Metabolomics analyses of cancer tissue from patients with colorectal cancer
The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehen...
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description | The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehensive untargeted metabolomics analysis was performed on the paired CRC tissues and adjacent normal tissues from patients with CRC (n=35) using ultra-high-performance liquid chromatography-mass spectrometry. Subsequently, bioinformatic analysis was performed on the differentially expressed metabolites. The changes in these differential metabolites were compared among groups of patients based on sex, anatomical tumor location, grade of tumor differentiation and stage of disease. A total of 927 metabolites were detected in the tissue samples, and 24 metabolites in the CRC tissue were significantly different compared with the adjacent normal tissue. The present study revealed that the levels of three amino acid metabolites were increased in the CRC tissue, specifically, N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, cyclo(Glu-Glu) and cyclo(Phe-Glu). The metabolites with decreased levels in the CRC tissue included quinaldic acid (also referred to as quinoline-2-carboxilic acid), 17[alpha]- and 17[beta]-estradioll, which are associated with tumor suppression activities, as well as other metabolites such as, anhydro-[beta]-glucose, Asp-Arg, lysophosphatidylcholine, lysophosphatidylethanolamine (lysoPE), lysophosphatidylinositol, carnitine, 5'-deoxy-5'-(methylthio) adenosine, 2'-deoxyinosine-5'-monophosphate and thiamine monophosphate. There was no difference in the levels of the differential metabolites between male and female patients. The differentiation of CRC also showed no impact on the levels of the differential metabolites. The levels of lysoPE were increased in the right side of the colon compared with the left side of the colon and rectum. Analysis of the different tumor stages indicated that 2-aminobenzenesulfonic acid, P-sulfanilic acid and quinoline-4-carboxylic acid were decreased in stage I CRC tissue compared with stage II, III and IV CRC tissue. The levels of N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, methylcysteine and 5'-deoxy-5'-(methylthio) adenosine varied at different stages of tumorigenesis. These differential metabolites were implicated in multiple metabolism pathways, including carbohydrate, amino acid, lipid, nucleotide and hormone. In conclus |
doi_str_mv | 10.3892/mmr.2023.13106 |
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fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10568249</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A770900364</galeid><sourcerecordid>A770900364</sourcerecordid><originalsourceid>FETCH-LOGICAL-c418t-6d115aeefeabff32f25970a650317a72f370899d12a77fd46d3b0264d157fe683</originalsourceid><addsrcrecordid>eNptkU1vFSEUhonR2Frdup7EjZt7PXwMDCvTNGqNbdzUNTmXObQ0M8MVZmz672XqjcamYQGBh4fDeRl7y2ErOys-jGPeChByyyUH_Ywdc2P5RgKo54e1sNYcsVel3ALoVrT2JTuSxhghrT5m3y5pxl0a0hh9aXDC4b5QaVJoPE6ecjPHUhZqQk5js8c50jSX5i7ON42vtzL5GYcD-5q9CDgUenOYT9iPz5-uzs43F9-_fD07vdh4xbt5o3vOWyQKhLsQpAi1JgOoW5DcoBFBGuis7blAY0KvdC93ILTqeWsC6U6esI9_vPtlN1Lva0kZB7fPccR87xJG9__JFG_cdfrlOLS6E8pWw_uDIaefC5XZjbF4GgacKC3Fic6AtUooVdF3j9DbtOTap5XqQCvTaf6PusaBXJxCqg_7VepOTXUBSL26tk9QdfRU258mCrHuP3XB51RKpvD3kxzcmr-r-bs1f_eQv_wNagSg_A</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2880647861</pqid></control><display><type>article</type><title>Metabolomics analyses of cancer tissue from patients with colorectal cancer</title><source>Spandidos Publications Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Kang, Chunbo ; Zhang, Jie ; Xue, Mei ; Li, Xiaowei ; Ding, Danyang ; Wang, Ye ; Jiang, Shujing ; Chu, Fong-Fong ; Gao, Qiang ; Zhang, Mengqiao</creator><creatorcontrib>Kang, Chunbo ; Zhang, Jie ; Xue, Mei ; Li, Xiaowei ; Ding, Danyang ; Wang, Ye ; Jiang, Shujing ; Chu, Fong-Fong ; Gao, Qiang ; Zhang, Mengqiao</creatorcontrib><description>The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehensive untargeted metabolomics analysis was performed on the paired CRC tissues and adjacent normal tissues from patients with CRC (n=35) using ultra-high-performance liquid chromatography-mass spectrometry. Subsequently, bioinformatic analysis was performed on the differentially expressed metabolites. The changes in these differential metabolites were compared among groups of patients based on sex, anatomical tumor location, grade of tumor differentiation and stage of disease. A total of 927 metabolites were detected in the tissue samples, and 24 metabolites in the CRC tissue were