Heinlein CA, Chang C. Androgen receptor in prostate most cancers. Endocr Rev. 2004;25:276–308.
Gibson DA, Saunders PTK, McEwan IJ. Androgens and androgen receptor: above and past. Mol Cell Endocrinol. 2018;465:1–3.
Dehm SM, Tindall DJ. Molecular regulation of androgen motion in prostate most cancers. J Cell Biochem. 2006;99:333–44.
Barfeld SJ, Itkonen HM, Urbanucci A, Mills IG. Androgen-regulated metabolism and biosynthesis in prostate most cancers. Endocr Relat Most cancers. 2014;21:T57–66.
Warburg O, Wind F, Negelein E. The metabolism of tumors within the physique. J Gen Physiol. 1927;8:519–30.
DeBerardinis RJ, Chandel NS. We have to speak in regards to the Warburg impact. Nat Metab. 2020;2:127–9.
Luengo A, Li Z, Gui DY, Sullivan LB, Zagorulya M, Do BT, et al. Elevated demand for NAD(+) relative to ATP drives cardio glycolysis. Mol Cell. 2021;81:691–707.e6.
Wang Y, Stancliffe E, Fowle-Grider R, Wang R, Wang C, Schwaiger-Haber M, et al. Saturation of the mitochondrial NADH shuttles drives cardio glycolysis in proliferating cells. Mol Cell. 2022;82:3270–83.e9.
Vaarwerk B, Breunis WB, Haveman LM, de Keizer B, Jehanno N, Borgwardt L, et al. Fluorine-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) computed tomography (CT) for the detection of bone, lung, and lymph node metastases in rhabdomyosarcoma. Cochrane Database Syst Rev. 2021;11:CD012325.
Graham NA, Minasyan A, Lomova A, Cass A, Balanis NG, Friedman M, et al. Recurrent patterns of DNA copy quantity alterations in tumors mirror metabolic choice pressures. Mol Syst Biol. 2017;13:914.
Wei J, Huang Ok, Chen Z, Hu M, Bai Y, Lin S, et al. Characterization of glycolysis-associated molecules within the tumor microenvironment revealed by pan-cancer tissues and lung most cancers single cell knowledge. Cancers (Basel). 2020;12:1788.
Mitchell KG, Amini B, Wang Y, Carter BW, Godoy MCB, Parra ER, et al. 18)F-fluorodeoxyglucose positron emission tomography correlates with tumor immunometabolic phenotypes in resected lung most cancers. Most cancers Immunol Immunother. 2020;69:1519–34.
Mathews EH, Liebenberg L, Pelzer R. Excessive-glycolytic cancers and their interaction with the physique’s glucose demand and provide cycle. Med Hypotheses. 2011;76:157–65.
Uo T, Sprenger CC, Plymate SR. Androgen receptor signaling and metabolic and mobile plasticity throughout development to castration resistant prostate most cancers. Entrance Oncol. 2020;10:580617.
White MA, Tsouko E, Lin C, Rajapakshe Ok, Spencer JM, Wilkenfeld SR, et al. GLUT12 promotes prostate most cancers cell development and is regulated by androgens and CaMKK2 signaling. Endocr Relat Most cancers. 2018;25:453–69.
Xu M, Sakamoto S, Matsushima J, Kimura T, Ueda T, Mizokami A, et al. Up-regulation of LAT1 throughout antiandrogen remedy contributes to development in prostate most cancers cells. J Urol. 2016;195:1588–97.
Wang J, Xu W, Wang B, Lin G, Wei Y, Abudurexiti M, et al. GLUT1 is an AR goal contributing to tumor development and glycolysis in castration-resistant and enzalutamide-resistant prostate cancers. Most cancers Lett. 2020;485:45–55.
de Moist L, Williams A, Gillard M, Kregel S, Lamperis S, Gutgesell LC, et al. SOX2 mediates metabolic reprogramming of prostate most cancers cells. Oncogene. 2022;41:1190–202.
Crowell PD, Giafaglione JM, Jones AE, Nunley NM, Hashimoto T, Delcourt AML, et al. MYC is a regulator of androgen receptor inhibition-induced metabolic necessities in prostate most cancers. Cell Rep. 2023;42:113221.
Liu Y, Zuckier LS, Ghesani NV. Dominant uptake of fatty acid over glucose by prostate cells: a possible new diagnostic and therapeutic method. Anticancer Res. 2010;30:369–74.
Sadeghi RN, Karami-Tehrani F, Salami S. Focusing on prostate most cancers cell metabolism: impression of hexokinase and CPT-1 enzymes. Tumour Biol. 2015;36:2893–905.
Twum-Ampofo J, Fu D-X, Passaniti A, Hussain A, Siddiqui MM. Metabolic targets for potential prostate most cancers therapeutics. Curr Opin Oncol. 2016;28:241–7.
Jadvar H. PET of glucose metabolism and mobile proliferation in prostate most cancers. J Nucl Med. 2016;57:25S–9S.
Vaz CV, Alves MG, Marques R, Moreira PI, Oliveira PF, Maia CJ, et al. Androgen-responsive and nonresponsive prostate most cancers cells current a definite glycolytic metabolism profile. Int J Biochem Cell Biol. 2012;44:2077–84.
Granlund KL, Tee S-S, Vargas HA, Lyashchenko SK, Reznik E, Nice S, et al. Hyperpolarized MRI of human prostate most cancers reveals elevated lactate with tumor grade pushed by monocarboxylate transporter 1. Cell Metab. 2020;31:105–14.e3.
Chen M-L, Xu P-Z, Peng X, Chen WS, Guzman G, Yang X, et al. The deficiency of Akt1 is enough to suppress tumor improvement in Pten + /− mice. Genes Dev. 2006;20:1569–74.
Grasso CS, Wu YM, Robinson DR, Cao X, Dhanasekaran SM, Khan AP, et al. The mutational panorama of deadly castration-resistant prostate most cancers. Nature. 2012;487:239–43.
Choi SYC, Ettinger SL, Lin D, Xue H, Ci X, Nabavi N, et al. Focusing on MCT4 to scale back lactic acid secretion and glycolysis for therapy of neuroendocrine prostate most cancers. Most cancers Med. 2018;7:3385–92.
Porporato PE, Filigheddu N, Pedro JMB-S, Kroemer G, Galluzzi L. Mitochondrial metabolism and most cancers. Cell Res. 2018;28:265–80.
