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Investigation of the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression
This study aimed to investigate the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression. This study included 88 patients diagnosed with prostate cancer and 91 healthy controls. Polymerase chain reaction (PCR) and restriction f...
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| description | This study aimed to investigate the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression.
This study included 88 patients diagnosed with prostate cancer and 91 healthy controls. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods were used to determine the genotype distributions of eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations.
In our study, the CC homozygous genotype of eNOS T786C gene variation was determined to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 2.343, 95%Cl: 0.990–5.544, p = 0.026), while the CT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was found to be significantly higher (OR: 0.589, 95%Cl: 0.325–1.068, p = 0.041). In addition, while the TT homozygous genotype of the eNOS G894T gene variation was found to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 9.068, 95%Cl: 4.396–18.777, p |
| doi_str_mv | 10.1016/j.niox.2024.09.008 |
| format | article |
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This study included 88 patients diagnosed with prostate cancer and 91 healthy controls. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods were used to determine the genotype distributions of eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations.
In our study, the CC homozygous genotype of eNOS T786C gene variation was determined to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 2.343, 95%Cl: 0.990–5.544, p = 0.026), while the CT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was found to be significantly higher (OR: 0.589, 95%Cl: 0.325–1.068, p = 0.041). In addition, while the TT homozygous genotype of the eNOS G894T gene variation was found to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 9.068, 95%Cl: 4.396–18.777, p < 0.001), the GT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was determined significantly higher (OR: 0.227, 95%Cl: 0.121–0.427, p < 0.001). For eNOS (4VNTR (4a/b) - G894T) gene variations, aa-TT (p = 0.042) and bb-TT (p < 0.001) haplotype frequencies were significantly higher in the prostate cancer patient group, while aa-GT (p = 0.017), bb-GG (p = 0.049) and bb-GT (p < 0.001) haplotype frequencies were found to be significantly higher in the healthy control group. For eNOS (4VNTR (4a/b) - T786C) gene variations, the bb-CC haplotype frequency was determined to be significantly higher in the patient group (p = 0.049), while the bb-CT haplotype frequency was determined to be significantly higher in the control group (p = 0.008). For eNOS (T786C -G894T) gene variations, TT-TT (p < 0.001) and CC-TT (p = 0.025) haplotype frequencies were found to be significantly higher in the patient group. On the other hand, TT-GT (p = 0.002) and CT-GT (p < 0.001) haplotype frequencies were determined to be significantly higher in the control group. The aa genotype of the intron 4 VNTR (4a/b) gene variation was determined to be significantly higher at Gleason score ≥7 compared to Gleason score <7 (OR: 0.184, 95%Cl: 0.050–0.677, p = 0.005). PSA levels were determined significantly higher in patients with Gleason score 7 and above (p = 0.008). The risk of developing prostate cancer was found to be significantly higher in patients carrying the CC homozygous mutant genotype of the eNOS T786C gene variation (p = 0.024) and in patients carrying the TT homozygous genotype of the G894T gene variation (p = 0.021).
In our study, the CC homozygous genotype of the eNOS T786C gene variation was determined as a genetic risk factor for the development of prostate cancer, while the CT heterozygous genotype was determined as a protective factor against prostate cancer. For the eNOS G894T gene variation, the TT homozygous genotype was determined as a genetic risk factor for the development of prostate cancer, while the GT heterozygous genotype was determined as a protective factor against prostate cancer. Additionally, for eNOS (4VNTR (4a/b) - G894T) gene variations, aa-TT and bb-TT haplotypes have been identified as genetic risk factors for the development of prostate cancer, while aa-GT, bb-GG and bb-GT haplotypes have been identified as protective factors against the disease has been determined. For eNOS (4VNTR (4a/b) - T786C) gene variations, the bb-CC haplotype was determined as a genetic risk factor in the development of prostate cancer, while the bb-CT haplotype was determined as a protective factor against the disease. TT-TT and CC-TT haplotypes for eNOS (T786C -G894T) gene variations have been identified as genetic risk factors for the development of prostate cancer. In contrast, TT-GT and CT-GT haplotypes were found to be protective factors against the disease. The aa genotype of the intron 4 VNTR (4a/b) gene variation has also been identified as an important genetic risk factor in prostate cancer progression. Significantly increased PSA levels in patients with Gleason score 7 and above, and significantly increased PSA levels in patients carrying the CC and TT homozygous mutant genotype for T786C and G894T gene variations were determined as important risk factors. It is thought that the genetic biomarkers in our study may play a role as personalized therapeutic agents in slowing down the development of prostate cancer, increasing the effectiveness of treatment in prostate cancer, affecting the responses to drugs that regulate NO signaling, predetermining genetic predisposition to prostate cancer, and risk assessment in patients with prostate cancer.
