Relevant bibliographies by topics / Metabolism, Cell Cycle, Cancer, Kras

Contents

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

Academic literature on the topic 'Metabolism, Cell Cycle, Cancer, Kras'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Metabolism, Cell Cycle, Cancer, Kras"

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Chiu, Ching-Feng, Ming-I. Hsu, Hsiu-Yen Yeh, et al. "Eicosapentaenoic Acid Inhibits KRAS Mutant Pancreatic Cancer Cell Growth by Suppressing Hepassocin Expression and STAT3 Phosphorylation." Biomolecules 11, no. 3 (2021): 370. http://dx.doi.org/10.3390/biom11030370.

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Background: The oncogenic Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation was reported to be the signature genetic event in most cases of pancreatic ductal adenocarcinoma (PDAC). Hepassocin (HPS/FGL1) is involved in regulating lipid metabolism and the progression of several cancer types; however, the underlying mechanism of HPS/FGL1 in the KRAS mutant PDAC cells undergoing eicosapentaenoic acid (EPA) treatment remains unclear. Methods: We measured HPS/FGL1 protein expressions in a human pancreatic ductal epithelial (HPNE) normal pancreas cell line, a KRAS-wild-type PDAC cell line (B
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Hatipoglu, Ahmet, Deepak Menon, Talia Levy, Maria A. Frias, and David A. Foster. "Inhibiting glutamine utilization creates a synthetic lethality for suppression of ATP citrate lyase in KRas-driven cancer cells." PLOS ONE 17, no. 10 (2022): e0276579. http://dx.doi.org/10.1371/journal.pone.0276579.

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Metabolic reprogramming is now considered a hallmark of cancer cells. KRas-driven cancer cells use glutaminolysis to generate the tricarboxylic acid cycle intermediate α-ketoglutarate via a transamination reaction between glutamate and oxaloacetate. We reported previously that exogenously supplied unsaturated fatty acids could be used to synthesize phosphatidic acid–a lipid second messenger that activates both mammalian target of rapamycin (mTOR) complex 1 (mTORC1) and mTOR complex 2 (mTORC2). A key target of mTORC2 is Akt–a kinase that promotes survival and regulates cell metabolism. We repor
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Chen, Yaoyu, Jinhong Chen, Yali Guo, et al. "Abstract B173: The anti-tumor activity of CDK2 inhibition alone or in combination with other anti-cancer agents in human cancers." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): B173. http://dx.doi.org/10.1158/1535-7163.targ-23-b173.

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Abstract Cyclin-dependent kinase 2 (CDK2) plays a crucial role in the regulation of the cell cycle and is involved in a variety of biological processes. It is responsible for phosphorylating proteins involved in G1 and S phase cell cycle progression, DNA damage response, intracellular transport, protein degradation, signal transduction, and DNA and RNA metabolism. CDK2 activity is particularly significant in cells exhibiting CCNE1 amplification or overexpression. Additionally, CDK2 activity has been linked to potential resistance against chemotherapy or targeted therapy. Several studies have i
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Shechter, Sharon, Sapir Ya’ar Bar, Hamdan Khattib, Matthew J. Gage, and Dorit Avni. "Riok1, A Novel Potential Target in MSI-High p53 Mutant Colorectal Cancer Cells." Molecules 28, no. 11 (2023): 4452. http://dx.doi.org/10.3390/molecules28114452.

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The vulnerabilities of cancer cells constitute a promising strategy for drug therapeutics. This paper integrates proteomics, bioinformatics, and cell genotype together with in vitro cell proliferation assays to identify key biological processes and potential novel kinases that could account, at least in part, for the clinical differences observed in colorectal cancer (CRC) patients. This study started by focusing on CRC cell lines stratified by their microsatellite (MS) state and p53 genotype. It shows that cell-cycle checkpoint, metabolism of proteins and RNA, signal transduction, and WNT sig
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Conroy, Lindsey R., Susan Dougherty, Traci Kruer, et al. "Loss of Rb1 Enhances Glycolytic Metabolism in Kras-Driven Lung Tumors In Vivo." Cancers 12, no. 1 (2020): 237. http://dx.doi.org/10.3390/cancers12010237.