significantly different compared with the adjacent normal tissue. The present study revealed that the levels of three amino acid metabolites were increased in the CRC tissue, specifically, N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, cyclo(Glu-Glu) and cyclo(Phe-Glu). The metabolites with decreased levels in the CRC tissue included quinaldic acid (also referred to as quinoline-2-carboxilic acid), 17[alpha]- and 17[beta]-estradioll, which are associated with tumor suppression activities, as well as other metabolites such as, anhydro-[beta]-glucose, Asp-Arg, lysophosphatidylcholine, lysophosphatidylethanolamine (lysoPE), lysophosphatidylinositol, carnitine, 5'-deoxy-5'-(methylthio) adenosine, 2'-deoxyinosine-5'-monophosphate and thiamine monophosphate. There was no difference in the levels of the differential metabolites between male and female patients. The differentiation of CRC also showed no impact on the levels of the differential metabolites. The levels of lysoPE were increased in the right side of the colon compared with the left side of the colon and rectum. Analysis of the different tumor stages indicated that 2-aminobenzenesulfonic acid, P-sulfanilic acid and quinoline-4-carboxylic acid were decreased in stage I CRC tissue compared with stage II, III and IV CRC tissue. The levels of N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, methylcysteine and 5'-deoxy-5'-(methylthio) adenosine varied at different stages of tumorigenesis. These differential metabolites were implicated in multiple metabolism pathways, including carbohydrate, amino acid, lipid, nucleotide and hormone. In conclusion, the present study demonstrated that CRC tumors had altered metabolites compared with normal tissue. The data from the metabolic profile of CRC tissues in the present study provided supportive evidence to understand tumorigenesis. Key words: colorectal cancer, mass spectrometry, metabolites, tissue metabolomics, ultra-high-performance liquid chromatography</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2023.13106</identifier><identifier>PMID: 37772396</identifier><language>eng</language><publisher>Athens: Spandidos Publications</publisher><subject>17β-Estradiol ; Amino acids ; Cancer ; Carbohydrate metabolism ; Carboxylic acids ; Care and treatment ; Carnitine ; Cell metabolism ; Chromatography ; Colonoscopy ; Colorectal cancer ; Colorectal carcinoma ; Development and progression ; Discriminant analysis ; Epigenetics ; Gene expression ; Genetic aspects ; Genotype ; Health aspects ; High-performance liquid chromatography ; Lysophosphatidylcholine ; Mass spectroscopy ; Medical prognosis ; Metabolism ; Metabolites ; Metabolomics ; Software ; Statistical analysis ; Sulfanilic acid ; Tumor suppression ; Tumorigenesis</subject><ispartof>Molecular medicine reports, 2023-11, Vol.28 (5), Article 219</ispartof><rights>COPYRIGHT 2023 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2023</rights><rights>Copyright: © Kang et al. 2023</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c418t-6d115aeefeabff32f25970a650317a72f370899d12a77fd46d3b0264d157fe683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids></links><search><creatorcontrib>Kang, Chunbo</creatorcontrib><creatorcontrib>Zhang, Jie</creatorcontrib><creatorcontrib>Xue, Mei</creatorcontrib><creatorcontrib>Li, Xiaowei</creatorcontrib><creatorcontrib>Ding, Danyang</creatorcontrib><creatorcontrib>Wang, Ye</creatorcontrib><creatorcontrib>Jiang, Shujing</creatorcontrib><creatorcontrib>Chu, Fong-Fong</creatorcontrib><creatorcontrib>Gao, Qiang</creatorcontrib><creatorcontrib>Zhang, Mengqiao</creatorcontrib><title>Metabolomics analyses of cancer tissue from patients with colorectal cancer</title><title>Molecular medicine reports</title><description>The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehensive untargeted metabolomics analysis was performed on the paired CRC tissues and adjacent normal tissues from patients with CRC (n=35) using ultra-high-performance liquid chromatography-mass spectrometry. Subsequently, bioinformatic analysis was performed on the differentially expressed metabolites. The changes in these differential metabolites were compared among groups of patients based on sex, anatomical tumor location, grade of tumor differentiation and stage of disease. A total of 927 metabolites were detected in the tissue samples, and 24 metabolites in the CRC tissue were significantly different compared with the adjacent normal tissue. The present study revealed that the levels of three amino acid metabolites were increased in the CRC tissue, specifically, N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, cyclo(Glu-Glu) and