•In our study, the CC homozygous genotype of the eNOS T786C gene variation was determined as a genetic risk factor for the development of prostate cancer, while the CT heterozygous genotype was determined as a protective factor against prostate cancer. For eNOS G894T gene variation, the TT homozygous genotype was determined as a genetic risk factor for the development of prostate cancer, while the GT heterozygous genotype was determined as a protective factor against prostate cancer.•For (4a/b - G894T) gene variations, aa-TT and bb-TT haplotypes have been identified as genetic risk factors for development of prostate cancer, while aa-GT, bb-GG and bb-GT haplotypes have been determined as protective factors against the disease. For (4a/b - T786C) gene variations, the bb-CC haplotype was determined as a genetic risk factor in the development of prostate cancer, while the bb-CT haplotype was determined as a protective factor against the disease. TT-TT and CC-TT haplotypes for (T786C-G894T) gene variations have been identified as genetic risk factors in the development of prostate cancer. In contrast, TT-GT and CT-GT haplotypes were found to be protective factors against the disease.•The aa genotype of the (4a/b) gene variation has also been identified as an important genetic risk factor in prostate cancer progression.•PSA levels were determined significantly higher in prostate cancer patients with a Gleason score of 7 and above. In addition, the risk of developing prostate cancer was determined to be significantly higher in patients carrying the CC homozygous mutant genotype of the T786C gene variation and the TT homozygous mutant genotype of the G894T gene variation.•Due to its versatile and diverse effects, NO is important as new anticancer strategies in slowing down cancer growth and increasing cancer treatment efficacy. eNOS regulation and NO production are affected by eNOS functional genetic variations, and these genetic variations are important in affecting the response to drugs that regulate NO signaling. It is thought that our findings may be effective in risk assessment and development of personalized therapeutic strategies in prostate cancer patients.]]></description><identifier>ISSN: 1089-8603</identifier><identifier>ISSN: 1089-8611</identifier><identifier>EISSN: 1089-8611</identifier><identifier>DOI: 10.1016/j.niox.2024.09.008</identifier><identifier>PMID: 39322022</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>eNOS gene variations ; Nitric oxide ; PCR ; Prostate cancer ; RFLP</subject><ispartof>Nitric oxide, 2024-11, Vol.152, p.69-77</ispartof><rights>2024 Elsevier Inc.</rights><rights>Copyright © 2024. Published by Elsevier Inc.</rights><rights>Copyright © 2024 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c237t-c80964d513d3d83a02b816c68c34c50a0653fb39b8f3b52c89735b73c058288f3</cites><orcidid>0000-0002-3745-8838 ; 0000-0002-8412-091X ; 0000-0001-5221-5132</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39322022$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alkanli, Nevra</creatorcontrib><creatorcontrib>Ay, Arzu</creatorcontrib><creatorcontrib>Cevik, Gokhan</creatorcontrib><title>Investigation of the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression</title><title>Nitric oxide</title><addtitle>Nitric Oxide</addtitle><description><![CDATA[This study aimed to investigate the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression.
This study included 88 patients diagnosed with prostate cancer and 91 healthy controls. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods were used to determine the genotype distributions of eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations.