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Dysregulated metabolism is a hallmark of cancer cells and is driven in part by specific genetic alterations in various oncogenes or tumor suppressors. The retinoblastoma protein (pRb) is a tumor suppressor that canonically regulates cell cycle progression; however, recent studies have highlighted a functional role for pRb in controlling cellular metabolism. Here, we report that loss of the gene encoding pRb (Rb1) in a transgenic mutant Kras-driven model of lung cancer results in metabolic reprogramming. Our tracer studies using bolus dosing of [U-13C]-glucose revealed an increase in glucose ca
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Der, Channing J. "Abstract IA06: Targeting the ERK-MYC signaling network for the treatment of KRAS-mutant cancers." Molecular Cancer Research 21, no. 5_Supplement (2023): IA06. http://dx.doi.org/10.1158/1557-3125.ras23-ia06.

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Abstract KRAS is mutationally activated in 95% of pancreatic ductal adenocarcinomas (PDAC) and essential for maintenance of PDAC tumorigenic growth. The recent clinical evaluation of inhibitors of one KRAS mutant (KRASG12C) supports the therapeutic value of direct targeting of KRAS for PDAC treatment. However, this mutant comprises less than 2% of KRAS mutations in PDAC. Therefore, we have evaluated direct inhibitors of the predominant KRAS mutations (G12D, G12V and G12R) in PDAC. Additionally, both innate and treatment-associated resistance mechanisms will limit the effectiveness of direct KR
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Singh, Pankaj Kumar. "Abstract SY13-01: Targeting the metabolic basis of resistance to Kras signaling inhibition in pancreatic cancer." Cancer Research 85, no. 8_Supplement_2 (2025): SY13–01—SY13–01. https://doi.org/10.1158/1538-7445.am2025-sy13-01.

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Abstract Pancreatic ductal adenocarcinoma patients show poor prognosis due in part to poor response to standard-of-care therapies. Hence, there is an urgent need to identify novel therapeutic strategies. Oncogenic Kras mutations are a key driver of PDAC tumorigenesis. Novel Kras-targeted therapies have demonstrated improved efficacies in preclinical models and are currently under trial in the clinic. However, resistance has been observed against these therapies. Metabolic alterations play a key role in regulating therapy responsiveness. Notably, Krasis a key regulator of metabolic reprogrammin
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Wang, Wenping, Samuel Wang, Ioana Dobrescu, et al. "Abstract 3803: CRISPR screening identifies methionine synthase as a potential therapeutic target in KRAS-driven NSCLC." Cancer Research 85, no. 8_Supplement_1 (2025): 3803. https://doi.org/10.1158/1538-7445.am2025-3803.

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Abstract One-carbon metabolism, which integrates the folate and methionine cycles, is crucial for cancer growth. Methionine synthase (MTR), a key enzyme in this pathway, converts 5-methyltetrahydrofolate (5-CH3-THF) to active tetrahydrofolate (THF), a cofactor required for nucleotide synthesis. Concurrently, MTR catalyzes the conversion of homocysteine to methionine, effectively linking the folate and methionine cycles. Given its central role, MTR has gained attention as a potential therapeutic target in cancer research, though its function in KRAS-driven lung cancer remains poorly understood.
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Vande Voorde, Johan, Rory T. Steven, Arafath K. Najumudeen, et al. "Metabolic profiling stratifies colorectal cancer and reveals adenosylhomocysteinase as a therapeutic target." Nature Metabolism 5, no. 8 (2023): 1303–18. http://dx.doi.org/10.1038/s42255-023-00857-0.

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AbstractThe genomic landscape of colorectal cancer (CRC) is shaped by inactivating mutations in tumour suppressors such as APC, and oncogenic mutations such as mutant KRAS. Here we used genetically engineered mouse models, and multimodal mass spectrometry-based metabolomics to study the impact of common genetic drivers of CRC on the metabolic landscape of the intestine. We show that untargeted metabolic profiling can be applied to stratify intestinal tissues according to underlying genetic alterations, and use mass spectrometry imaging to identify tumour, stromal and normal adjacent tissues. B
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Rana, Manjul, Rita G. Kansal, Jie Fang, Benjamin T. Allen, Jun Yang, and Evan S. Glazer. "Abstract B044: Bromodomain and Extra-Terminal Protein inhibition decreases pancreatic cancer proliferation via MYC-independent pathways." Cancer Research 82, no. 22_Supplement (2022): B044. http://dx.doi.org/10.1158/1538-7445.panca22-b044.