Jia D, Lu M, Jung KH, Park JH, Yu L, Onuchic JN, et al. Elucidating most cancers metabolic plasticity by coupling gene regulation with metabolic pathways. Proc Natl Acad Sci USA. 2019;116:3909–18.
Cassim S, Vučetić M, Ždralević M, Pouyssegur J. Warburg and past: the ability of mitochondrial metabolism to collaborate or substitute fermentative glycolysis in most cancers. Cancers (Basel). 2020;12:1119.
Grasso D, Zampieri LX, Capelôa T, Van de Velde JA, Sonveaux P. Mitochondria in most cancers. Cell Stress. 2020;4:114–46.
Roth KG, Mambetsariev I, Kulkarni P, Salgia R. The mitochondrion as an rising therapeutic goal in most cancers. Developments Mol Med. 2020;26:119–34.
Mosier JA, Schwager SC, Boyajian DA, Reinhart-King CA. Most cancers cell metabolic plasticity in migration and metastasis. Clin Exp Metastasis. 2021;38:343–59.
Tan YQ, Zhang X, Zhang S, Zhu T, Garg M, Lobie PE, et al. Mitochondria: the metabolic change of mobile oncogenic transformation. Biochim Biophys Acta Rev Most cancers. 2021;1876:188534.
Zhang X, Su Q, Zhou J, Yang Z, Liu Z, Ji L, et al. To betray or to battle? The twin id of the mitochondria in most cancers. Future Oncol. 2021;17:723–43.
Uo T, Ojo KK, Sprenger CCT, Soriano Epilepsia Ok, Perera BGK, Damodarasamy, M et al. A Compound that Inhibits Glycolysis in Prostate Most cancers Controls Development of Superior Prostate Most cancers. Mol Most cancers Ther. 2024; https://doi.org/10.1158/1535-7163.MCT-23-0540.
Bartman CR, Weilandt DR, Shen Y, Lee WD, Han Y, TeSlaa T, et al. Sluggish TCA flux and ATP manufacturing in main strong tumours however not metastases. Nature. 2023;614:349–57.
Fischer GM, Jalali A, Kircher DA, Lee W-C, McQuade JL, Haydu LE, et al. Molecular profiling reveals distinctive immune and metabolic options of melanoma mind metastases. Most cancers Discov. 2019;9:628–45.
Yap TA, Daver N, Mahendra M, Zhang J, Kamiya-Matsuoka C, Meric-Bernstam F, et al. Complicated I inhibitor of oxidative phosphorylation in superior strong tumors and acute myeloid leukemia: section I trials. Nat Med. 2023;29:115–26.
Mullen AR, Hu Z, Shi X, Jiang L, Boroughs LK, Kovacs Z, et al. Oxidation of alpha-ketoglutarate is required for reductive carboxylation in most cancers cells with mitochondrial defects. Cell Rep. 2014;7:1679–90.
Tomlinson IPM, Alam NA, Rowan AJ, Barclay E, Jaeger EEM, Kelsell D, et al. Germline mutations in FH predispose to dominantly inherited uterine fibroids, pores and skin leiomyomata and papillary renal cell most cancers. Nat Genet. 2002;30:406–10.
Baysal BE, Ferrell RE, Willett-Brozick JE, Lawrence EC, Myssiorek D, Bosch A, et al. Mutations in SDHD, a mitochondrial advanced II gene, in hereditary paraganglioma. Science. 2000;287:848–51.
Mullen AR, Wheaton WW, Jin ES, Chen P-H, Sullivan LB, Cheng T, et al. Reductive carboxylation helps development in tumour cells with faulty mitochondria. Nature. 2011;481:385–8.
Astuti D, Latif F, Dallol A, Dahia PL, Douglas F, George E, et al. Gene mutations within the succinate dehydrogenase subunit SDHB trigger susceptibility to familial pheochromocytoma and to familial paraganglioma. Am J Hum Genet. 2001;69:49–54.
Killian JK, Kim SY, Miettinen M, Smith C, Merino M, Tsokos M, et al. Succinate dehydrogenase mutation underlies world epigenomic divergence in gastrointestinal stromal tumor. Most cancers Discov. 2013;3:648–57.
Niemann S, Müller U. Mutations in SDHC trigger autosomal dominant paraganglioma, sort 3. Nat Genet. 2000;26:268–70.
Arnold PK, Jackson BT, Paras KI, Brunner JS, Hart ML, Newsom OJ, et al. A non-canonical tricarboxylic acid cycle underlies mobile id. Nature. 2022;603:477–81.
Cutruzzolà F, Giardina G, Marani M, Macone A, Paiardini A, Rinaldo S, et al. Glucose metabolism within the development of prostate most cancers. Entrance Physiol. 2017;8:97.
Costello LC, Franklin RB. Citrate metabolism of regular and malignant prostate epithelial cells. Urology. 1997;50:3–12.
Costello LC, Franklin RB. The scientific relevance of the metabolism of prostate most cancers; zinc and tumor suppression: connecting the dots. Mol Most cancers. 2006;5:17.
Costello LC, Feng P, Milon B, Tan M, Franklin RB. Function of zinc within the pathogenesis and therapy of prostate most cancers: important points to resolve. Prostate Most cancers Prostatic Dis. 2004;7:111–7.
Cooper JF, Farid I. The function of citric acid within the physiology of the prostate. 3. Lactate/citrate ratios in benign and malignant prostatic homogenates as an index of prostatic malignancy. J Urol. 1964;92:533–6.
Giafaglione JM, Crowell PD, Delcourt AML, Hashimoto T, Ha SM, Atmakuri A, et al. Prostate lineage-specific metabolism governs luminal differentiation and response to antiandrogen therapy. Nat Cell Biol. 2023;25:1821–32.
Costello LC, Franklin RB, Feng P. Mitochondrial perform, zinc, and middleman metabolism relationships in regular prostate and prostate most cancers. Mitochondrion. 2005;5:143–53.
Frégeau-Proulx L, Lacouture A, Berthiaume L, Weidmann C, Harvey M, Gonthier Ok, et al. A number of metabolic pathways gas the truncated tricarboxylic acid cycle of the prostate to maintain fixed citrate manufacturing and secretion. Mol Metab. 2022;62:101516.
Zou J, Milon BC, Desouki MM, Costello LC, Franklin RB. hZIP1 zinc transporter down-regulation in prostate most cancers includes the overexpression of ras responsive ingredient binding protein-1 (RREB-1). Prostate. 2011;71:1518–24.