In our study, the CC homozygous genotype of eNOS T786C gene variation was determined to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 2.343, 95%Cl: 0.990–5.544, p = 0.026), while the CT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was found to be significantly higher (OR: 0.589, 95%Cl: 0.325–1.068, p = 0.041). In addition, while the TT homozygous genotype of the eNOS G894T gene variation was found to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 9.068, 95%Cl: 4.396–18.777, p < 0.001), the GT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was determined significantly higher (OR: 0.227, 95%Cl: 0.121–0.427, p < 0.001). For eNOS (4VNTR (4a/b) - G894T) gene variations, aa-TT (p = 0.042) and bb-TT (p < 0.001) haplotype frequencies were significantly higher in the prostate cancer patient group, while aa-GT (p = 0.017), bb-GG (p = 0.049) and bb-GT (p < 0.001) haplotype frequencies were found to be significantly higher in the healthy control group. For eNOS (4VNTR (4a/b) - T786C) gene variations, the bb-CC haplotype frequency was determined to be significantly higher in the patient group (p = 0.049), while the bb-CT haplotype frequency was determined to be significantly higher in the control group (p = 0.008). For eNOS (T786C -G894T) gene variations, TT-TT (p < 0.001) and CC-TT (p = 0.025) haplotype frequencies were found to be significantly higher in the patient group. On the other hand, TT-GT (p = 0.002) and CT-GT (p < 0.001) haplotype frequencies were determined to be significantly higher in the control group. The aa genotype of the intron 4 VNTR (4a/b) gene variation was determined to be significantly higher at Gleason score ≥7 compared to Gleason score <7 (OR: 0.184, 95%Cl: 0.050–0.677, p = 0.005). PSA levels were determined significantly higher in patients with Gleason score 7 and above (p = 0.008). The risk of developing prostate cancer was found to be significantly higher in patients carrying the CC homozygous mutant genotype of the eNOS T786C gene variation (p = 0.024) and in patients carrying the TT homozygous genotype of the G894T gene variation (p = 0.021).
In our study, the CC homozygous genotype of the eNOS T786C gene variation was determined as a genetic risk factor for the development of prostate cancer, while the CT heterozygous genotype was determined as a protective factor against prostate cancer. For the eNOS G894T gene variation, the TT homozygous genotype was determined as a genetic risk factor for the development of prostate cancer, while the GT heterozygous genotype was determined as a protective factor against prostate cancer. Additionally, for eNOS (4VNTR (4a/b) - G894T) gene variations, aa-TT and bb-TT haplotypes have been identified as genetic risk factors for the development of prostate cancer, while aa-GT, bb-GG and bb-GT haplotypes have been identified as protective factors against the disease has been determined. For eNOS (4VNTR (4a/b) - T786C) gene variations, the bb-CC haplotype was determined as a genetic risk factor in the development of prostate cancer, while the bb-CT haplotype was determined as a protective factor against the disease. TT-TT and CC-TT haplotypes for eNOS (T786C -G894T) gene variations have been identified as genetic risk factors for the development of prostate cancer. In contrast, TT-GT and CT-GT haplotypes were found to be protective factors against the disease. The aa genotype of the intron 4 VNTR (4a/b) gene variation has also been identified as an important genetic risk factor in prostate cancer progression. Significantly increased PSA levels in patients with Gleason score 7 and above, and significantly increased PSA levels in patients carrying the CC and TT homozygous mutant genotype for T786C and G894T gene variations were determined as important risk factors. It is thought that the genetic biomarkers in our study may play a role as personalized therapeutic agents in slowing down the development of prostate cancer, increasing the effectiveness of treatment in prostate cancer, affecting the responses to drugs that regulate NO signaling, predetermining genetic predisposition to prostate cancer, and risk assessment in patients with prostate cancer.
