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Folate and choline metabolism gene variants in relation to ovarian cancer risk in the Polish population
Data indicates that genetic factors alone do not account for ovarian tumorigenesis, suggesting that epigenetic status additionally affects this process. Therefore, we assessed the possible contribution of polymorphic variants of genes that may affect DNA methylation to the risk of ovarian cancer inc...
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| Published in: | Molecular biology reports 2012-05, Vol.39 (5), p.5553-5560 |
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| creator | Pawlik, Piotr Mostowska, Adrianna Lianeri, Margarita Sajdak, Stefan Kędzia, Helena Jagodzinski, Paweł P. |
| description | Data indicates that genetic factors alone do not account for ovarian tumorigenesis, suggesting that epigenetic status additionally affects this process. Therefore, we assessed the possible contribution of polymorphic variants of genes that may affect DNA methylation to the risk of ovarian cancer incidence in the Polish population. Using PCR-RFLP and HRM analyses, we studied the distribution of
BHMT
(rs3733890),
MTHFD1
(rs2236225),
MTHFR
(rs1801133),
MTR
(rs1805087),
MTRR
(rs1801394) and
TCN2
(rs1801198) genotypes and alleles in patients with ovarian cancer (
n
= 136) and controls (
n
= 160). Moreover, using DNA and methylation-specific PCR (MSP) we also determined the methylation of the
Cadherin 13
(CDH13)
promoter in cancerous tissue from these patients. We did not observe a significant association between all studied gene variants and the incidence of ovarian cancer. The lowest
P
trend
= 0.1226 was observed for the
MTHFR
Ala222Val polymorphism. Moreover, the lowest
P
= 0.0772 was found in the comparison of
MTHFR
Ala/Ala versus Val/Val and Val/Ala genotypes in patients and control groups. The multifactor dimensionality reduction analysis also did not indicate a significant interactive genetic effect on ovarian cancer incidence for all analyzed SNPs. However, we observed frequent methylation of the
CDH13
promoter in approximately 21% (29/136) patients with ovarian carcinomas. Our results might suggest that the selected polymorphic gene variants may not contribute to ovarian cancer incidence. |
| doi_str_mv | 10.1007/s11033-011-1359-0 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_948897163</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>948897163</sourcerecordid><originalsourceid>FETCH-LOGICAL-c403t-4f7576292c0b970ab66944e8d4479f47b48f933c1606decf10c234d9b336f5db3</originalsourceid><addsrcrecordid>eNp9kcFqFTEUhoNY7LX6AG5KcFM3Y89JMpNkWYqtQqFd1HXIZDL3Tp1JbpMZoW9vLlMVhLpKwvn-_xA-Qj4gfEYAeZ4RgfMKECvkta7gFdlgLXkltFSvyQY4YCVUjcfkbc4PACBQ1m_IMWOoOAe2IdurONrZUxs66nZxHIKnk59tW655oltf3j9tGmyYMx0CTb7gQwx0jjSuA-pscD7RNOQfB2TeeXp3iO_oPu6XlX9Hjno7Zv_--Twh36--3F9-rW5ur79dXtxUTgCfK9HLWjZMMwetlmDbptFCeNUJIXUvZCtUrzl32EDTedcjOMZFp1vOm77uWn5CztbefYqPi8-zmYbs_Dja4OOSjRZKaYkNL-Sn_5IITAEqpkRBP_6DPsQlhfIPo7moWQOoC4Qr5FLMOfne7NMw2fRUmsxBl1l1maLLHHQZKJnT5-KlnXz3J_HbTwHYCuQyCluf_m5-ufUXNHGeyQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>934526019</pqid></control><display><type>article</type><title>Folate and choline metabolism gene variants in relation to ovarian cancer risk in the Polish population</title><source>Springer Nature</source><creator>Pawlik, Piotr ; Mostowska, Adrianna ; Lianeri, Margarita ; Sajdak, Stefan ; Kędzia, Helena ; Jagodzinski, Paweł P.</creator><creatorcontrib>Pawlik, Piotr ; Mostowska, Adrianna ; Lianeri, Margarita ; Sajdak, Stefan ; Kędzia, Helena ; Jagodzinski, Paweł P.</creatorcontrib><description>Data indicates that genetic factors alone do not account for ovarian tumorigenesis, suggesting that epigenetic status additionally affects this process. Therefore, we assessed the possible contribution of polymorphic variants of genes that may affect DNA methylation to the risk of ovarian cancer incidence in the Polish population. Using PCR-RFLP and HRM analyses, we studied the distribution of
BHMT
(rs3733890),
MTHFD1
(rs2236225),
MTHFR
(rs1801133),
MTR
(rs1805087),
MTRR
(rs1801394) and
TCN2
(rs1801198) genotypes and alleles in patients with ovarian cancer (
n
= 136) and controls (
n
= 160). Moreover, using DNA and methylation-specific PCR (MSP) we also determined the methylation of the