Milon BC, Agyapong A, Bautista R, Costello LC, Franklin RB. Ras responsive ingredient binding protein-1 (RREB-1) down-regulates hZIP1 expression in prostate most cancers cells. Prostate. 2010;70:288–96.
Shao Y, Ye G, Ren S, Piao H-L, Zhao X, Lu X, et al. Metabolomics and transcriptomics profiles reveal the dysregulation of the tricarboxylic acid cycle and associated mechanisms in prostate most cancers. Int J Most cancers. 2018;143:396–407.
Ahmad F, Cherukuri MK, Choyke PL. Metabolic reprogramming in prostate most cancers. Br J Most cancers. 2021;125:1185–96.
Mahmood M, Liu EM, Shergold AL, Tolla E, Tait-Mulder J, Huerta-Uribe A, et al. Mitochondrial DNA mutations drive cardio glycolysis to boost checkpoint blockade response in melanoma. Nat Most cancers. 2024. https://doi.org/10.1038/s43018-023-00721-w.
Wheaton WW, Weinberg SE, Hamanaka RB, Soberanes S, Sullivan LB, Anso E, et al. Metformin inhibits mitochondrial advanced I of most cancers cells to scale back tumorigenesis. Elife. 2014;3:e02242.
Heinz S, Freyberger A, Lawrenz B, Schladt L, Schmuck G, Ellinger-Ziegelbauer H. Mechanistic investigations of the mitochondrial advanced I inhibitor rotenone within the context of pharmacological and security analysis. Sci Rep. 2017;7:45465.
Zaidi S, Gandhi J, Joshi G, Smith NL, Khan SA. The anticancer potential of metformin on prostate most cancers. Prostate Most cancers Prostatic Dis. 2019;22:351–61.
Naguib A, Mathew G, Reczek CR, Watrud Ok, Ambrico A, Herzka T, et al. Mitochondrial advanced I inhibitors expose a vulnerability for selective killing of Pten-null cells. Cell Rep. 2018;23:58–67.
Bader DA, McGuire SE. Tumour metabolism and its distinctive properties in prostate adenocarcinoma. Nat Rev Urol. 2020;17:214–31.
Bader DA, Hartig SM, Putluri V, Foley C, Hamilton MP, Smith EA, et al. Mitochondrial pyruvate import is a metabolic vulnerability in androgen receptor-driven prostate most cancers. Nat Metab. 2019;1:70–85.
Patra KC, Hay N. The pentose phosphate pathway and most cancers. Developments Biochem Sci. 2014;39:347–54.
Jin L, Zhou Y. Essential function of the pentose phosphate pathway in malignant tumors. Oncol Lett. 2019;17:4213–21.
Ronquist G, Theodorsson E. Inherited, non-spherocytic haemolysis on account of deficiency of glucose-6-phosphate dehydrogenase. Scand J Clin Lab Make investments. 2007;67:105–11.
Mehta A, Mason PJ, Vulliamy TJ. Glucose-6-phosphate dehydrogenase deficiency. Baillieres Finest Pr Res Clin Haematol. 2000;13:21–38.
Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008;371:64–74.
Dore MP, Davoli A, Longo N, Marras G, Pes GM. Glucose-6-phosphate dehydrogenase deficiency and danger of colorectal most cancers in Northern Sardinia: a retrospective observational research. Drugs. 2016;95:e5254.
Kowalik MA, Columbano A, Perra A. Rising function of the pentose phosphate pathway in hepatocellular carcinoma. Entrance Oncol. 2017;7:87.
Chen M, Shen M, Li Y, Liu C, Zhou Ok, Hu W, et al. GC-MS-based metabolomic evaluation of human papillary thyroid carcinoma tissue. Int J Mol Med. 2015;36:1607–14.
Cohen HJ, Elizalde A, Miller SP. Cytologic research of glucose-6-phosphate dehydrogenase in malignancy. Most cancers. 1968;21:1055–60.
Langbein S, Frederiks WM, zur Hausen A, Popa J, Lehmann J, Weiss C, et al. Metastasis is promoted by a bioenergetic change: new targets for progressive renal cell most cancers. Int J Most cancers. 2008;122:2422–8.
Lu M, Lu L, Dong Q, Yu G, Chen J, Qin L, et al. Elevated G6PD expression contributes to migration and invasion of hepatocellular carcinoma cells by inducing epithelial-mesenchymal transition. Acta Biochim Biophys Sin (Shanghai). 2018;50:370–80.
Dong T, Kang X, Liu Z, Zhao S, Ma W, Xuan Q, et al. Altered glycometabolism impacts each scientific options and prognosis of triple-negative and neoadjuvant chemotherapy-treated breast most cancers. Tumour Biol. 2016;37:8159–68.
Pu H, Zhang Q, Zhao C, Shi L, Wang Y, Wang J, et al. Overexpression of G6PD is related to excessive dangers of recurrent metastasis and poor progression-free survival in main breast carcinoma. World J Surg Oncol. 2015;13:323.
Zampella EJ, Bradley ELJ, Pretlow TG 2nd. Glucose-6-phosphate dehydrogenase: a potential scientific indicator for prostatic carcinoma. Most cancers. 1982;49:384–7.
Tsouko E, Khan AS, White MA, Han JJ, Shi Y, Service provider FA, et al. Regulation of the pentose phosphate pathway by an androgen receptor-mTOR-mediated mechanism and its function in prostate most cancers cell development. Oncogenesis. 2014;3:e103.
Whitburn J, Rao SR, Morris EV, Tabata S, Hirayama A, Soga T, et al. Metabolic profiling of prostate most cancers in skeletal microenvironments identifies G6PD as a key mediator of development and survival. Sci Adv. 2022;8:eabf9096.
Gillis JL, Hinneh JA, Ryan NK, Irani S, Moldovan M, Quek L-E, et al. A suggestions loop between the androgen receptor and 6-phosphogluoconate dehydrogenase (6PGD) drives prostate most cancers development. Elife. 2021;10:e62592.
Marshall S, Bacote V, Traxinger RR. Discovery of a metabolic pathway mediating glucose-induced desensitization of the glucose transport system. Function hexosamine biosynth induction insulin resistance. J Biol Chem. 1991;266:4706–12.
Ying H, Kimmelman AC, Lyssiotis CA, Hua S, Chu GC, Fletcher-Sananikone E, et al. Oncogenic Kras maintains pancreatic tumors by regulation of anabolic glucose metabolism. Cell. 2012;149:656–70.
