capacité à résister à la chimiothérapie après xénogreffes, conduisant à des retards importants de rechute tumorale après traitements par chimiothérapies in vivo. Cette étude suggère fortement que l'inhibition ciblée de PXR peut représenter une stratégie de traitement néo-adjuvant afin de diminuer la résistance aux médicaments et la récidive des patients CCR via la sensibilisation des cellules souches cancéreuses aux chimiothérapies classiques
Tumor recurrence is one of the major obstacles to overcome in the future to improve overall survival of patients with colon cancer. High rates and patterns of therapeutic failure seen in patients are consistent with a steady accumulation of drug-resistant cancer stem cells (CSCs). Here, we demonstrate that the nuclear receptor PXR (NR1I2) acts as a key regulator of colon CSC chemoresistance and of their ability to generate post-treatment tumor relapse. We first determined that the enrichment of PXR paralleled that of CSC markers upon treatment of colon cancer cells with standard of care chemotherapy. We found that PXR was highly expressed in colorectal cancer cells displaying CSC markers and function and that it was instrumental for the emergence of CSCs following chemotherapy in vitro and in vivo. mRNA profiling experiments in colon CSCs indicated that PXR transcriptionally controls a large network of genes including markers of stemness, genes involved in resistance to drug/apoptosis or migration/invasion. Finally, PXR down-regulation altered the survival and self-renewal of colon CSCs in vitro and hampered their capacity to resist chemotherapy in vivo, leading to significant delays of post-chemotherapy tumor relapse. This study strongly suggests that targeting PXR may represent a novel treatment strategy to prevent drug resistance and recurrence through the sensitization of CSCs to standard chemotherapy. Taken together, our data strongly suggest that PXR plays an instrumental role in the so-called "intrinsic" pan-resistance of CSCs against therapy
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Iliopoulos, Dimitrios. "The role of the WWOX tumor suppressor in breast and lung cancer." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1155142398.

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IPPOLITO, LUIGI. "OXPHOS - a metabolic switch driven by tumor microenvironment and resistance to therapy in prostate carcinoma." Doctoral thesis, Università di Siena, 2016. http://hdl.handle.net/11365/1006820.

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Tumor cells exhibit metabolic reprogramming according to microenvironmental scenarios (i.e. stroma composition and/or anticancer drugs burden) to meet their demands for energy, rapid proliferation, metastasis and progression. In our experimental model, a vicious metabolic synergy between CAFs and prostate cancer (PCa) cells has been described as a pivotal engine allowing cancer cells to achieve aggressive features and evolve their malignancy. Such metabolic crosstalk is mainly based on the OXPHOS rewiring of PCa cells induced by highly glycolytic CAFs through the establishment of tumor:stroma lactate shuttle. In the first part of this study, we highlighted a peculiar CAFs conditioning of PCa cells in terms of OXPHOS upgrading and enhancement. Indeed, we observed that CAFs induce a SIRT1/PGC-1α axis activation in PCa cells, leading to the accumulation of mitochondrial ROS and TCA cycle oncometabolites (succinate/fumarate) that are both closely related to EMT engagement and PCa invasiveness. Indeed, we found that CAFs-exacerbated mitochondrial ROS are crucial for the oxidation of critical targets (Src, PKM2) needed for the metabolic reprogramming toward OXPHOS established in CAFs-exposed PCa cells. On the other hand, succinate is able to maintain CAFs-induced HIF-1α activation and the HIF-1- dependent malignant phenotype of PCa cells. Furthermore, we intriguingly observed a mechanism of mitochondrial transfer elicited by CAFs in order to further boost OXPHOS exploitation, mitochondrial ROS generation and invasiveness of PCa cells. Among microenvironmental cues, chemotherapy resistance has been increasingly and finely associated to the metabolic reprogramming of resistant cancer cells. In the second part of this study, we metabolically characterized docetaxel-resistant PCa cells and we clearly outlined a metabolic adaptation of resistant cancer cells compared to the sensitive counterpart. Docetaxel-resistant PCa cells undergo a Warburg escape towards OXPHOS addiction in order to ensure metabolic advantages during acquisition of resistant phenotype. Together with lactate and glucose, we also found an higher glutamine mitochondrial exploitation by docetaxel-resistant cells. Furthermore, we appreciated a role of CAFs in modulating the response to drug exposure by protecting sensitive and resistant PCa cells. We found that such metabolic/resistant phenotype can be counteracted either by metformin (or other mitocans) treatment or by overexpressing miR-205, a downregulated miRNA orchestrating prostate tumor:stroma crosstalk. Taken together, all the data obtained in our study highlight the role of OXPHOS as an important shared metabolic state between chemotherapy resistance and symbiosis with microenvironment PCa cells.
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Wang, Xuan. "Internalization of Extracellular ATP by Cancer Cells and its Functional Roles in Cancer Drug Resistance." Ohio University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1505834714683835.