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Abstract Introduction: The bromodomain and extra-terminal (BET) protein family contains proteins which have evolutionarily conserved bromodomains (BRDs) that specifically recognize acetylated lysine residues on the histone tails of chromatin and regulate gene transcription. Deregulation of these BRD-containing proteins has been seen in carcinogenesis as they are also known to play role in the regulation of the cell-cycle and MYC oncogenes. BMS-986158 is an oral BET inhibitor which has been used in the clinical trials for both hematologic and advanced solid tumor cancers. We hypothesized that B
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Dissertations / Theses on the topic "Metabolism, Cell Cycle, Cancer, Kras"

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GAGLIO, DANIELA. "Role of nutrient availability on proliferation and cell cycle excution of immortalized and kras transformed mouse fibroblastic." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/7548.

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Mammalian cells proliferate, differentiate or die in response to extracellular signals as growth factors and nutrients. Cancer is essentially a disease in which cells have lost responsiveness to many of these signals and to normal checks on cell proliferation. Therefore, it may not be surprising that tumor cells, in order to meet the increased requirements of proliferation, often display fundamental changes in pathways of energy metabolism and nutrient uptake (Garber, 2006). In particular, several studies shown that the process of tumorigenesis is often associated with altered metabolism of tw
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Toda, Kosuke. "Metabolic Alterations Caused by KRAS Mutations in Colorectal Cancer Contribute to Cell Adaptation to Glutamine Depletion by Upregulation of Asparagine Synthetase." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225464.

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Maddula, Sasidhar [Verfasser]. "Cell cycle phase specific metabolism of colon cancer cells: a metabolome study / Sasidhar Maddula." München : Verlag Dr. Hut, 2011. http://d-nb.info/1018980911/34.

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Neumann, Chase K. A. "Phosphatidylinositol Remodeling through Membrane Bound O-acyl Transferase Domain-7 (MBOAT7) Promotes the Progression of Clear Cell Renal Cell Carcinoma (ccRCC)." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1586250046745924.

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Yang, Jie. "Prediction of combination efficacy in cancer therapy." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/prediction-of-combination-efficacy-in-cancer-therapy(1b49824b-9d5f-4d21-89d7-6160a810d05e).html.

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The cell cycle is an essential process in all living organisms that must be carefully regulated to ensure successful cell growth and division. Disregulation of the cell cycle is a key contributing factor towards the formation of cancerous cells. Understanding events at a cellular level is the first step towards comprehending how cancer manifests at an organismal level. Mathematical modelling can be used as a means of formalising and predicting the behaviour of the biological systems involved in cancer. In response, cell cycle models have been constructed to simulate and predict what happens to
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Moulin, Cécile. "Analyse des voies métaboliques au cours du cycle cellulaire : application au métabolisme du cancer." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASG022.

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L’objectif de cette thèse est d’étudier comment la cellule mammifère adapte son métabolisme aux étapes du cycle cellulaire. Le cycle cellulaire est l’ensemble des étapes menant une cellule à se diviser. Le rôle du métabolisme est de fournir à la cellule les éléments et l’énergie dont elle a besoin pour fonctionner. En particulier, à chaque étape du cycle cellulaire, la cellule a besoin de différents éléments pour pouvoir, à terme, se diviser correctement. Il est donc crucial pour la cellule de coordonner le métabolisme et le cycle cellulaire et en particulier de contrôler ce que le métabolisme
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Silva, Alinne Costa. "Aparato de importação de proteínas mitocondriais em Aspergillus fumigatus: caracterização fenotípica da deleção da menor subunidade do complexo TIM23." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17131/tde-06062017-161751/.