•In our study, the CC homozygous genotype of the eNOS T786C gene variation was determined as a genetic risk factor for the development of prostate cancer, while the CT heterozygous genotype was determined as a protective factor against prostate cancer. For eNOS G894T gene variation, the TT homozygous genotype was determined as a genetic risk factor for the development of prostate cancer, while the GT heterozygous genotype was determined as a protective factor against prostate cancer.•For (4a/b - G894T) gene variations, aa-TT and bb-TT haplotypes have been identified as genetic risk factors for development of prostate cancer, while aa-GT, bb-GG and bb-GT haplotypes have been determined as protective factors against the disease. For (4a/b - T786C) gene variations, the bb-CC haplotype was determined as a genetic risk factor in the development of prostate cancer, while the bb-CT haplotype was determined as a protective factor against the disease. TT-TT and CC-TT haplotypes for (T786C-G894T) gene variations have been identified as genetic risk factors in the development of prostate cancer. In contrast, TT-GT and CT-GT haplotypes were found to be protective factors against the disease.•The aa genotype of the (4a/b) gene variation has also been identified as an important genetic risk factor in prostate cancer progression.•PSA levels were determined significantly higher in prostate cancer patients with a Gleason score of 7 and above. In addition, the risk of developing prostate cancer was determined to be significantly higher in patients carrying the CC homozygous mutant genotype of the T786C gene variation and the TT homozygous mutant genotype of the G894T gene variation.•Due to its versatile and diverse effects, NO is important as new anticancer strategies in slowing down cancer growth and increasing cancer treatment efficacy. eNOS regulation and NO production are affected by eNOS functional genetic variations, and these genetic variations are important in affecting the response to drugs that regulate NO signaling. It is thought that our findings may be effective in risk assessment and development of personalized therapeutic strategies in prostate cancer patients.]]></description><subject>eNOS gene variations</subject><subject>Nitric oxide</subject><subject>PCR</subject><subject>Prostate cancer</subject><subject>RFLP</subject><issn>1089-8603</issn><issn>1089-8611</issn><issn>1089-8611</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kc1uEzEUhS0EoqXwAiyQl0Vqptf2jMeW2FQRLZWqVoLA1vJ47qSOJp5gO4G-Bk-MQ9ouWfnvfMe65xDynkHFgMnzVRX89LviwOsKdAWgXpBjBkrPlGTs5fMexBF5k9IKAGqh5GtyJLTgBePH5M912GHKfmmznwKdBprvkUYc_53Tvd8k2mH-hRgo3t59o4tWyfkZvVK6XpxRH3IsWE1_3C6-0tPanncf6RID0p2N_uBBbejpJk4p24zU2eAw0h53OE6bNYb89L6MmFIB3pJXgx0TvntcT8j3y8-L-ZfZzd3V9fziZua4aPPMKdCy7hsmetErYYF3ikknlRO1a8CCbMTQCd2pQXQNd0q3oula4aBRXJXLE3J68C1__9yWEMzaJ4fjaANO22QEA61bybQsUn6QujJGijiYTfRrGx8MA7PvwqzMvguz78KANqWLAn149N92a-yfkafwi-DTQYBlyp3HaJLzWOLpfUSXTT_5__n_BfFImdg</recordid><startdate>20241101</startdate><enddate>20241101</enddate><creator>Alkanli, Nevra</creator><creator>Ay, Arzu</creator><creator>Cevik, Gokhan</creator><general>Elsevier Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3745-8838</orcidid><orcidid>https://orcid.org/0000-0002-8412-091X</orcidid><orcidid>https://orcid.org/0000-0001-5221-5132</orcidid></search><sort><creationdate>20241101</creationdate><title>Investigation of the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression</title><author>Alkanli, Nevra ; Ay, Arzu ; Cevik, Gokhan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c237t-c80964d513d3d83a02b816c68c34c50a0653fb39b8f3b52c89735b73c058288f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>eNOS gene variations</topic><topic>Nitric oxide</topic><topic>PCR</topic><topic>Prostate cancer</topic><topic>RFLP</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alkanli, Nevra</creatorcontrib><creatorcontrib>Ay, Arzu</creatorcontrib><creatorcontrib>Cevik, Gokhan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Nitric oxide</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alkanli, Nevra</au><au>Ay, Arzu</au><au>Cevik, Gokhan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigation of the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression</atitle><jtitle>Nitric oxide</jtitle><addtitle>Nitric Oxide</addtitle><date>2024-11-01</date><risdate>2024</risdate><volume>152</volume><spage>69</spage><epage>77</epage><pages>69-77</pages><issn>1089-8603</issn><issn>1089-8611</issn><eissn>1089-8611</eissn><abstract><![CDATA[This study aimed to investigate the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression.
