Organ-Specific Cancer Metabolism and Its Potential for Therapy
Targeting cancer metabolism has the potential to lead to major advances in tumor therapy. Numerous promising metabolic drug targets have been identified. Yet, it has emerged that there is no singular metabolism that defines the oncogenic state of the cell. Rather, the metabolism of cancer cells is a...
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description | Targeting cancer metabolism has the potential to lead to major advances in tumor therapy. Numerous promising metabolic drug targets have been identified. Yet, it has emerged that there is no singular metabolism that defines the oncogenic state of the cell. Rather, the metabolism of cancer cells is a function of the requirements of a tumor. Hence, the tissue of origin, the (epi)genetic drivers, the aberrant signaling, and the microenvironment all together define these metabolic requirements. In this chapter we discuss in light of (epi)genetic, signaling, and environmental factors the diversity in cancer metabolism based on triple-negative and estrogen receptor-positive breast cancer, early- and late-stage prostate cancer, and liver cancer. These types of cancer all display distinct and partially opposing metabolic behaviors (e.g., Warburg versus reverse Warburg metabolism). Yet, for each of the cancers, their distinct metabolism supports the oncogenic phenotype. Finally, we will assess the therapeutic potential of metabolism based on the concepts of metabolic normalization and metabolic depletion. |
doi_str_mv | 10.1007/164_2015_10 |
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Numerous promising metabolic drug targets have been identified. Yet, it has emerged that there is no singular metabolism that defines the oncogenic state of the cell. Rather, the metabolism of cancer cells is a function of the requirements of a tumor. Hence, the tissue of origin, the (epi)genetic drivers, the aberrant signaling, and the microenvironment all together define these metabolic requirements. In this chapter we discuss in light of (epi)genetic, signaling, and environmental factors the diversity in cancer metabolism based on triple-negative and estrogen receptor-positive breast cancer, early- and late-stage prostate cancer, and liver cancer. These types of cancer all display distinct and partially opposing metabolic behaviors (e.g., Warburg versus reverse Warburg metabolism). Yet, for each of the cancers, their distinct metabolism supports the oncogenic phenotype. Finally, we will assess the therapeutic potential of metabolism based on the concepts of metabolic normalization and metabolic depletion.</description><subject>Breast Neoplasms - metabolism</subject><subject>Cancer metabolism</subject><subject>Epigenetic drivers</subject><subject>Estrogen receptor-positive breast cancer</subject><subject>Fatty acid metabolism</subject><subject>Female</subject><subject>Genetic drivers</subject><subject>Gluconeogenesis</subject><subject>Glucose metabolism</subject><subject>Glutamine metabolism</subject><subject>Humans</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - metabolism</subject><subject>Male</subject><subject>Medical research</subject><subject>Metabolic depletion</subject><subject>Metabolic normalization</subject><subject>Metabolic therapy</subject><subject>Metabolism</subject><subject>Microenvironment</subject><subject>Mixed Warburg effect</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Organ Specificity</subject><subject>Pharmacology</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Reverse Warburg effect</subject><subject>Serine metabolism</subject><subject>Tissue-specific metabolism</subject><subject>Triple-negative breast cancer</subject><subject>Tumor Microenvironment</subject><subject>Warburg effect</subject><issn>0171-2004</issn><issn>1865-0325</issn><isbn>3319298046</isbn><isbn>9783319298047</isbn><isbn>9783319298061</isbn><isbn>3319298062</isbn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1v1DAQhs13l2VP3FGOcAjM2B47viChFR-ViopEOVsTx2kD2SS1s4f-e1y1lRCnObzPvKN5hHiN8B4B7Ac02ktA8giPxM7ZRil00jVg8LHYYGOoBiXpiXj5EGjzVGwALdYSQD8XG6epscpCcyJ2Of8GADSkweELcSLJYanXG_HxPF3yVP9cYhj6IVR7nkJM1fe4cjuPQz5UPHXV6ZqrH_Map3XgsernVF1cxcTLzSvxrOcxx9393IpfXz5f7L_VZ-dfT_efzuqgXLPWThmjOPRMoQMyTDpwE1u0ZHTsrGYpsfwNINuWDPWdU8iObRuJgupRbcXbu94lzdfHmFd_GHKI48hTnI_Zo7WaFMkiaive3KPH9hA7v6ThwOnGP_xcgHd3QC7RdBmTb-f5T-kAf-ve_-O-sPq_u_EWDsVE4jFc8bLGlL3WpKUp-856JVH9BZnifF8</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Elia, Ilaria</creator><creator>Schmieder, Roberta</creator><creator>Christen, Stefan</creator><creator>Fendt, Sarah-Maria</creator><general>Springer