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O câncer de ovário (OvCa) se destaca dentre as neoplasias ginecológicas por ser um dos mais letais e de difícil diagnóstico. O OvCa ocorre devido ao acúmulo de alterações celulares progressivas promovidas por mutações no genoma de uma célula que, consequentemente, alteram as complexas vias de regulação celular que respondem a fatores internos, como reprogramação genética, ou externos, como a resposta a fatores de crescimento, que juntamente com outras alterações moleculares favorecem a progressão e a metástase. Uma importante etapa da cascata metastática é a transição epitélio-mesenquimal (EMT
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Kinkade, Rebecca. "Rb-Raf-1 interaction as a therapeutic target for proliferative disorders." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002426.

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Nandagopal, Neethi. "Identification of copper metabolism as a KRAS-specific vulnerability in colorectal cancer." Thesis, 2020. http://hdl.handle.net/1866/25272.

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KRAS est parmi les gènes les plus fréquemment mutés dans les cancers humains, tel que ~ 45% des cancers colorectaux (CCR). Malgré les efforts déployés pour réduire son potentiel oncogénique, KRAS muté est fréquemment associé à la résistance aux médicaments et est extrêmement difficile à cibler sur le plan thérapeutique. Les protéines à la surface cellulaire sont souvent dérégulées dans les cancers et sont des cibles thérapeutiques attrayantes en raison de leur accessibilité aux anticorps. Nous avons séquençé les ARNm de cellules épithéliales intestinales exprimant KRAS muté et observé que ces
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Przybytkowski, Ewa. "Fatty acid metabolism and modulation of human breast cancer cell survival." Thèse, 2006. http://hdl.handle.net/1866/15602.

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Books on the topic "Metabolism, Cell Cycle, Cancer, Kras"

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Whitfield, James F. Calcium in cell cycles and cancer. 2nd ed. CRC Press, 1995.

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Calcium, cell cycles, and cancer. CRC Press, 1990.

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Book chapters on the topic "Metabolism, Cell Cycle, Cancer, Kras"

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Çoban, Esra Aydemir, Didem Tecimel, Fikrettin Şahin, and Ayşen Aslı Hızlı Deniz. "Targeting Cancer Metabolism and Cell Cycle by Plant-Derived Compounds." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/5584_2019_449.

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Li, Ting, Christopher Copeland, and Anne Le. "Glutamine Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_2.

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AbstractMetabolism is a fundamental process for all cellular functions. For decades, there has been growing evidence of a relationship between metabolism and malignant cell proliferation. Unlike normal differentiated cells, cancer cells have reprogrammed metabolism in order to fulfill their energy requirements. These cells display crucial modifications in many metabolic pathways, such as glycolysis and glutaminolysis, which include the tricarboxylic acid (TCA) cycle, the electron transport chain (ETC), and the pentose phosphate pathway (PPP) [1]. Since the discovery of the Warburg effect, it h
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Schulze, Almut, Karim Bensaad, and Adrian L. Harris. "Cancer metabolism." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0016.

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Abnormalities in cancer metabolism have been noted since Warburg first described the phenomenon of glycolysis in normoxic conditions. This chapter reviews the major pathways in metabolism known to be modified in cancer, including glycolysis and the Krebs cycle, the pentose shunt, and new data implicating the role of different metabolic adaptations, including oncometabolism. It highlights the genetic changes that effect metabolism including many of the commonly occurring oncogenes but also rare mutations that specifically target metabolism. Nutrient and oxygen limitation and proliferation creat
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"Cell Cycle and Energy Metabolism in Tumor Cells: Strategies for Drug Therapy." In Topics in Anti-Cancer Research, edited by Nivea D. Amoêdo, Tatiana El-Bacha Porto, Mariana F. Rodrigues, and Franklin D. Rumjanek. BENTHAM SCIENCE PUBLISHERS, 2013. http://dx.doi.org/10.2174/9781608051366113020008.

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Piris, M. A., M. Sanchez-Beato, R. Villuendas, and J. C. Martinez. "Oncogenes and tumour-suppressor genes." In Cell Proliferation in Cancer. Oxford University PressOxford, 1995. http://dx.doi.org/10.1093/oso/9780198547914.003.0003.

