Expression of the mutated transketolase TKTL1, a molecular marker in gastric cancer
The nonoxidative pentose phosphate pathway allows glucose conversion to ribose for DNA or RNA synthesis and glucose degradation to lactate controlled by transketolase enzyme reactions. It has been postulated, that this pathway is of the utmost importance in tumors for the proliferation process. We d...
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| Veröffentlicht in: | Oncology reports 2006-10, Vol.16 (4), p.657-661 |
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| creator | STAIGER, Wilko I COY, Johannes F GROBHOLZ, Rainer HOFHEINZ, Ralf-Dieter LUKAN, Nadine POST, Stefan SCHWARZBACH, Matthias H WILLEKE, Frank |
| description | The nonoxidative pentose phosphate pathway allows glucose conversion to ribose for DNA or RNA synthesis and glucose degradation to lactate controlled by transketolase enzyme reactions. It has been postulated, that this pathway is of the utmost importance in tumors for the proliferation process. We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in a considerable number of patients with gastric cancer (GC) or cancer of the gastroesophageal junction (GEJ). While only 10.8% of the cancer tissues revealed a significant mRNA upregulation, 36.9% of the cancer tissues demonstrated a protein overexpression. We propose that TKTL1 upregulation is a common phenomenon in GC and cancer of the GEJ leading to an enhanced, oxygen-independent glucose usage which might contribute to a more aggressive tumor growth. Since molecular targeted inhibition of transketolase enzyme reactions suppresses tumor growth and metastasis, TKTL1 could be a relevant target for anti-transketolase therapies in gastric cancer. |
| doi_str_mv | 10.3892/or.16.4.657 |
| format | Article |
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It has been postulated, that this pathway is of the utmost importance in tumors for the proliferation process. We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in a considerable number of patients with gastric cancer (GC) or cancer of the gastroesophageal junction (GEJ). While only 10.8% of the cancer tissues revealed a significant mRNA upregulation, 36.9% of the cancer tissues demonstrated a protein overexpression. We propose that TKTL1 upregulation is a common phenomenon in GC and cancer of the GEJ leading to an enhanced, oxygen-independent glucose usage which might contribute to a more aggressive tumor growth. Since molecular targeted inhibition of transketolase enzyme reactions suppresses tumor growth and metastasis, TKTL1 could be a relevant target for anti-transketolase therapies in gastric cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.16.4.657</identifier><identifier>PMID: 16969476</identifier><language>eng</language><publisher>Athens: S.n.</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Biomarkers, Tumor ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Medical sciences ; Middle Aged ; Mutation ; Neoplasm Metastasis ; Oxygen - metabolism ; RNA, Messenger - metabolism ; Stomach Neoplasms - metabolism ; Stomach. Duodenum. Small intestine. Colon. Rectum. 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It has been postulated, that this pathway is of the utmost importance in tumors for the proliferation process. We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in a considerable number of patients with gastric cancer (GC) or cancer of the gastroesophageal junction (GEJ). While only 10.8% of the cancer tissues revealed a significant mRNA upregulation, 36.9% of the cancer tissues demonstrated a protein overexpression. We propose that TKTL1 upregulation is a common phenomenon in GC and cancer of the GEJ leading to an enhanced, oxygen-independent glucose usage which might contribute to a more aggressive tumor growth. Since molecular targeted inhibition of transketolase enzyme reactions suppresses tumor growth and metastasis, TKTL1 could be a relevant target for anti-transketolase therapies in gastric cancer.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Metastasis</subject><subject>Oxygen - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasm Metastasis</topic><topic>Oxygen - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Transketolase - biosynthesis</topic><topic>Transketolase - genetics</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>STAIGER, Wilko I</creatorcontrib><creatorcontrib>COY, Johannes F</creatorcontrib><creatorcontrib>GROBHOLZ, Rainer</creatorcontrib><creatorcontrib>HOFHEINZ, Ralf-Dieter</creatorcontrib><creatorcontrib>LUKAN, Nadine</creatorcontrib><creatorcontrib>POST, Stefan</creatorcontrib><creatorcontrib>SCHWARZBACH, Matthias H</creatorcontrib><creatorcontrib>WILLEKE, Frank</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>STAIGER, Wilko I</au><au>COY, Johannes F</au><au>GROBHOLZ, Rainer</au><au>HOFHEINZ, Ralf-Dieter</au><au>LUKAN, Nadine</au><au>POST, Stefan</au><au>SCHWARZBACH, Matthias H</au><au>WILLEKE, Frank</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of the mutated transketolase TKTL1, a molecular marker in gastric cancer</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2006-10-01</date><risdate>2006</risdate><volume>16</volume><issue>4</issue><spage>657</spage><epage>661</epage><pages>657-661</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>The nonoxidative pentose phosphate pathway allows glucose conversion to ribose for DNA or RNA synthesis and glucose degradation to lactate controlled by transketolase enzyme reactions. It has been postulated, that this pathway is of the utmost importance in tumors for the proliferation process. We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in a considerable number of patients with gastric cancer (GC) or cancer of the gastroesophageal junction (GEJ). While only 10.8% of the cancer tissues revealed a significant mRNA upregulation, 36.9% of the cancer tissues demonstrated a protein overexpression. We propose that TKTL1 upregulation is a common phenomenon in GC and cancer of the GEJ leading to an enhanced, oxygen-independent glucose usage which might contribute to a more aggressive tumor growth. 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| subjects | Adult Aged Aged, 80 and over Biological and medical sciences Biomarkers, Tumor Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Humans Male Medical sciences Middle Aged Mutation Neoplasm Metastasis Oxygen - metabolism RNA, Messenger - metabolism Stomach Neoplasms - metabolism Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Transketolase - biosynthesis Transketolase - genetics Tumors |
| title | Expression of the mutated transketolase TKTL1, a molecular marker in gastric cancer |
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