International Publishing AG</general><general>Springer International Publishing</general><scope>FFUUA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20160101</creationdate><title>Organ-Specific Cancer Metabolism and Its Potential for Therapy</title><author>Elia, Ilaria ; Schmieder, Roberta ; Christen, Stefan ; Fendt, Sarah-Maria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-93663acfa5cd056a54ca8eb17564ed74a221100002bb565fd931a9a7be55c3f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Breast Neoplasms - metabolism</topic><topic>Cancer metabolism</topic><topic>Epigenetic drivers</topic><topic>Estrogen receptor-positive breast cancer</topic><topic>Fatty acid metabolism</topic><topic>Female</topic><topic>Genetic drivers</topic><topic>Gluconeogenesis</topic><topic>Glucose metabolism</topic><topic>Glutamine metabolism</topic><topic>Humans</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - metabolism</topic><topic>Male</topic><topic>Medical research</topic><topic>Metabolic depletion</topic><topic>Metabolic normalization</topic><topic>Metabolic therapy</topic><topic>Metabolism</topic><topic>Microenvironment</topic><topic>Mixed Warburg effect</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Organ Specificity</topic><topic>Pharmacology</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Reverse Warburg effect</topic><topic>Serine metabolism</topic><topic>Tissue-specific metabolism</topic><topic>Triple-negative breast cancer</topic><topic>Tumor Microenvironment</topic><topic>Warburg effect</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Elia, Ilaria</creatorcontrib><creatorcontrib>Schmieder, Roberta</creatorcontrib><creatorcontrib>Christen, Stefan</creatorcontrib><creatorcontrib>Fendt, Sarah-Maria</creatorcontrib><collection>ProQuest Ebook Central - Book Chapters - Demo use only</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Handbook of experimental pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Elia, Ilaria</au><au>Schmieder, Roberta</au><au>Christen, Stefan</au><au>Fendt, Sarah-Maria</au><au>Herzig, Stephan</au><au>Herzig, Stephan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Organ-Specific Cancer Metabolism and Its Potential for Therapy</atitle><jtitle>Handbook of experimental pharmacology</jtitle><addtitle>Handb Exp Pharmacol</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>233</volume><spage>321</spage><epage>353</epage><pages>321-353</pages><issn>0171-2004</issn><eissn>1865-0325</eissn><isbn>3319298046</isbn><isbn>9783319298047</isbn><eisbn>9783319298061</eisbn><eisbn>3319298062</eisbn><abstract>Targeting cancer metabolism has the potential to lead to major advances in tumor therapy. Numerous promising metabolic drug targets have been identified. Yet, it has emerged that there is no singular metabolism that defines the oncogenic state of the cell. Rather, the metabolism of cancer cells is a function of the requirements of a tumor. Hence, the tissue of origin, the (epi)genetic drivers, the aberrant signaling, and the microenvironment all together define these metabolic requirements. In this chapter we discuss in light of (epi)genetic, signaling, and environmental factors the diversity in cancer metabolism based on triple-negative and estrogen receptor-positive breast cancer, early- and late-stage prostate cancer, and liver cancer. These types of cancer all display distinct and partially opposing metabolic behaviors (e.g., Warburg versus reverse Warburg metabolism). Yet, for each of the cancers, their distinct metabolism supports the oncogenic phenotype. 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subjects | Breast Neoplasms - metabolism Cancer metabolism Epigenetic drivers Estrogen receptor-positive breast cancer Fatty acid metabolism Female Genetic drivers Gluconeogenesis Glucose metabolism Glutamine metabolism Humans Liver cancer Liver Neoplasms - metabolism Male Medical research Metabolic depletion Metabolic normalization Metabolic therapy Metabolism Microenvironment Mixed Warburg effect Neoplasms - drug therapy Neoplasms - metabolism Organ Specificity Pharmacology Prostate cancer Prostatic Neoplasms - metabolism Reverse Warburg effect Serine metabolism Tissue-specific metabolism Triple-negative breast cancer Tumor Microenvironment Warburg effect |
title | Organ-Specific Cancer Metabolism and Its Potential for Therapy |
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