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Abstract The process of oncogenesis at the cellular level appears to be related to disorders in the control of cell proliferation, differentiation, and programmed cell death. These processes in higher organisms are regulated by multiple mechanisms involving intracellular and extracellular loops of control. Most, if not all, cancer cells contain multiple genetic aberrations that appear to contribute to tumorigenesis by perturbing these pathways. Two basic types of genetic damage are encountered frequently in cancer cells, dominant with targets known as proto-oncogenes, and recessive with target
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Jain, Aakanchha, Shiv Kumar Prajapati Prajapati, Dolly Jain, et al. "Cancer Biology." In Therapeutic Nanocarriers in Cancer Treatment: Challenges and Future Perspective. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815080506123010004.

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As stated by Globocan, there were around 82 lakh cancer-related deaths and 141 lakh new cancer diagnoses worldwide in 2012. Normal genes that are expressed improperly or exhibit aberrant expression may cause neoplasia, often known as cancer. Oncogenes are mutated forms of normal cellular genes that contribute to the development of cancer. Typically, oncogenes govern cell development and differentiation. Proapoptotic genes initiate cell death and decrease the number of cells. Antioncogens, or tumour suppressor genes, regulate cell division negatively. Tumours are caused by genes that directly o
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Zhan, Xianquan, and Na Li. "The Anti-Cancer Effects of Anti-Parasite Drug Ivermectin in Ovarian Cancer." In Ovarian Cancer - Updates in Tumour Biology and Therapeutics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95556.

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Ivermectin is an old, common, and classic anti-parasite drug, which has been found to have a broad-spectrum anti-cancer effect on multiple human cancers. This chapter will focus on the anti-cancer effects of ivermectin on ovarian cancer. First, ivermectin was found to suppress cell proliferation and growth, block cell cycle progression, and promote cell apoptosis in ovarian cancer. Second, drug pathway network, qRT-PCR, and immunoaffinity blot analyses found that ivermectin acts through molecular networks to target the key molecules in energy metabolism pathways, including PFKP in glycolysis,
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Joshi, Mit, and Bhoomika M. Patel. "Sphingosine Kinase as a Target to Treat Gastrointestinal Cancers." In Promising Cancer Therapeutic Drug Targets: Recent Advancements. BENTHAM SCIENCE PUBLISHERS, 2025. https://doi.org/10.2174/9789815238570125010008.

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Gastrointestinal cancer is a malignant condition of the gastrointestinal tract including the esophagus, stomach, small and large intestine, rectum, and anus. About 4.8 million new cases of gastrointestinal cancer were recorded in 2020. Current treatment options of gastrointestinal cancers have failed to treat the disease condition and newer approaches are under investigation. One such approach includes targeting the sphingosine kinase, a critical enzyme in sphingolipid metabolism. Known as structural molecules of the cellular membrane, sphingolipids, and their metabolism have emerged as import
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Gomes Morais, Mariana, Francisca Guilherme Carvalho Dias, João Alexandre Velho Prior, Ana Luísa Pereira Teixeira, and Rui Manuel de Medeiros Melo Silva. "The Impact of Oxidoreductases-Related MicroRNAs in Glucose Metabolism of Renal Cell Carcinoma and Prostate Cancer." In Oxidoreductase. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.93932.

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The reprogramming of metabolism is one of cancer hallmarks. Glucose’s metabolism, as one of the main fuels of cancer cells, has been the focus of several research studies in the oncology field. However, because cancer is a heterogeneous disease, the disruptions in glucose metabolism are highly variable depending of the cancer. In fact, Renal Cell Carcinoma (RCC) and Prostate Cancer (PCa), the most lethal and common urological neoplasia, respectively, show different disruptions in the main pathways of glucose catabolism: glycolysis, lactate fermentation and Krebs Cycle. Oxidoreductases are a cl
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Alam, Waqas, Haroon Khan, Michael Ascher, and Imad Ahmad. "Flavonoids in the Treatment of Gastrointestinal Tract Cancer." In Phytonutrients in the Treatment of Gastrointestinal Cancer. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815049633123010007.

