Results 121 to 130 of about 1,574,651 (334)
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani+14 more
wiley +1 more source
Haitang Qiu,1,* Shajidan Abudureyimu,1,* Mengjia Liu,1 Fen Liu,2 Ying Gao1 1Department of Comprehensive Internal Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, People’s Republic of China; 2State Key ...
Qiu H+4 more
doaj
Estimation of the Gene-Environment Interaction in Breast Cancer Patients
Background and objectives: There is growing interest in assessing gene-environment interaction in the course of case-control studies. Difficulties related to the sampling of controls have led to the development of a range of non-traditional methods that
P Yavari, MA Pourhosseingholi
doaj
Ubiquitination of transcription factors in cancer: unveiling therapeutic potential
In cancer, dysregulated ubiquitination of transcription factors contributes to the uncontrolled growth and survival characteristics of tumors. Tumor suppressors are degraded by aberrant ubiquitination, or oncogenic transcription factors gain stability through ubiquitination, thereby promoting tumorigenesis.
Dongha Kim, Hye Jin Nam, Sung Hee Baek
wiley +1 more source
Gene-environment interaction and maternal arsenic methylation efficiency during pregnancy
Background: Single nucleotide polymorphisms (SNPs) may influence arsenic methylation efficiency, affecting arsenic metabolism. Whether gene-environment interactions affect arsenic metabolism during pregnancy remains unclear, which may have implications ...
Shangzhi Gao+9 more
doaj
The missing person in gene‐environment interactions [PDF]
Oluwatobiloba Osikoya, Myles Axton
openaire +4 more sources
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen+12 more
wiley +1 more source
Breast cancer metastasis is associated with myeloid cell dysregulation and the lung‐specific accumulation of tumor‐supportive Gr1+ cells. Gr1+ cells support metastasis, in part, through a CHI3L1‐mediated mechanism, which can be targeted and inhibited with cargo‐free, polymeric nanoparticles.
Jeffrey A. Ma+9 more
wiley +1 more source