cyclo(Phe-Glu). The metabolites with decreased levels in the CRC tissue included quinaldic acid (also referred to as quinoline-2-carboxilic acid), 17[alpha]- and 17[beta]-estradioll, which are associated with tumor suppression activities, as well as other metabolites such as, anhydro-[beta]-glucose, Asp-Arg, lysophosphatidylcholine, lysophosphatidylethanolamine (lysoPE), lysophosphatidylinositol, carnitine, 5'-deoxy-5'-(methylthio) adenosine, 2'-deoxyinosine-5'-monophosphate and thiamine monophosphate. There was no difference in the levels of the differential metabolites between male and female patients. The differentiation of CRC also showed no impact on the levels of the differential metabolites. The levels of lysoPE were increased in the right side of the colon compared with the left side of the colon and rectum. Analysis of the different tumor stages indicated that 2-aminobenzenesulfonic acid, P-sulfanilic acid and quinoline-4-carboxylic acid were decreased in stage I CRC tissue compared with stage II, III and IV CRC tissue. The levels of N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, methylcysteine and 5'-deoxy-5'-(methylthio) adenosine varied at different stages of tumorigenesis. These differential metabolites were implicated in multiple metabolism pathways, including carbohydrate, amino acid, lipid, nucleotide and hormone. In conclusion, the present study demonstrated that CRC tumors had altered metabolites compared with normal tissue. The data from the metabolic profile of CRC tissues in the present study provided supportive evidence to understand tumorigenesis. Key words: colorectal cancer, mass spectrometry, metabolites, tissue metabolomics, ultra-high-performance liquid chromatography</description><subject>17β-Estradiol</subject><subject>Amino acids</subject><subject>Cancer</subject><subject>Carbohydrate metabolism</subject><subject>Carboxylic acids</subject><subject>Care and treatment</subject><subject>Carnitine</subject><subject>Cell metabolism</subject><subject>Chromatography</subject><subject>Colonoscopy</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Development and progression</subject><subject>Discriminant analysis</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genotype</subject><subject>Health aspects</subject><subject>High-performance liquid chromatography</subject><subject>Lysophosphatidylcholine</subject><subject>Mass spectroscopy</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Sulfanilic acid</subject><subject>Tumor suppression</subject><subject>Tumorigenesis</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkU1vFSEUhonR2Frdup7EjZt7PXwMDCvTNGqNbdzUNTmXObQ0M8MVZmz672XqjcamYQGBh4fDeRl7y2ErOys-jGPeChByyyUH_Ywdc2P5RgKo54e1sNYcsVel3ALoVrT2JTuSxhghrT5m3y5pxl0a0hh9aXDC4b5QaVJoPE6ecjPHUhZqQk5js8c50jSX5i7ON42vtzL5GYcD-5q9CDgUenOYT9iPz5-uzs43F9-_fD07vdh4xbt5o3vOWyQKhLsQpAi1JgOoW5DcoBFBGuis7blAY0KvdC93ILTqeWsC6U6esI9_vPtlN1Lva0kZB7fPccR87xJG9__JFG_cdfrlOLS6E8pWw_uDIaefC5XZjbF4GgacKC3Fic6AtUooVdF3j9DbtOTap5XqQCvTaf6PusaBXJxCqg_7VepOTXUBSL26tk9QdfRU258mCrHuP3XB51RKpvD3kxzcmr-r-bs1f_eQv_wNagSg_A</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Kang, Chunbo</creator><creator>Zhang, Jie</creator><creator>Xue, Mei</creator><creator>Li, Xiaowei</creator><creator>Ding, Danyang</creator><creator>Wang, Ye</creator><creator>Jiang, Shujing</creator><creator>Chu, Fong-Fong</creator><creator>Gao, Qiang</creator><creator>Zhang, Mengqiao</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20231101</creationdate><title>Metabolomics analyses of cancer tissue from patients with colorectal cancer</title><author>Kang, Chunbo ; Zhang, Jie ; Xue, Mei ; Li, Xiaowei ; Ding, Danyang ; Wang, Ye ; Jiang, Shujing ; Chu, Fong-Fong ; Gao, Qiang ; Zhang, Mengqiao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c418t-6d115aeefeabff32f25970a650317a72f370899d12a77fd46d3b0264d157fe683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>17β-Estradiol</topic><topic>Amino acids</topic><topic>Cancer</topic><topic>Carbohydrate metabolism</topic><topic>Carboxylic acids</topic><topic>Care and treatment</topic><topic>Carnitine</topic><topic>Cell metabolism</topic><topic>Chromatography</topic><topic>Colonoscopy</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Development and progression</topic><topic>Discriminant analysis</topic><topic>Epigenetics</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genotype</topic><topic>Health aspects</topic><topic>High-performance liquid chromatography</topic><topic>Lysophosphatidylcholine</topic><topic>Mass spectroscopy</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metabolomics</topic><topic>Software</topic><topic>Statistical