Moloughney JG, Kim PK, Vega-Cotto NM, Wu C-C, Zhang S, Adlam M, et al. mTORC2 responds to glutamine catabolite ranges to modulate the hexosamine biosynthesis enzyme GFAT1. Mol Cell. 2016;63:811–26.
Moloughney JG, Vega-Cotto NM, Liu S, Patel C, Kim PK, Wu C-C, et al. mTORC2 modulates the amplitude and period of GFAT1 Ser-243 phosphorylation to take care of flux by the hexosamine pathway throughout hunger. J Biol Chem. 2018;293:16464–78.
Lucena MC, Carvalho-Cruz P, Donadio JL, Oliveira IA, de Queiroz RM, Marinho-Carvalho MM, et al. Epithelial mesenchymal transition induces aberrant glycosylation by hexosamine biosynthetic pathway activation. J Biol Chem. 2016;291:12917–29.
Caldwell SA, Jackson SR, Shahriari KS, Lynch TP, Sethi G, Walker S, et al. Nutrient sensor O-GlcNAc transferase regulates breast most cancers tumorigenesis by focusing on of the oncogenic transcription issue FoxM1. Oncogene. 2010;29:2831–42.
Champattanachai V, Netsirisawan P, Chaiyawat P, Phueaouan T, Charoenwattanasatien R, Chokchaichamnankit D, et al. Proteomic evaluation and abrogated expression of O-GlcNAcylated proteins related to main breast most cancers. Proteomics. 2013;13:2088–99.
Mi W, Gu Y, Han C, Liu H, Fan Q, Zhang X, et al. O-GlcNAcylation is a novel regulator of lung and colon most cancers malignancy. Biochim Biophys Acta. 2011;1812:514–9.
Zhu Q, Zhou L, Yang Z, Lai M, Xie H, Wu L, et al. O-GlcNAcylation performs a job in tumor recurrence of hepatocellular carcinoma following liver transplantation. Med Oncol. 2012;29:985–93.
Krześlak A, Wójcik-Krowiranda Ok, Forma E, Bieńkiewicz A, Bryś M. Expression of genes encoding for enzymes related to O-GlcNAcylation in endometrial carcinomas: clinicopathologic correlations. Ginekol Pol. 2012;83:22–26.
Kim MJ, Choi MY, Lee DH, Roh GS, Kim HJ, Kang SS, et al. O-linked N-acetylglucosamine transferase enhances secretory clusterin expression through liver X receptors and sterol response ingredient binding protein regulation in cervical most cancers. Oncotarget. 2018;9:4625–36.
Ma Z, Vocadlo DJ, Vosseller Ok. Hyper-O-GlcNAcylation is anti-apoptotic and maintains constitutive NF-κB exercise in pancreatic most cancers cells. J Biol Chem. 2013;288:15121–30.
Itkonen HM, Minner S, Guldvik IJ, Sandmann MJ, Tsourlakis MC, Berge V, et al. O-GlcNAc transferase integrates metabolic pathways to manage the soundness of c-MYC in human prostate most cancers cells. Most cancers Res. 2013;73:5277–87.
Munkley J, Vodak D, Livermore KE, James Ok, Wilson BT, Knight B, et al. Glycosylation is an androgen-regulated course of important for prostate most cancers cell viability. EBioMedicine. 2016;8:103–16.
Albitar M, Ma W, Lund L, Albitar F, Diep Ok, Fritsche HA, et al. Predicting prostate biopsy outcomes utilizing a panel of plasma and urine biomarkers mixed in a scoring system. J Most cancers. 2016;7:297–303.
Itkonen HM, Engedal N, Babaie E, Luhr M, Guldvik IJ, Minner S, et al. UAP1 is overexpressed in prostate most cancers and is protecting towards inhibitors of N-linked glycosylation. Oncogene. 2015;34:3744–50.
Scott E, Hodgson Ok, Calle B, Turner H, Cheung Ok, Bermudez A, et al. Upregulation of GALNT7 in prostate most cancers modifies O-glycosylation and promotes tumour development. Oncogene. 2023;42:926–37.
Rossi M, Altea-Manzano P, Demicco M, Doglioni G, Bornes L, Fukano M, et al. PHGDH heterogeneity potentiates most cancers cell dissemination and metastasis. Nature. 2022;605:747–53.
Samaržija I. Put up-translational modifications that drive prostate most cancers development. Biomolecules. 2021;11:247.
Itkonen HM, Gorad SS, Duveau DY, Martin SES, Barkovskaya A, Bathen TF, et al. Inhibition of O-GlcNAc transferase exercise reprograms prostate most cancers cell metabolism. Oncotarget. 2016;7:12464–76.
de Queiroz RM, Madan R, Chien J, Dias WB, Slawson C. Adjustments in O-linked N-acetylglucosamine (O-GlcNAc) homeostasis activate the p53 pathway in ovarian most cancers cells. J Biol Chem. 2016;291:18897–914.
Kaushik AK, Shojaie A, Panzitt Ok, Sonavane R, Venghatakrishnan H, Manikkam M, et al. Inhibition of the hexosamine biosynthetic pathway promotes castration-resistant prostate most cancers. Nat Commun. 2016;7:11612.
Baenke F, Peck B, Miess H, Schulze A. Hooked on fats: the function of lipid synthesis in most cancers metabolism and tumour improvement. Dis Mannequin Mech. 2013;6:1353–63.
Broadfield LA, Pane AA, Talebi A, Swinnen JV, Fendt SM. Lipid metabolism in most cancers: new views and rising mechanisms. Dev Cell. 2021;56:1363–93.
Giunchi F, Fiorentino M, Loda M. The metabolic panorama of prostate most cancers. Eur Urol Oncol. 2019;2:28–36.
Butler LM, Centenera MM, Swinnen JV. Androgen management of lipid metabolism in prostate most cancers: novel insights and future purposes. Endocr Relat Most cancers. 2016;23:R219–27.
Swinnen JV, Verhoeven G. Androgens and the management of lipid metabolism in human prostate most cancers cells. J Steroid Biochem Mol Biol. 1998;65:191–8.
Pardo JC, de Porras VR, Gil J, Font A, Puig-Domingo M, Jordà M. Lipid metabolism and epigenetics crosstalk in prostate most cancers. Vitamins. 2022;14:851.
Lounis MA, Péant B, Leclerc-Desaulniers Ok, Ganguli D, Daneault C, Ruiz M, et al. Modulation of de novo lipogenesis improves response to enzalutamide therapy in prostate most cancers. Cancers (Basel). 2020;12:1–21.
