The Significant Role of a Functional Polymorphism in the
            <i>NF-κB1</i>
            Gene in Breast Cancer: Evidence from an Iranian Cohort

Alidoust, Maryam; Shamshiri, Asma Khorshid; Tajbakhsh, Amir; Gheibihayat, Seyed Mohammad; Mazloom, Seyed Mostafa; Alizadeh, Farzaneh; Pasdar, Alireza

doi:10.2217/fon-2021-0197

Cited by 2 publications

(3 citation statements)

References 41 publications

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“…This p65/p50 heterodimer plays a key role in NF-κB function [ 33 , 34 , 35 ]. In several cancer types, including CRC, lung cancer, blood cancer, and pancreatic cancer, etc., researchers have observed constitutive activation of this particular family [ 36 , 37 , 38 , 39 ].…”

Section: Genetic Changes Of Nf-κb Signaling In Crcmentioning

confidence: 99%

“…Importantly, a recent study has detected a genetic variation within the promoter segment of the NF-κB1 gene. This genetic variation entails a 4-base pair (bp) insertion/deletion (94ins/delATTG) positioned between two presumed critical regulatory components in the promoter, specifically AP-1 and κB [ 36 ]. Interestingly, the research found that people who have two copies of this deletion (94del/delATTG) are more likely to develop ulcerative colitis, a chronic inflammatory bowel disease predominantly affecting the colon.…”

Section: Genetic Changes Of Nf-κb Signaling In Crcmentioning

confidence: 99%

“…If left untreated, ulcerative colitis-related inflammation in the colon can result in an increased risk in developing CRC. The study observed that the deletion variant of the 94ins/delATTG polymorphism in the NF-κB1 gene’s promoter region, whether homozygous (DD) or heterozygous (WD), was linked to an increased risk in CRC among Swedish patients, including those with both unselected and sporadic forms of the disease [ 36 , 40 ].…”

Section: Genetic Changes Of Nf-κb Signaling In Crcmentioning

confidence: 99%

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Genetic Alterations of NF-κB and Its Regulators: A Rich Platform to Advance Colorectal Cancer Diagnosis and Treatment

Alipourgivi,

Motolani,

Qiu

et al. 2023

IJMS

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Colorectal cancer (CRC) is the third leading cause of cancer mortality in the United States, with an estimated 52,000 deaths in 2023. Though significant progress has been made in both diagnosis and treatment of CRC in recent years, genetic heterogeneity of CRC—the culprit for possible CRC relapse and drug resistance, is still an insurmountable challenge. Thus, developing more effective therapeutics to overcome this challenge in new CRC treatment strategies is imperative. Genetic and epigenetic changes are well recognized to be responsible for the stepwise development of CRC malignancy. In this review, we focus on detailed genetic alteration information about the nuclear factor (NF)-κB signaling, including both NF-κB family members, and their regulators, such as protein arginine methyltransferase 5 (PRMT5), and outer dynein arm docking complex subunit 2 (ODAD2, also named armadillo repeat-containing 4, ARMC4), etc., in CRC patients. Moreover, we provide deep insight into different CRC research models, with a particular focus on patient-derived xenografts (PDX) and organoid models, and their potential applications in CRC research. Genetic alterations on NF-κB signaling components are estimated to be more than 50% of the overall genetic changes identified in CRC patients collected by cBioportal for Cancer Genomics; thus, emphasizing its paramount importance in CRC progression. Consequently, various genetic alterations on NF-κB signaling may hold great promise for novel therapeutic development in CRC. Future endeavors may focus on utilizing CRC models (e.g., PDX or organoids, or isogenic human embryonic stem cell (hESC)-derived colonic cells, or human pluripotent stem cells (hPSC)-derived colonic organoids, etc.) to further uncover the underpinning mechanism of these genetic alterations in NF-κB signaling in CRC progression. Moreover, establishing platforms for drug discovery in dishes, and developing Biobanks, etc., may further pave the way for the development of innovative personalized medicine to treat CRC in the future.

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