Cadherin 13
(CDH13)
promoter in cancerous tissue from these patients. We did not observe a significant association between all studied gene variants and the incidence of ovarian cancer. The lowest
P
trend
= 0.1226 was observed for the
MTHFR
Ala222Val polymorphism. Moreover, the lowest
P
= 0.0772 was found in the comparison of
MTHFR
Ala/Ala versus Val/Val and Val/Ala genotypes in patients and control groups. The multifactor dimensionality reduction analysis also did not indicate a significant interactive genetic effect on ovarian cancer incidence for all analyzed SNPs. However, we observed frequent methylation of the
CDH13
promoter in approximately 21% (29/136) patients with ovarian carcinomas. Our results might suggest that the selected polymorphic gene variants may not contribute to ovarian cancer incidence.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-011-1359-0</identifier><identifier>PMID: 22183302</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Betaine-homocysteine S-methyltransferase ; Biomedical and Life Sciences ; Cadherin ; Cadherins - genetics ; Case-Control Studies ; Choline ; Choline - metabolism ; Data processing ; Databases, Genetic ; DNA ; DNA methylation ; DNA Methylation - genetics ; epigenetics ; Epistasis, Genetic ; Female ; Folic acid ; Folic Acid - metabolism ; Gene Frequency - genetics ; Gene polymorphism ; Genes, Neoplasm ; Genetic effects ; Genetic factors ; Genetic Predisposition to Disease ; Genotype & phenotype ; Genotypes ; Histology ; Humans ; Incidence ; Life Sciences ; Metabolic Networks and Pathways - genetics ; Metabolism ; Methylenetetrahydrofolate reductase ; Middle Aged ; Molecular biology ; Morphology ; Ovarian cancer ; Ovarian carcinoma ; Ovarian Neoplasms - epidemiology ; Ovarian Neoplasms - genetics ; Poland - epidemiology ; Polymerase chain reaction ; Polymorphism, Single Nucleotide - genetics ; Population genetics ; Promoter Regions, Genetic - genetics ; Promoters ; Restriction fragment length polymorphism ; Risk Factors ; Single-nucleotide polymorphism ; Tumorigenesis</subject><ispartof>Molecular biology reports, 2012-05, Vol.39 (5), p.5553-5560</ispartof><rights>Springer Science+Business Media B.V. 2011</rights><rights>Springer Science+Business Media B.V. 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-4f7576292c0b970ab66944e8d4479f47b48f933c1606decf10c234d9b336f5db3</citedby><cites>FETCH-LOGICAL-c403t-4f7576292c0b970ab66944e8d4479f47b48f933c1606decf10c234d9b336f5db3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22183302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pawlik, Piotr</creatorcontrib><creatorcontrib>Mostowska, Adrianna</creatorcontrib><creatorcontrib>Lianeri, Margarita</creatorcontrib><creatorcontrib>Sajdak, Stefan</creatorcontrib><creatorcontrib>Kędzia, Helena</creatorcontrib><creatorcontrib>Jagodzinski, Paweł P.</creatorcontrib><title>Folate and choline metabolism gene variants in relation to ovarian cancer risk in the Polish population</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Data indicates that genetic factors alone do not account for ovarian tumorigenesis, suggesting that epigenetic status additionally affects this process. Therefore, we assessed the possible contribution of polymorphic variants of genes that may affect DNA methylation to the risk of ovarian cancer incidence in the Polish population. Using PCR-RFLP and HRM analyses, we studied the distribution of
BHMT
(rs3733890),
MTHFD1
(rs2236225),
MTHFR
(rs1801133),
MTR
(rs1805087),
MTRR
(rs1801394) and
TCN2
(rs1801198) genotypes and alleles in patients with ovarian cancer (
n
= 136) and controls (
n
= 160). Moreover, using DNA and methylation-specific PCR (MSP) we also determined the methylation of the
Cadherin 13
(CDH13)
promoter in cancerous tissue from these patients. We did not observe a significant association between all studied gene variants and the incidence of ovarian cancer. The lowest
P
trend
= 0.1226 was observed for the
MTHFR
Ala222Val polymorphism. Moreover, the lowest
P
= 0.0772 was found in the comparison of
MTHFR
Ala/Ala versus Val/Val and Val/Ala genotypes in patients and control groups. The multifactor dimensionality reduction analysis also did not indicate a significant interactive genetic effect on ovarian cancer incidence for all analyzed SNPs. However, we observed frequent methylation of the