Butler LM, Mah CY, Machiels J, Vincent AD, Irani S, Mutuku SM, et al. Lipidomic profiling of scientific prostate most cancers reveals targetable alterations in membrane lipid composition. Most cancers Res. 2021;81:4981–93.
Mounier C, Bouraoui L, Rassart E. Lipogenesis in most cancers development (assessment). Int J Oncol. 2014;45:485–92.
Huang WC, Li X, Liu J, Lin J, Chung LWK. Activation of androgen receptor, lipogenesis, and oxidative stress converged by SREBP-1 is liable for regulating development and development of prostate most cancers cells. Mol Most cancers Res. 2012;10:133–42.
Lee MY, Moon JS, Park SW, Koh YK, Ahn YH, Kim KS. KLF5 enhances SREBP-1 motion in androgen-dependent induction of fatty acid synthase in prostate most cancers cells. Biochem J. 2009;417:313–22.
Hamada S, Horiguchi A, Kuroda Ok, Ito Ok, Asano T, Miyai Ok, et al. Elevated fatty acid synthase expression in prostate biopsy cores predicts greater Gleason rating in radical prostatectomy specimen. BMC Clin Pathol. 2014;14:3.
Bastos DC, Ribeiro CF, Ahearn T, Nascimento J, Pakula H, Clohessy J, et al. Genetic ablation of FASN attenuates the invasive potential of prostate most cancers pushed by Pten loss. J Pathol. 2021;253:292–303.
Li X, Chen YT, Hu P, Huang WC. Fatostatin shows excessive antitumor exercise in prostate most cancers by blocking SREBP-regulated metabolic pathways and androgen receptor signaling. Mol Most cancers Ther. 2014;13:855–66.
Schmidt LJ, Ballman KV, Tindall DJ. Inhibition of fatty acid synthase exercise in prostate most cancers cells by dutasteride. Prostate. 2007;67:1111–20.
Rae C, Fragkoulis GI, Chalmers AJ. Cytotoxicity and radiosensitizing exercise of the fatty acid synthase inhibitor C75 is enhanced by blocking fatty acid uptake in prostate most cancers cells. Adv Radiat Oncol. 2020;5:994–1005.
Chuang HY, Lee YP, Lin WC, Lin YH, Hwang JJ. Fatty acid inhibition sensitizes androgen-dependent and -independent prostate most cancers to radiotherapy through FASN/NF-κB pathway. Sci Rep. 2019;9:13284.
Centenera MM, Scott JS, Machiels J, Nassar ZD, Miller DC, Zinonos I, et al. ELOVL5 is a important and targetable fatty acid elongase in prostate most cancers. Most cancers Res. 2021;81:1704–18.
Xu H, Li S, Solar Y, Xu L, Hong X, Wang Z, et al. ELOVL5-mediated lengthy chain fatty acid elongation contributes to enzalutamide resistance of prostate most cancers. Cancers (Basel). 2021;13:1–12.
Kaini RR, Sillerud LO, Zhaorigetu S, Hu CAA. Autophagy regulates lipolysis and cell survival by lipid droplet degradation in androgen-sensitive prostate most cancers cells. Prostate. 2012;72:1412–22.
Nomura DK, Lombardi DP, Chang JW, Niessen S, Ward AM, Lengthy JZ, et al. Monoacylglycerol lipase exerts twin management over endocannabinoid and fatty acid pathways to assist prostate most cancers. Chem Biol. 2011;18:846–56.
Awad D, Cao PHA, Pulliam TL, Spradlin M, Subramani E, Tellman TV, et al. Adipose triglyceride lipase is a therapeutic goal in superior prostate most cancers that promotes metabolic plasticity. Most cancers Res. 2024;84:703–24.
Liu Y. Fatty acid oxidation is a dominant bioenergetic pathway in prostate most cancers. Prostate Most cancers Prostatic Dis. 2006;9:230–4.
Flaig TW, Salzmann-Sullivan M, Su LJ, Zhang Z, Joshi M, Gijón MA, et al. Lipid catabolism inhibition sensitizes prostate most cancers cells to antiandrogen blockade. Oncotarget. 2017;8:56051–65.
Schlaepfer IR, Rider L, Rodrigues LU, Gijón MA, Pac CT, Romero L, et al. Lipid catabolism through CPT1 as a therapeutic goal for prostate most cancers. Mol Most cancers Ther. 2014;13:2361–71.
Blomme A, Ford CA, Mui E, Patel R, Ntala C, Jamieson LE, et al. 2,4-dienoyl-CoA reductase regulates lipid homeostasis in treatment-resistant prostate most cancers. Nat Commun. 2020;11:1–17.
Nassar ZD, Mah CY, Dehairs J, Burvenich IJG, Irani S, Centenera MM, et al. Human DECR1 is an androgen-repressed survival issue that regulates PUFA oxidation to guard prostate tumor cells from ferroptosis. Elife. 2020;9:1–34.
O’Sullivan SE, Kaczocha M. FABP5 as a novel molecular goal in prostate most cancers. Drug Discov At the moment. 2020;25:2056–61.
Hillowe A, Gordon C, Wang L, Rizzo RC, Trotman LC, Ojima I, et al. Fatty acid binding protein 5 regulates docetaxel sensitivity in taxane-resistant prostate most cancers cells. PLoS One. 2023;18:e0292483.
Carbonetti G, Converso C, Clement T, Wang C, Trotman LC, Ojima I, et al. Docetaxel/cabazitaxel and fatty acid binding protein 5 inhibitors produce synergistic inhibition of prostate most cancers development. Prostate. 2020;80:88–98.
M Swamynathan M, Mathew G, Aziz A, Gordon C, Hillowe A, Wang H, et al. FABP5 inhibition towards PTEN-mutant remedy resistant prostate most cancers. Cancers (Basel). 2023;16:60.
Watt MJ, Clark AK, Selth LA, Haynes VR, Lister N, Rebello R, et al. Suppressing fatty acid uptake has therapeutic results in preclinical fashions of prostate most cancers. Sci Transl Med. 2019;11:1–12.
Pascual G, Avgustinova A, Mejetta S, Martín M, Castellanos A, Attolini CSO, et al. Focusing on metastasis-initiating cells by the fatty acid receptor CD36. Nature. 2017;541:41–45.