This study included 88 patients diagnosed with prostate cancer and 91 healthy controls. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods were used to determine the genotype distributions of eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations.
In our study, the CC homozygous genotype of eNOS T786C gene variation was determined to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 2.343, 95%Cl: 0.990–5.544, p = 0.026), while the CT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was found to be significantly higher (OR: 0.589, 95%Cl: 0.325–1.068, p = 0.041). In addition, while the TT homozygous genotype of the eNOS G894T gene variation was found to be significantly higher in the prostate cancer patient group compared to the healthy control group (OR: 9.068, 95%Cl: 4.396–18.777, p < 0.001), the GT heterozygous genotype was found to be significantly higher in the healthy control group compared to the prostate cancer patient group was determined significantly higher (OR: 0.227, 95%Cl: 0.121–0.427, p < 0.001). For eNOS (4VNTR (4a/b) - G894T) gene variations, aa-TT (p = 0.042) and bb-TT (p < 0.001) haplotype frequencies were significantly higher in the prostate cancer patient group, while aa-GT (p = 0.017), bb-GG (p = 0.049) and bb-GT (p < 0.001) haplotype frequencies were found to be significantly higher in the healthy control group. For eNOS (4VNTR (4a/b) - T786C) gene variations, the bb-CC haplotype frequency was determined to be significantly higher in the patient group (p = 0.049), while the bb-CT haplotype frequency was determined to be significantly higher in the control group (p = 0.008). For eNOS (T786C -G894T) gene variations, TT-TT (p < 0.001) and CC-TT (p = 0.025) haplotype frequencies were found to be significantly higher in the patient group. On the other hand, TT-GT (p = 0.002) and CT-GT (p < 0.001) haplotype frequencies were determined to be significantly higher in the control group. The aa genotype of the intron 4 VNTR (4a/b) gene variation was determined to be significantly higher at Gleason score ≥7 compared to Gleason score <7 (OR: 0.184, 95%Cl: 0.050–0.677, p = 0.005). PSA levels were determined significantly higher in patients with Gleason score 7 and above (p = 0.008). The risk of developing prostate cancer was found to be significantly higher in patients carrying the CC homozygous mutant genotype of the eNOS T786C gene variation (p = 0.024) and in patients carrying the TT homozygous genotype of the G894T gene variation (p = 0.021).
In our study, the CC homozygous genotype of the eNOS T786C gene variation was determined as a genetic risk factor for the development of prostate cancer, while the CT heterozygous genotype was determined as a protective factor against prostate cancer. For the eNOS G894T gene variation, the TT homozygous genotype was determined as a genetic risk factor for the development of prostate cancer, while the GT heterozygous genotype was determined as a protective factor against prostate cancer. Additionally, for eNOS (4VNTR (4a/b) - G894T) gene variations, aa-TT and bb-TT haplotypes have been identified as genetic risk factors for the development of prostate cancer, while aa-GT, bb-GG and bb-GT haplotypes have been identified as protective factors against the disease has been determined. For eNOS (4VNTR (4a/b) - T786C) gene variations, the bb-CC haplotype was determined as a genetic risk factor in the development of prostate cancer, while the bb-CT haplotype was determined as a protective factor against the disease. TT-TT and CC-TT haplotypes for eNOS (T786C -G894T) gene variations have been identified as genetic risk factors for the development of prostate cancer. In contrast, TT-GT and CT-GT haplotypes were found to be protective factors against the disease. The aa genotype of the intron 4 VNTR (4a/b) gene variation has also been identified as an important genetic risk factor in prostate cancer progression. Significantly increased PSA levels in patients with Gleason score 7 and above, and significantly increased PSA levels in patients carrying the CC and TT homozygous mutant genotype for T786C and G894T gene variations were determined as important risk factors. It is thought that the genetic biomarkers in our study may play a role as personalized therapeutic agents in slowing down the development of prostate cancer, increasing the effectiveness of treatment in prostate cancer, affecting the responses to drugs that regulate NO signaling, predetermining genetic predisposition to prostate cancer, and risk assessment in patients with prostate cancer.