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Globally, cancer is a leading cause of death next to cardiovascular disease. Gastrointestinal malignancies (GI) are extremely widespread malignancies, but their prevalence varies significantly amongst nations and communities. Existing cancer treatments are primarily concerned with low tissue availability, adverse drug reactions related to the demand for larger dose levels and non-specificity of the medicine. Phytochemicals have been important resources of preventive and curative entities for a variety of diseases, such as cancer. To a certain extent, enough investigation has been made over the
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Conference papers on the topic "Metabolism, Cell Cycle, Cancer, Kras"

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Salvucci, Manuela, Robert O’Byrne, Natalia Niewidok, et al. "Abstract 1012: Systems analysis of colon cancer cell metabolism rewired by p53 and KRAS mutations." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1012.

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Rozeveld, Cody, Ryan Schulze, Lizhi Zhang, and Gina L. Razidlo. "Abstract PR09: KRas modulates pancreatic cancer cell metabolism and invasive potential through the lipase HSL." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-pr09.

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Gwinn, Dana M., and Alejandro Sweet-Cordero. "Abstract B27: Kras alters expression of asparagine synthetase (Asns) in non-small cell lung cancer (NSCLC) and protects tumors during nutrient stress." 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-b27.

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Andrew, Angeline S., Jiang Gui, Jason H. Moore, et al. "Abstract A66: Apoptosis, cell cycle, DNA repair, immune, and metabolism pathway SNPs modify bladder cancer risk, recurrence, and survival." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a66.

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Gut, Ivan, Marie Ehrlichova, Radka Vaclavikova, Iwao Ojima, and Petr Simek. "Abstract A147: Novel fluorinated taxane SB‐T‐12854 active in drug‐resistant and sensitive cell lines: Human, pig, rat metabolism, cell transport, and effects on cell cycle." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a147.

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Váraljai, Renáta, Abul B. M. M. K. Islam, Nicholas J. Dyson, and Elizaveta V. Benevolenskaya. "Abstract B01: pRb activates mitochondrial metabolism and promotes differentiation through the histone demethylase Kdm5a." In Abstracts: AACR Precision Medicine Series: Cancer Cell Cycle - Tumor Progression and Therapeutic Response; February 28 - March 2, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.cellcycle16-b01.

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Okano, Larissa Miyuki, Alexandre Luiz Korte de Azevedo, Tamyres Mingorance Carvalho, Tathiane Maistro Malta, Mauro Antonio Alves Castro, and Luciane Regina Cavalli. "Characterization of an epigenetic regulatory network on basal-like breast cancer subtype and its impact on signaling pathways and biological processes." In Brazilian Breast Cancer Symposium 2024. Mastology, 2024. http://dx.doi.org/10.29289/259453942024v34s1029.

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Objective: The main objective of this study was to identify DNA methylation at the distal cis-regulatory genomic regions associated with the basal-like breast cancer (BLBC) subtype, construct an epigenetic regulatory network, and determine its impact on cancer-associated signaling pathways and biological processes. Methodology: BLBC (n=134) and non- -tumoral breast (n=84) samples with DNA methylation, mRNA, and miRNA expression data were downloaded from The Cancer Genome Atlas (TCGA) database using a pipeline of computational tools. DNA methylation patterns on cancer- -specific enhancers enric
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Jovičić Milić, Sandra S., Marko Antonijević, Đorđe S. Petrović, Verica V. Jevtić, and Danijela Lj Stojković. "Investigation of the anticancer activity of 2-amino-6-methylbenzothiazole and corresponding Pd(II) complex using molecular docking simulations." In 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.535jm.

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In our prior investigations, it has been established that compound di(2-amino-6-methylbenzothiazole)dichloridopalladate(II) (C1) exhibits promising efficacy in inhibiting the growth of colon carcinoma, thereby demonstrating potential as an anticancer agent. To elucidate the underlying mechanism of action against cancer, a comprehensive investigation involving DNA binding analysis and a series of assays to evaluate the inhibitory potential of compound C1 against key proteins involved in cancer metabolism were conducted. The significant inhibitory potential of C1 towards Bcl-2, Ki-67, and CDK-4
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