Pascual G, Domínguez D, Elosúa-Bayes M, Beckedorff F, Laudanna C, Bigas C, et al. Dietary palmitic acid promotes a prometastatic reminiscence through Schwann cells. Nature. 2021;599:485–90.
Stopsack KH, Gerke TA, Sinnott JA, Penney KL, Tyekucheva S, Sesso HD, et al. Ldl cholesterol metabolism and prostate most cancers lethality. Most cancers Res. 2016;76:4785–90.
Tibbo AJ, Hartley A, Vasan R, Shaw R, Galbraith L, Mui E, et al. MBTPS2 acts as a regulator of lipogenesis and ldl cholesterol synthesis by SREBP signalling in prostate most cancers. Br J Most cancers. 2023;128:1991–9.
Jiang S, Wang X, Track D, Liu XJ, Gu Y, Xu Z, et al. Ldl cholesterol induces epithelial-to-mesenchymal transition of prostate most cancers cells by suppressing degradation of EGFR by APMAP. Most cancers Res. 2019;79:3063–75.
Solanki AA, Liauw SL. Function of HMG-CoA reductase inhibitors with healing radiotherapy in males with prostate most cancers. Open Entry J Urol. 2011;3:95–104.
Dillard PR, Lin MF, Khan SA. Androgen-independent prostate most cancers cells purchase the whole steroidogenic potential of synthesizing testosterone from ldl cholesterol. Mol Cell Endocrinol. 2008;295:115–20.
Locke JA, Nelson CC, Adomat HH, Hendy SC, Gleave ME, Weapons EST. Steroidogenesis inhibitors alter however don’t remove androgen synthesis mechanisms throughout development to castration-resistance in LNCaP prostate xenografts. J Steroid Biochem Mol Biol. 2009;115:126–36.
Locke JA, Weapons ES, Lubik AA, Adomat HH, Hendy SC, Wooden CA, et al. Androgen ranges improve by intratumoral de novo steroidogenesis throughout development of castration-resistant prostate most cancers. Most cancers Res. 2008;68:6407–15.
Raftopulos NL, Washaya TC, Niederprüm A, Egert A, Hakeem-Sanni MF, Varney B, et al. Prostate most cancers cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover. Most cancers Metab. 2022;10:1–15.
Murtola TJ, Siltari A. Statins for prostate most cancers: when and the way a lot? Clin Most cancers Res. 2021;27:4947–9.
Pan T, Lin SC, Lee YC, Yu G, Track JH, Pan J, et al. Statins scale back castration-induced bone marrow adiposity and prostate most cancers development in bone. Oncogene. 2021;40:4592–603.
Hoque A, Chen H, Xu XC. Statin induces apoptosis and cell development arrest in prostate most cancers cells. Most cancers Epidemiol Biomark Prev. 2008;17:88–94.
Caro-Maldonado A, Camacho L, Zabala-Letona A, Torrano V, Fernández-Ruiz S, Zamacola-Bascaran Ok, et al. Low-dose statin therapy will increase prostate most cancers aggressiveness. Oncotarget. 2017;9:1494–504.
Shangguan X, Ma Z, Yu M, Ding J, Xue W, Qi J. Squalene epoxidase metabolic dependency is a targetable vulnerability in castration-resistant prostate most cancers. Most cancers Res. 2022;82:3032–44.
Kalogirou C, Linxweiler J, Schmucker P, Snaebjornsson MT, Schmitz W, Wach S, et al. MiR-205-driven downregulation of ldl cholesterol biosynthesis by SQLE-inhibition identifies therapeutic vulnerability in aggressive prostate most cancers. Nat Commun. 2021;12:5066.
El-Kenawi A, Dominguez-Viqueira W, Liu M, Awasthi S, Abraham-Miranda J, Keske A, et al. Macrophage-derived ldl cholesterol contributes to therapeutic resistance in prostate most cancers. Most cancers Res. 2021;81:5477–90.
Ducker GS, Rabinowitz JD. One-carbon metabolism in well being and illness. Cell Metab. 2017;25:27–42.
Islam A, Shaukat Z, Hussain R, Gregory SL. One-carbon and polyamine metabolism as most cancers remedy targets. Biomolecules. 2022;12:1902.
Newman AC, Maddocks ODK. One-carbon metabolism in most cancers. Br J Most cancers. 2017;116:1499–504.
Yang M, Vousden KH. Serine and one-carbon metabolism in most cancers. Nat Rev Most cancers. 2016;16:650–62.
Corbin JM, Ruiz-Echevarría MJ. One-carbon metabolism in prostate most cancers: the function of androgen signaling. Int J Mol Sci. 2016;17:1208.
Inexperienced T, Chen X, Ryan S, Asch AS, Ruiz-Echevarría MJ. TMEFF2 and SARDH cooperate to modulate one-carbon metabolism and invasion of prostate most cancers cells. Prostate. 2013;73:1561–75.
Track YH, Shiota M, Kuroiwa Ok, Naito S, Oda Y. The essential function of glycine N-methyltransferase within the carcinogenesis and development of prostate most cancers. Mod Pathol. 2011;24:1272–80.
Khan AP, Rajendiran TM, Ateeq B, Asangani IA, Athanikar JN, Yocum AK, et al. The function of sarcosine metabolism in prostate most cancers development. Neoplasia. 2013;15:491–501.
Jentzmik F, Stephan C, Lein M, Miller Ok, Kamlage B, Bethan B, et al. Sarcosine in prostate most cancers tissue is just not a differential metabolite for prostate most cancers aggressiveness and biochemical development. J Urol. 2011;185:706–11.
Sreekumar A, Poisson LM, Rajendiran TM, Khan AP, Cao Q, Yu J, et al. Metabolomic profiles delineate potential function for sarcosine in prostate most cancers development. Nature. 2009;457:910–4.
Luka Z, Mudd SH, Wagner C. Glycine N-methyltransferase and regulation of S-adenosylmethionine ranges. J Biol Chem. 2009;284:22507–11.
Ottaviani S, Brooke GN, O’Hanlon-Brown C, Waxman J, Ali S, Buluwela L. Characterisation of the androgen regulation of glycine N-methyltransferase in prostate most cancers cells. J Mol Endocrinol. 2013;51:301–12.
Mulholland DJ, Tran LM, Li Y, Cai H, Morim A, Wang S, et al. Cell autonomous function of PTEN in regulating castration-resistant prostate most cancers development. Most cancers Cell. 2011;19:792–804.