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Balcells, Nadal Cristina. "The supramolecular organization of cancer metabolism: From macromolecular crowding to metabolic reprogramming underlying cancer metastasis and drug resistance." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668321.

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Metastasis and drug resistance represent the two main causes of therapeutic failure in oncology. In the present dissertation, the interplay between them has been interrogated using metabolomics, systems biology and biophysical approaches, in an attempt to find common phenotypic adaptations and metabolic vulnerabilities of metastatic and resistant cancer cells, potentially exploitable in novel combination therapies. The obtained results unveil that highly metastatic e-CSC phenotypes of CRPC present particular metabolic vulnerabilities that can potentially lead to establishing putative biomarkers and metabolic targets that are specific for PCa subsets with high tumorigenic potential. Moreover, by generating isogenic cell models of multiplatinum resistance in CRPC and CRC we also identified that metastatic solid tumors with originally opposed metabolic profiles can lead to different metabolic adaptations as they acquire platinum resistance, but that a common metabolic signature of acquired platinum resistance arises, which also includes alterations in proline and one carbon metabolism, glutathione synthesis and ROS production. In addition to characterizing in deep the metabolic reprogramming associated to resistance to platinum compounds already used in the clinics, we also explored the possibility to design of novel platinum drugs able to counter platinum-resistant tumors. In this regard, we identified novel families of cyclometallated platinum (II) and platinum (IV) compounds exhibit strong antiproliferative effects in the low micromolar range against a wide variety of solid tumors. The leading compounds of each series also exhibit remarkable selectivity for cancer cells and the capacity to arrest the cell cycle at S and G2/M phases, induce apoptosis and increase intracellular ROS levels. The multiple combinations of equatorial and axial ligands explored in this work, allowed us to conclude that octahedral Pt (IV) compounds containing tridentate [C,N,N’] ligands are the optimal design to improve efficacy and selectivity against cancer cell lines. Remarkably, we have also identified that these novel cyclometallated Pt (IV) exhibit a complete absence of cross-resistance with the platinum-resistant CRC and CRPC models generated in this work. Indeed, platinum-based chemotherapy can severely affect internal cell architecture, causing fluctuations in the levels of macromolecular crowding inside cells and having an impact on the supramolecular organization of cell metabolism. In turn, this has been proved to have a profound impact on the kinetic behavior of metabolic enzymes that govern the rate of metabolic pathways that we have identified as important throughout this work. Thus, we have explored the kinetic behavior of lactate dehydrogenase (LDH), as a representative of aerobic glycolysis, under the presence of globular obstacles that do not introduce specific interactions with either LDH or its substrates, dextran polymers, obtaining that LDH kinetics is impaired in an obstacle size- and concentration-dependent manner. Additionally, we unveiled that LDH kinetic behavior shifts from activation control to diffusion control as crowding increases, implying that the behavior of LDH inside cells could be significantly different than previous dilute solution kinetic studies of this enzyme had predicted. On the other hand, the effect of macromolecular crowding on glutaminolysis had not been explored prior to this work. By studying the kinetic behavior of glutamate dehydrogenase (GLDH) in crowded media and characterizing its negative cooperativity, we have concluded that its kinetics is impaired by crowding in an obstacle size- and concentration-dependent manner, but that negative cooperativity is not significantly altered by macromolecular crowding. The actual impact of macromolecular crowding on cell metabolism has been scarcely explored and we are just scratching the surface of the understanding of the multiple implications that this phenomenon may entail for cell physiology and, in particular, for the metabolic alterations of cancer cells. Our observations throughout this work will hopefully have contributed to set grounds onto this enthralling enterprise, as long as meaningfully contributed to encounter valuable therapeutic tools against metastatic CRPC and CRC that can circumvent platinum resistance, both with new generations of platinum compounds and novel metabolic targets that selectively target metastatic solid tumors.
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Books on the topic "Cancer drug resistance, tumor metabolism"

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

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Benjamin, Bonavida, ed. Sensitization of cancer cells for chemo/immuno/radio-therapy. Totowa, NJ: Humana Press, 2008.