analysis</topic><topic>Sulfanilic acid</topic><topic>Tumor suppression</topic><topic>Tumorigenesis</topic><toplevel>online_resources</toplevel><creatorcontrib>Kang, Chunbo</creatorcontrib><creatorcontrib>Zhang, Jie</creatorcontrib><creatorcontrib>Xue, Mei</creatorcontrib><creatorcontrib>Li, Xiaowei</creatorcontrib><creatorcontrib>Ding, Danyang</creatorcontrib><creatorcontrib>Wang, Ye</creatorcontrib><creatorcontrib>Jiang, Shujing</creatorcontrib><creatorcontrib>Chu, Fong-Fong</creatorcontrib><creatorcontrib>Gao, Qiang</creatorcontrib><creatorcontrib>Zhang, Mengqiao</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kang, Chunbo</au><au>Zhang, Jie</au><au>Xue, Mei</au><au>Li, Xiaowei</au><au>Ding, Danyang</au><au>Wang, Ye</au><au>Jiang, Shujing</au><au>Chu, Fong-Fong</au><au>Gao, Qiang</au><au>Zhang, Mengqiao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolomics analyses of cancer tissue from patients with colorectal cancer</atitle><jtitle>Molecular medicine reports</jtitle><date>2023-11-01</date><risdate>2023</risdate><volume>28</volume><issue>5</issue><artnum>219</artnum><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehensive untargeted metabolomics analysis was performed on the paired CRC tissues and adjacent normal tissues from patients with CRC (n=35) using ultra-high-performance liquid chromatography-mass spectrometry. Subsequently, bioinformatic analysis was performed on the differentially expressed metabolites. The changes in these differential metabolites were compared among groups of patients based on sex, anatomical tumor location, grade of tumor differentiation and stage of disease. A total of 927 metabolites were detected in the tissue samples, and 24 metabolites in the CRC tissue were significantly different compared with the adjacent normal tissue. The present study revealed that the levels of three amino acid metabolites were increased in the CRC tissue, specifically, N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, cyclo(Glu-Glu) and cyclo(Phe-Glu). The metabolites with decreased levels in the CRC tissue included quinaldic acid (also referred to as quinoline-2-carboxilic acid), 17[alpha]- and 17[beta]-estradioll, which are associated with tumor suppression activities, as well as other metabolites such as, anhydro-[beta]-glucose, Asp-Arg, lysophosphatidylcholine, lysophosphatidylethanolamine (lysoPE), lysophosphatidylinositol, carnitine, 5'-deoxy-5'-(methylthio) adenosine, 2'-deoxyinosine-5'-monophosphate and thiamine monophosphate. There was no difference in the levels of the differential metabolites between male and female patients. The differentiation of CRC also showed no impact on the levels of the differential metabolites. The levels of lysoPE were increased in the right side of the colon compared with the left side of the colon and rectum. Analysis of the different tumor stages indicated that 2-aminobenzenesulfonic acid, P-sulfanilic acid and quinoline-4-carboxylic acid were decreased in stage I CRC tissue compared with stage II, III and IV CRC tissue. The levels of N-[alpha]-acetyl-[epsilon]-(2-propenal)-Lys, methylcysteine and 5'-deoxy-5'-(methylthio) adenosine varied at different stages of tumorigenesis. These differential metabolites were implicated in multiple metabolism pathways, including carbohydrate, amino acid, lipid, nucleotide and hormone. In conclusion, the present study demonstrated that CRC tumors had altered metabolites compared with normal tissue. The data from the metabolic profile of CRC tissues in the present study provided supportive evidence to understand tumorigenesis. Key words: colorectal cancer, mass spectrometry, metabolites, tissue metabolomics, ultra-high-performance liquid chromatography</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><pmid>37772396</pmid><doi>10.3892/mmr.2023.13106</doi><oa>free_for_read</oa></addata></record> |
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subjects | 17β-Estradiol Amino acids Cancer Carbohydrate metabolism Carboxylic acids Care and treatment Carnitine Cell metabolism Chromatography Colonoscopy Colorectal cancer Colorectal carcinoma Development and progression Discriminant analysis Epigenetics Gene expression Genetic aspects Genotype Health aspects High-performance liquid chromatography Lysophosphatidylcholine Mass spectroscopy Medical prognosis Metabolism Metabolites Metabolomics Software Statistical analysis Sulfanilic acid Tumor suppression Tumorigenesis |
title | Metabolomics analyses of cancer tissue from patients with colorectal cancer |
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