Carver BS, Chapinski C, Wongvipat J, Hieronymus H, Chen Y, Chandarlapaty S, et al. Reciprocal suggestions regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate most cancers. Most cancers Cell. 2011;19:575–86.
Zabala-Letona A, Arruabarrena-Aristorena A, Fernandez-Ruiz S, Viera C, Carlevaris O, Ercilla A, et al. PI3K-regulated Glycine N-methyltransferase is required for the event of prostate most cancers. Oncogenesis. 2022;11:10.
Obata F, Miura M. Enhancing S-adenosyl-methionine catabolism extends Drosophila lifespan. Nat Commun. 2015;6:1–9.
Reina-Campos M, Linares JF, Duran A, Cordes T, L’Hermitte A, Badur MG, et al. Elevated serine and one-carbon pathway metabolism by PKCλ/ι deficiency promotes neuroendocrine prostate most cancers. Most cancers Cell. 2019;35:385–400.e9.
Zhang HF, Klein Geltink RI, Parker SJ, Sorensen PH. Transsulfuration, minor participant or essential for cysteine homeostasis in most cancers. Developments Cell Biol. 2022;32:800–14.
Prudova A, Albin M, Bauman Z, Lin A, Vitvitsky V, Banerjee R. Testosterone regulation of homocysteine metabolism modulates redox standing in human prostate most cancers cells. Antioxid Redox Sign. 2007;9:1875–81.
Guo H, Gai JW, Wang Y, Jin HF, Du JB, Jin J. Characterization of hydrogen sulfide and its synthases, cystathionine β-synthase and cystathionine γ-lyase, in human prostatic tissue and cells. Urology. 2012;79:483.e1–483.e5.
Zhang W, Braun A, Bauman Z, Olteanu H, Madzelan P, Banerjee R. Expression profiling of homocysteine junction enzymes within the NCI60 panel of human most cancers cell traces. Most cancers Res. 2005;65:1554–60.
Stabler S, Koyama T, Zhao Z, Martinez-Ferrer M, Allen RH, Luka Z et al. Serum methionine metabolites are danger elements for metastatic prostate most cancers development. PLoS One 2011;6:8.
Saha A, Zhao S, Kindall A, Wilder C, Friedman CA, Clark R et al. Cysteine depletion sensitizes prostate most cancers cells to brokers that improve DNA harm and to immune checkpoint inhibition. J Exp Clin Most cancers Res. 2023;42:119.
Pegg AE. Capabilities of polyamines in mammals. J Biol Chem. 2016;291:14904–12.
Nowotarski SL, Woster PM, Casero RA Jr. Polyamines and most cancers: implications for chemoprevention and chemotherapy. Knowledgeable Rev Mol Med. 2014;15:1–28.
Jänne OA, Crozat A, Palvimo J, Eisenberg LM. Androgen-regulation of ornithine decarboxylase and S-adenosylmethionine decarboxylase genes. J Steroid Biochem Mol Biol. 1991;40:307–15.
Fjösne HE, Strand H, Sunde A. Dose-dependent induction of ornithine decarboxylase and S-adenosyl-methionine decarboxylase exercise by testosterone within the accent intercourse organs of male rats. Prostate. 1992;21:239–45.
Cohen RJ, Fujiwara Ok, Holland JW, McNeal JE. Polyamines in prostatic epithelial cells and adenocarcinoma; the results of androgen blockade. Prostate. 2001;49:278–84.
Bello-Fernandez C, Packham G, Cleveland JL. The ornithine decarboxylase gene is a transcriptional goal of c-Myc. Proc Natl Acad Sci USA. 1993;90:7804–8.
Kaminski L, Torrino S, Dufies M, Djabari Z, Haider R, Roustan FR, et al. PGC1α inhibits polyamine synthesis to suppress prostate most cancers aggressiveness. Most cancers Res. 2019;79:3268–80.
Torrano V, Valcarcel-Jimenez L, Cortazar AR, Liu X, Urosevic J, Castillo-Martin M, et al. The metabolic co-regulator PGC1α suppresses prostate most cancers metastasis. Nat Cell Biol. 2016;18:645–56.
Valcarcel-Jimenez L, Macchia A, Crosas-Molist E, Schaub-Clerigue A, Camacho L, Martín-Martín N, et al. PGC1α suppresses prostate most cancers cell invasion by ERRα transcriptional management. Most cancers Res. 2019;79:6153–65.
Zabala-Letona A, Arruabarrena-Aristorena A, Martín-Martín N, Fernandez-Ruiz S, Sutherland JD, Clasquin M, et al. MTORC1-dependent AMD1 regulation sustains polyamine metabolism in prostate most cancers. Nature. 2017;547:109–13.
Monelli E, Villacampa P, Zabala-Letona A, Martinez-Romero A, Llena J, Beiroa D, et al. Angiocrine polyamine manufacturing regulates adiposity. Nat Metab. 2022;4:327–43.
de Visser KE, Joyce JA. The evolving tumor microenvironment: from most cancers initiation to metastatic outgrowth. Most cancers Cell. 2023;41:374–403.
Qin Y, Lu F, Lyu Ok, Chang AE, Li Q. Rising ideas relating to pro- and anti tumor properties of B cells in tumor immunity. Entrance Immunol. 2022;13:881427.
Chen S, Zhu G, Yang Y, Wang F, Xiao YT, Zhang N, et al. Single-cell evaluation reveals transcriptomic remodellings in distinct cell varieties that contribute to human prostate most cancers development. Nat Cell Biol. 2021;23:87–98.
Wong HY, Sheng Q, Hesterberg AB, Croessmann S, Rios BL, Giri Ok, et al. Single cell evaluation of cribriform prostate most cancers reveals cell intrinsic and tumor microenvironmental pathways of aggressive illness. Nat Commun. 2022;13:6036.
Lopez-Bujanda ZA, Haffner MC, Chaimowitz MG, Chowdhury N, Venturini NJ, Patel RA, et al. Castration-mediated IL-8 promotes myeloid infiltration and prostate most cancers development. Nat Most cancers. 2021;2:803–18.
Chang C-H, Qiu J, O’Sullivan D, Buck MD, Noguchi T, Curtis JD, et al. Metabolic competitors within the tumor microenvironment is a driver of most cancers development. Cell. 2015;162:1229–41.
Beckermann KE, Dudzinski SO, Rathmell JC. Dysfunctional T cell metabolism within the tumor microenvironment. Cytokine Development Issue Rev. 2017;35:7–14.