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S, El-Deiry Wafik, ed. Tumor progression and therapeutic resistance. New York, NY: New York Academy of Sciences, 2005.

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B, Roninson Igor, ed. Molecular and cellular biology of multidrug resistance in tumor cells. New York: Plenum Press, 1991.

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Lauricella, Marianna, and Sonia Emanuele. Novel apoptotic drugs in targeting tumor cells. Trivandrum, Kerala, India: Researh Signpost, 2007.

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Kim, Kŏn-hong. Yubangam ŭi taje yangmul naesŏng saengchʻe chipʻyo palgul mit kŭ yuyongsŏng kŏmjŭng =: Identification of biomarkers for multidrug resistance and validation of markers in breast cancer tissue. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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Bonavida, Benjamin. Chemo-immunosensitization of resistant tumor cells to cell death by apoptosis, 2006. Trivandrum: Transworld Research Network, 2006.

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Julia, Gee, Nicholson Robert I, and SpringerLink (Online service), eds. Therapeutic Resistance to Anti-Hormonal Drugs in Breast Cancer: New Molecular Aspects and their Potential as Targets. Dordrecht: Springer Netherlands, 2009.

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1940-, Tabuchi K., ed. Biological aspects of brain tumors: Proceedings of the 8th Nikko Brain Tumor Conference, Karatsu (Saga) 1990. Tokyo: Springer-Verlag, 1991.

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Gregory, Bock, Goode Jamie, Novartis Foundation, and Symposium on Mechanisms of Drug Resistance in Epilepsy : Lessons from Oncology (2001 : London, England), eds. Mechanisms of drug resistance in epilepsy: Lessons from oncology. Chichester, England: Wiley, 2002.

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Book chapters on the topic "Cancer drug resistance, tumor metabolism"

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Park, Joshua K., Nathan J. Coffey, Aaron Limoges, and Anne Le. "The Heterogeneity of Lipid Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 39–56. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_3.

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AbstractThe study of cancer cell metabolism has traditionally focused on glycolysis and glutaminolysis. However, lipidomic technologies have matured considerably over the last decade and broadened our understanding of how lipid metabolism is relevant to cancer biology [1–3]. Studies now suggest that the reprogramming of cellular lipid metabolism contributes directly to malignant transformation and progression [4, 5]. For example, de novo lipid synthesis can supply proliferating tumor cells with phospholipid components that comprise the plasma and organelle membranes of new daughter cells [6, 7]. Moreover, the upregulation of mitochondrial β-oxidation can support tumor cell energetics and redox homeostasis [8], while lipid-derived messengers can regulate major signaling pathways or coordinate immunosuppressive mechanisms [9–11]. Lipid metabolism has, therefore, become implicated in a variety of oncogenic processes, including metastatic colonization, drug resistance, and cell differentiation [10, 12–16]. However, whether we can safely and effectively modulate the underlying mechanisms of lipid metabolism for cancer therapy is still an open question.
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Wahl, Daniel, Michael Petronek, Rashmi Ramachandran, John Floberg, Bryan G. Allen, and Julie K. Schwarz. "Targeting Tumor Metabolism to Overcome Radioresistance." In Cancer Drug Discovery and Development, 219–63. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49701-9_10.

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Mashima, Tetsuo, Hiroyuki Seimiya, Zhihong Chen, Shiro Kataoka, and Takashi Tsuruo. "Apoptosis resistance in tumor cells." In Multiple Drug Resistance in Cancer 2, 293–308. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2374-9_20.

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Boros, László G., Richard D. Beger, Emmanuelle J. Meuillet, Jerry R. Colca, Sándor Szalma, Patricia A. Thompson, László Dux, Gyula Farkas, and Gábor Somlyai. "Targeted 13C-Labeled Tracer Fate Associations for Drug Efficacy Testing in Cancer." In Tumor Cell Metabolism, 349–72. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5_15.

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Saeed, Mohamed, Henry Johannes Greten, and Thomas Efferth. "Collateral Sensitivity in Drug-Resistant Tumor Cells." In Resistance to Targeted Anti-Cancer Therapeutics, 187–211. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7070-0_10.

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Lundholm, Kent G. "Tumor Host Metabolism and Nutrient Delivery in Cancer Treatment." In Drug Delivery in Cancer Treatment, 29–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73077-1_4.