CDH13
promoter in approximately 21% (29/136) patients with ovarian carcinomas. Our results might suggest that the selected polymorphic gene variants may not contribute to ovarian cancer incidence.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Betaine-homocysteine S-methyltransferase</subject><subject>Biomedical and Life Sciences</subject><subject>Cadherin</subject><subject>Cadherins - genetics</subject><subject>Case-Control Studies</subject><subject>Choline</subject><subject>Choline - metabolism</subject><subject>Data processing</subject><subject>Databases, Genetic</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>epigenetics</subject><subject>Epistasis, Genetic</subject><subject>Female</subject><subject>Folic acid</subject><subject>Folic Acid - metabolism</subject><subject>Gene Frequency - genetics</subject><subject>Gene polymorphism</subject><subject>Genes, Neoplasm</subject><subject>Genetic effects</subject><subject>Genetic factors</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Histology</subject><subject>Humans</subject><subject>Incidence</subject><subject>Life Sciences</subject><subject>Metabolic Networks and Pathways - genetics</subject><subject>Metabolism</subject><subject>Methylenetetrahydrofolate reductase</subject><subject>Middle Aged</subject><subject>Molecular biology</subject><subject>Morphology</subject><subject>Ovarian cancer</subject><subject>Ovarian carcinoma</subject><subject>Ovarian Neoplasms - epidemiology</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Poland - epidemiology</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Population genetics</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Promoters</subject><subject>Restriction fragment length polymorphism</subject><subject>Risk Factors</subject><subject>Single-nucleotide polymorphism</subject><subject>Tumorigenesis</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp9kcFqFTEUhoNY7LX6AG5KcFM3Y89JMpNkWYqtQqFd1HXIZDL3Tp1JbpMZoW9vLlMVhLpKwvn-_xA-Qj4gfEYAeZ4RgfMKECvkta7gFdlgLXkltFSvyQY4YCVUjcfkbc4PACBQ1m_IMWOoOAe2IdurONrZUxs66nZxHIKnk59tW655oltf3j9tGmyYMx0CTb7gQwx0jjSuA-pscD7RNOQfB2TeeXp3iO_oPu6XlX9Hjno7Zv_--Twh36--3F9-rW5ur79dXtxUTgCfK9HLWjZMMwetlmDbptFCeNUJIXUvZCtUrzl32EDTedcjOMZFp1vOm77uWn5CztbefYqPi8-zmYbs_Dja4OOSjRZKaYkNL-Sn_5IITAEqpkRBP_6DPsQlhfIPo7moWQOoC4Qr5FLMOfne7NMw2fRUmsxBl1l1maLLHHQZKJnT5-KlnXz3J_HbTwHYCuQyCluf_m5-ufUXNHGeyQ</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Pawlik, Piotr</creator><creator>Mostowska, Adrianna</creator><creator>Lianeri, Margarita</creator><creator>Sajdak, Stefan</creator><creator>Kędzia, Helena</creator><creator>Jagodzinski, Paweł P.</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7T2</scope><scope>7U1</scope><scope>7U2</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20120501</creationdate><title>Folate and choline metabolism gene variants in relation to ovarian cancer risk in the Polish population</title><author>Pawlik, Piotr ; Mostowska, Adrianna ; Lianeri, Margarita ; Sajdak, Stefan ; Kędzia, Helena ; Jagodzinski, Paweł P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c403t-4f7576292c0b970ab66944e8d4479f47b48f933c1606decf10c234d9b336f5db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Betaine-homocysteine S-methyltransferase</topic><topic>Biomedical and Life Sciences</topic><topic>Cadherin</topic><topic>Cadherins - genetics</topic><topic>Case-Control Studies</topic><topic>Choline</topic><topic>Choline - metabolism</topic><topic>Data processing</topic><topic>Databases, Genetic</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>epigenetics</topic><topic>Epistasis, Genetic</topic><topic>Female</topic><topic>Folic acid</topic><topic>Folic Acid - metabolism</topic><topic>Gene Frequency - genetics</topic><topic>Gene polymorphism</topic><topic>Genes, Neoplasm</topic><topic>Genetic effects</topic><topic>Genetic factors</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Histology</topic><topic>Humans</topic><topic>Incidence</topic><topic>Life Sciences</topic><topic>Metabolic Networks and Pathways - genetics</topic><topic>Metabolism</topic><topic>Methylenetetrahydrofolate reductase</topic><topic>Middle Aged</topic><topic>Molecular biology</topic><topic>Morphology</topic><topic>Ovarian cancer</topic><topic>Ovarian