Estrella V, Chen T, Lloyd M, Wojtkowiak J, Cornnell HH, Ibrahim-Hashim A, et al. Acidity generated by the tumor microenvironment drives native invasion. Most cancers Res. 2013;73:1524–35.
Liberti MV, Locasale JW. The Warburg impact: how does it profit most cancers cells? Developments Biochem Sci. 2016;41:211–8.
Niu D, Wu Y, Lei Z, Zhang M, Xie Z, Tang S. Lactic acid, a driver of tumor-stroma interactions. Int Immunopharmacol. 2022;106:108597.
Fischer Ok, Hoffmann P, Voelkl S, Meidenbauer N, Ammer J, Edinger M, et al. Inhibitory impact of tumor cell-derived lactic acid on human T cells. Blood. 2007;109:3812–9.
Inamdar S, Suresh AP, Mangal JL, Ng ND, Sundem A, Wu C, et al. Rescue of dendritic cells from glycolysis inhibition improves most cancers immunotherapy in mice. Nat Commun. 2023;14:5333.
Chang C-H, Curtis JD, Maggi LBJ, Faubert B, Villarino AV, O’Sullivan D, et al. Posttranscriptional management of T cell effector perform by cardio glycolysis. Cell. 2013;153:1239–51.
Jacobs SR, Herman CE, Maciver NJ, Wofford JA, Wieman HL, Hammen JJ, et al. Glucose uptake is limiting in T cell activation and requires CD28-mediated Akt-dependent and unbiased pathways. J Immunol. 2008;180:4476–86.
Notarangelo G, Spinelli JB, Perez EM, Baker GJ, Kurmi Ok, Elia I, et al. Oncometabolite d-2HG alters T cell metabolism to impair CD8( + ) T cell perform. Science. 2022;377:1519–29.
Lim SA, Wei J, Nguyen TLM, Shi H, Su W, Palacios G, et al. Lipid signalling enforces purposeful specialization of Treg cells in tumours. Nature. 2021;591:306–11.
Discipline CS, Baixauli F, Kyle RL, Puleston DJ, Cameron AM, Sanin DE, et al. Mitochondrial integrity regulated by lipid metabolism is a cell-intrinsic checkpoint for treg suppressive perform. Cell Metab. 2020;31:422–37.e5.
Yang P, Qin H, Li Y, Xiao A, Zheng E, Zeng H, et al. CD36-mediated metabolic crosstalk between tumor cells and macrophages impacts liver metastasis. Nat Commun. 2022;13:5782.
Nava Lauson CB, Tiberti S, Corsetto PA, Conte F, Tyagi P, Machwirth M, et al. Linoleic acid potentiates CD8 + T cell metabolic health and antitumor immunity. Cell Metab. 2023;35:633–50.e9.
Rowe JH, Elia I, Shahid O, Gaudiano EF, Sifnugel NE, Johnson S, et al. Formate supplementation enhances antitumor CD8 + T-cell health and efficacy of PD-1 blockade. Most cancers Discov. 2023;13:2566–83.
Cheng H, Qiu Y, Xu Y, Chen L, Ma Ok, Tao M, et al. Extracellular acidosis restricts one-carbon metabolism and preserves T cell stemness. Nat Metab. 2023;5:314–30.
Kurniawan H, Franchina DG, Guerra L, Bonetti L, Baguet LS, Grusdat M, et al. Glutathione restricts serine metabolism to protect regulatory T cell perform. Cell Metab. 2020;31:920–36.e7.
Valera PS, Plou J, García I, Astobiza I, Viera C, Aransay AM, et al. SERS evaluation of most cancers cell-secreted purines reveals a novel paracrine crosstalk in MTAP-deficient tumors. Proc Natl Acad Sci USA. 2023;120:52.
Terry AR, Nogueira V, Rho H, Ramakrishnan G, Li J, Kang S, et al. CD36 maintains lipid homeostasis through selective uptake of monounsaturated fatty acids throughout matrix detachment and tumor development. Cell Metab. 2023;35:2060–2076.e9.
Kalaany NY, Sabatini DM. Tumours with PI3K activation are immune to dietary restriction. Nature. 2009;458:725–31.
Lien EC, Westermark AM, Zhang Y, Yuan C, Li Z, Lau AN, et al. Low glycaemic diets alter lipid metabolism to affect tumour development. Nature. 2021;599:302–7.
Vidal AC, Freedland SJ. Weight problems and prostate most cancers: a targeted replace on lively surveillance, race, and molecular subtyping. Eur Urol. 2017;72:78.
Cantarutti A, Bonn SE, Adami HO, Grönberg H, Bellocco R, Bälter Ok. Physique mass index and mortality in males with prostate most cancers. Prostate. 2015;75:1129–36.
Zhong S, Yan X, Wu Y, Zhang X, Chen L, Tang J, et al. Physique mass index and mortality in prostate most cancers sufferers: a dose-response meta-analysis. Prostate Most cancers Prostatic Dis. 2016;19:122–31.
Liu J, Ramakrishnan SK, Khuder SS, Kaw MK, Muturi HT, Lester SG, et al. Excessive-calorie food plan exacerbates prostate neoplasia in mice with haploinsufficiency of Pten tumor suppressor gene. Mol Metab. 2015;4:186–98.
Wang H, Yan W, Solar Y, Yang CS. Excessive-fat diet-induced hyperinsulinemia promotes the event of prostate adenocarcinoma in prostate-specific Pten−/− mice. Carcinogenesis. 2022;43:504–16.
Labbé DP, Uetani N, Vinette V, Lessard L, Aubry I, Migon E, et al. PTP1B deficiency permits the power of a high-fat food plan to drive the invasive character of PTEN-deficient prostate cancers. Most cancers Res. 2016;76:3130–5.
Hayashi T, Fujita Ok, Nojima S, Hayashi Y, Nakano Ok, Ishizuya Y, et al. Excessive-fat diet-induced irritation accelerates prostate most cancers development through IL6 signaling. Clin Most cancers Res. 2018;24:4309–18.
Chen M, Zhang J, Sampieri Ok, Clohessy JG, Mendez L, Gonzalez-Billalabeitia E, et al. An aberrant SREBP-dependent lipogenic program promotes metastatic prostate most cancers. Nat Genet. 2018;50:206.
Carreño DV, Corro NBNB, Cerda-Infante JF, Echeverría CE, Asencio-Barría CA, Torres-Estay VAVA, et al. Dietary fructose promotes prostate most cancers development. Most cancers Res. 2021;81:2824–32.

