ArticleBiochemical genetics2026
Molecular Study of the Poly (ADP-ribose) Polymerase-1 Gene as a Promotor of Inflammation-Driven Colorectal Carcinoma.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related deaths worldwide. Chronic inflammation is a risk factor for various cancers, including CRC. However, the specific mechanisms by which inflammation contributes to cancer development are not fully understood. Our study assessed PARP1 and NF-κB mRNA expression in different stages of CRC, aiming to elucidate their roles in inflammation-driven CRC pathogenesis and define their stage-specific expression patterns. The study involved 35 CRC tissue samples and a control group of 25 samples from the healthy margins of colon cancer. PARP1 and NF-κB mRNA levels were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in tumor tissue samples, as well as the adjacent part of normal tissue. Our results revealed that PARP1 and NF-κB/p50 gene expression was significantly higher in CRC vs. control. Furthermore, there was a positive correlation between PARP1 and NF-κB/p50 mRNA expression levels. PARP1 was found to be responsible for 14.5% of the change in NF-κB/p50. Both PARP1 and NF-κB/p50 had high accuracy in the diagnosis of CRC with AUC = 0.905 and 0.956, respectively. This study revealed the overexpression of PARP1 and NF-κB genes in CRC cases, which suggests that the use of PARP1 inhibitors and anti-inflammatory drugs could be effective in CRC treatment. PARP1/NF-κB showed preliminary associations with CRC that merit diagnostic evaluation in larger studies. Our data suggest that PARP1 and NF-κB expression may complement CEA in characterizing CRC biology though future studies must determine whether these markers have independent prognostic value.
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