carcinoma</topic><topic>Ovarian Neoplasms - epidemiology</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Poland - epidemiology</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Population genetics</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Promoters</topic><topic>Restriction fragment length polymorphism</topic><topic>Risk Factors</topic><topic>Single-nucleotide polymorphism</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pawlik, Piotr</creatorcontrib><creatorcontrib>Mostowska, Adrianna</creatorcontrib><creatorcontrib>Lianeri, Margarita</creatorcontrib><creatorcontrib>Sajdak, Stefan</creatorcontrib><creatorcontrib>Kędzia, Helena</creatorcontrib><creatorcontrib>Jagodzinski, Paweł P.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pawlik, Piotr</au><au>Mostowska, Adrianna</au><au>Lianeri, Margarita</au><au>Sajdak, Stefan</au><au>Kędzia, Helena</au><au>Jagodzinski, Paweł P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Folate and choline metabolism gene variants in relation to ovarian cancer risk in the Polish population</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>39</volume><issue>5</issue><spage>5553</spage><epage>5560</epage><pages>5553-5560</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Data indicates that genetic factors alone do not account for ovarian tumorigenesis, suggesting that epigenetic status additionally affects this process. Therefore, we assessed the possible contribution of polymorphic variants of genes that may affect DNA methylation to the risk of ovarian cancer incidence in the Polish population. Using PCR-RFLP and HRM analyses, we studied the distribution of
BHMT
(rs3733890),
MTHFD1
(rs2236225),
MTHFR
(rs1801133),
MTR
(rs1805087),
MTRR
(rs1801394) and
TCN2
(rs1801198) genotypes and alleles in patients with ovarian cancer (
n
= 136) and controls (
n
= 160). Moreover, using DNA and methylation-specific PCR (MSP) we also determined the methylation of the
Cadherin 13
(CDH13)
promoter in cancerous tissue from these patients. We did not observe a significant association between all studied gene variants and the incidence of ovarian cancer. The lowest
P
trend
= 0.1226 was observed for the
MTHFR
Ala222Val polymorphism. Moreover, the lowest
P
= 0.0772 was found in the comparison of
MTHFR
Ala/Ala versus Val/Val and Val/Ala genotypes in patients and control groups. The multifactor dimensionality reduction analysis also did not indicate a significant interactive genetic effect on ovarian cancer incidence for all analyzed SNPs. However, we observed frequent methylation of the
CDH13
promoter in approximately 21% (29/136) patients with ovarian carcinomas. Our results might suggest that the selected polymorphic gene variants may not contribute to ovarian cancer incidence.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>22183302</pmid><doi>10.1007/s11033-011-1359-0</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Molecular biology reports, 2012-05, Vol.39 (5), p.5553-5560 |
| issn | 0301-4851 1573-4978 |
| language | eng |
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| source | Springer Nature |
| subjects | Animal Anatomy Animal Biochemistry Betaine-homocysteine S-methyltransferase Biomedical and Life Sciences Cadherin Cadherins - genetics Case-Control Studies Choline Choline - metabolism Data processing Databases, Genetic DNA DNA methylation DNA Methylation - genetics epigenetics Epistasis, Genetic Female Folic acid Folic Acid - metabolism Gene Frequency - genetics Gene polymorphism Genes, Neoplasm Genetic effects Genetic factors Genetic Predisposition to Disease Genotype & phenotype Genotypes Histology Humans Incidence Life Sciences Metabolic Networks and Pathways - genetics Metabolism Methylenetetrahydrofolate reductase Middle Aged Molecular biology Morphology Ovarian cancer Ovarian carcinoma Ovarian Neoplasms - epidemiology Ovarian Neoplasms - genetics Poland - epidemiology Polymerase chain reaction Polymorphism, Single Nucleotide - genetics Population genetics Promoter Regions, Genetic - genetics Promoters Restriction fragment length polymorphism Risk Factors Single-nucleotide polymorphism Tumorigenesis |
| title | Folate and choline metabolism gene variants in relation to ovarian cancer risk in the Polish population |
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