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Siddik, Zahid H. "Drug Resistance and the Tumor Suppressor p53: The Paradox of Wild-Type Genotype in Chemorefractory Cancers." In Drug Resistance in Cancer Cells, 209–31. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89445-4_9.

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Mitchell, James B., Angelo Russo, John A. Cook, and Eli Glatstein. "Tumor cell drug and radiation resistance: Does an interrelationship exist?" In Cancer Treatment and Research, 189–203. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1601-5_12.

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Davis, Alison J., and Ian F. Tannock. "Tumor Physiology and Resistance to Chemotherapy: Repopulation and Drug Penetration." In Cancer Treatment and Research, 1–26. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1173-1_1.

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Broxterman, Henk J., and Carolien H. M. Versantvoort. "Pharmacology of Drug Transport in Multidrug Resistant Tumor Cells." In Alternative Mechanisms of Multidrug Resistance in Cancer, 67–80. Boston, MA: Birkhäuser Boston, 1995. http://dx.doi.org/10.1007/978-1-4615-9852-7_3.

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Conference papers on the topic "Cancer drug resistance, tumor metabolism"

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Taylor, Holly, Jaroslav Slamecka, Alla Musiyenko, Elaine Gavin, Tiffany S. Norton, Ileana Aragon, Taylor Young, et al. "Abstract B31: Tumor-intrinsic B7-H3 regulates drug resistance, metabolism, and pathogenesis in ovarian cancer." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-b31.

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Liu, Jiawei. "Metabolism, Metastasis and Drug Resistance in Cancer." In The International Conference on Biomedical Engineering and Bioinformatics. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011311900003443.

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Okon, Imoh S., Kathleen A. Coughlan, and Ming-Hui Zou. "Abstract B24: Attenuated expression of a novel mitochondrial and metabolic gene contributes to acquired gefitinib resistance in lung tumors." 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-b24.

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Achuthan, Santhi, Richard Callaghan, and Anneke C. Blackburn. "Abstract A90: Dichloroacetate can overcome drug resistance via decreased ABC drug transporter expression and PDK2 inhibition." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a90.

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Yu, Tengfei, Ying Yan, Wei Du, Yuefei Yang, Tingting Tan, Xuqin Yang, Jiali Gu, Liang Hua, Xin K. Ye, and Zhenyu Gu. "Abstract 1212: Studying cancer drug resistance in patient derived xenograft tumor models." 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.am2014-1212.

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Nwosu, ZC, W. Pioronska, MP Ebert, C. Meyer, and S. Dooley. "Glutamine deprivation link impaired metabolism to ERK pathway activation and drug resistance in liver cancer." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677176.

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Jayaprakash, Priyamvada, Michael Curran, Brittany Morrow, Joseph Marszalek, Krithikaa Rajkumar Bhanu, Meghan Rice, Jason Gay, Christopher Vellano, Benjamin Cowen, and Dean Welsch. "831 Targeting tumor oxidative metabolism to overcome hypoxia-induced immunotherapy resistance in prostate cancer." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0831.

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Settleman, Jeffrey. "Modeling drug sensitivity and resistance in human tumor-derived cell lines." In AACR International Conference: Molecular Diagnostics in Cancer Therapeutic Development– Sep 27-30, 2010; Denver, CO. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/diag-10-pl1-1.

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Raja, Vaishnavi, Shailendra Giri, Suhail Hamid, Adnan R. Munkarah, and Ramandeep Rattan. "Abstract GMM-049: STAT3 PROMOTES OVARIAN CANCER GROWTH AND DRUG RESISTANCE BY MODULATING THE ENERGY METABOLISM." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-gmm-049.

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Stuart, Shawn D., Moises Guardado, Michael Dahan, Paul M. Bingham, and Zuzana Zachar. "Abstract A61: Tumor metabolic remodeling can modulate anticancer drug response: CPI-613 attack on tumor cell mitochondrial metabolism is mediated by metabolite availability." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a61.

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Reports on the topic "Cancer drug resistance, tumor metabolism"

1

Liu, Shuang, Zheng-Miao Wang, Dong-Mei Lv, and Yi-Xuan Zhao. Advances in highly active one-carbon metabolism in cancer diagnosis, treatment, and drug resistance: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0099.

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Spanjaard, Remco A. Role of ei24/PIG8, A Putative Pro-Apoptotic Tumor Suppressor, in Breast Cancer Development and Resistance to Drug Therapy. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada433856.

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