•In our study, the CC homozygous genotype of the eNOS T786C gene variation was determined as a genetic risk factor for the development of prostate cancer, while the CT heterozygous genotype was determined as a protective factor against prostate cancer. For eNOS G894T gene variation, the TT homozygous genotype was determined as a genetic risk factor for the development of prostate cancer, while the GT heterozygous genotype was determined as a protective factor against prostate cancer.•For (4a/b - G894T) gene variations, aa-TT and bb-TT haplotypes have been identified as genetic risk factors for development of prostate cancer, while aa-GT, bb-GG and bb-GT haplotypes have been determined as protective factors against the disease. For (4a/b - T786C) gene variations, the bb-CC haplotype was determined as a genetic risk factor in the development of prostate cancer, while the bb-CT haplotype was determined as a protective factor against the disease. TT-TT and CC-TT haplotypes for (T786C-G894T) gene variations have been identified as genetic risk factors in the development of prostate cancer. In contrast, TT-GT and CT-GT haplotypes were found to be protective factors against the disease.•The aa genotype of the (4a/b) gene variation has also been identified as an important genetic risk factor in prostate cancer progression.•PSA levels were determined significantly higher in prostate cancer patients with a Gleason score of 7 and above. In addition, the risk of developing prostate cancer was determined to be significantly higher in patients carrying the CC homozygous mutant genotype of the T786C gene variation and the TT homozygous mutant genotype of the G894T gene variation.•Due to its versatile and diverse effects, NO is important as new anticancer strategies in slowing down cancer growth and increasing cancer treatment efficacy. eNOS regulation and NO production are affected by eNOS functional genetic variations, and these genetic variations are important in affecting the response to drugs that regulate NO signaling. It is thought that our findings may be effective in risk assessment and development of personalized therapeutic strategies in prostate cancer patients.]]></abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>39322022</pmid><doi>10.1016/j.niox.2024.09.008</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3745-8838</orcidid><orcidid>https://orcid.org/0000-0002-8412-091X</orcidid><orcidid>https://orcid.org/0000-0001-5221-5132</orcidid></addata></record> |
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| identifier | ISSN: 1089-8603 |
| ispartof | Nitric oxide, 2024-11, Vol.152, p.69-77 |
| issn | 1089-8603 1089-8611 1089-8611 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3109976196 |
| source | ScienceDirect Freedom Collection |
| subjects | eNOS gene variations Nitric oxide PCR Prostate cancer RFLP |
| title | Investigation of the relationships between eNOS T786C, G894T, intron 4 VNTR (4a/b) gene variations and prostate cancer development and progression |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T05%3A50%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Investigation%20of%20the%20relationships%20between%20eNOS%20T786C,%20G894T,%20intron%204%20VNTR%20(4a/b)%20gene%20variations%20and%20prostate%20cancer%20development%20and%20progression&rft.jtitle=Nitric%20oxide&rft.au=Alkanli,%20Nevra&rft.date=2024-11-01&rft.volume=152&rft.spage=69&rft.epage=77&rft.pages=69-77&rft.issn=1089-8603&rft.eissn=1089-8611&rft_id=info:doi/10.1016/j.niox.2024.09.008&rft_dat=%3Cproquest_cross%3E3109976196%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c237t-c80964d513d3d83a02b816c68c34c50a0653fb39b8f3b52c89735b73c058288f3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=3109976196&rft_id=info:pmid/39322022&rfr_iscdi=true |