There is an increasing understanding of the molecular and cytogenetic background of various tumors that helps us better conceptualize the pathogenesis of specific diseases. Additionally, in many cases, these molecular and cytogenetic alterations have diagnostic, prognostic, and/or therapeutic applications that are heavily used in clinical practice. Given that there is always room for improvement in cancer treatments and in cancer patient management, it is important to discover new therapeutic targets for affected individuals. In this review, we discuss mitochondrial changes in breast and gynecological (endometrial and ovarian) cancers. In addition, we review how the frequently altered genes in these diseases (BRCA1/2, HER2, PTEN, PIK3CA, CTNNB1, RAS, CTNNB1, FGFR, TP53, ARID1A, and TERT) affect the mitochondria, highlighting the possible associated individual therapeutic targets. With this approach, drugs targeting mitochondrial glucose or fatty acid metabolism, reactive oxygen species production, mitochondrial biogenesis, mtDNA transcription, mitophagy, or cell death pathways could provide further tailored treatment.

Papillary thyroid cancer (PTC) is the most common thyroid malignancy, with significant racial/ethnic disparities in incidence and survival. Asians have the highest incidence, and recurrence, while African Americans experience the lowest survival rates, suggesting contributions from genetic, environmental, and healthcare-related factors. While socioeconomic disparities play a role, emerging evidence highlights genetic and molecular mechanisms underlying these differences. This study examines differentially expressed genes (DEGs) to identify potential molecular drivers of PTC disparities. Bulk RNA-sequencing (RNA-seq) data from 20 PTC tumors (5 White, 5 African American, 5 Hispanic, and 5 Asian) were analyzed using the UseGalaxy platform. Preprocessing included quality control, adapter trimming, and genome alignment. Differential expression analysis identified genes with p < 0.01 and fold change ≥ 2.5. Volcano plots visualized significant DEGs. Gene Set Enrichment Analysis (GSEA) via eVITTA identified enriched pathways. TCGA data analysis validated racial/ethnic differences in gene expression. Ethnic groups exhibited distinct gene expression profiles. GSEA revealed differences in cell proliferation, immune regulation, and thyroid hormone metabolism. African Americans showed immune suppression and reduced tumor suppressor activity, while Asians exhibited enriched cell cycle and DNA repair pathways. Significant differences were confirmed in some of the genes in TCGA data analysis. This study identifies genetic factors contributing to racial disparities in PTC, emphasizing the need for further validation in larger cohorts and functional studies. Understanding these molecular differences may inform personalized treatment strategies and improve PTC outcomes across diverse populations.

Enigma protein, encoded by the PDLIM7 gene, is overexpressed in thyroid cancer in a stage-dependent manner, suggesting a potential involvement in the initiation and progression of thyroid cancer. The Enigma interacts with several cellular pathways, including PI3K/AKT, MDM2, and BMP-1. The Enigma is regulated by microRNAs. Specifically, we showed that the Enigma protein upregulation corresponds to the downregulation of Let-7 family genes. There is limited research on the interactions and regulation of the Enigma with other proteins/genes in thyroid cancer tissues, indicating a gap in current knowledge. Our aim is to establish the Enigma as a biomarker. We also aim to study the interacting partners of the Enigma signaling pathways and their probable miRNA regulation in thyroid cancer progression. Using Western blotting, densitometric analysis, immunoprecipitation (IP), and reverse IP, we detected the protein expression and protein–protein interactions in the corresponding papillary thyroid carcinomas (PTCs). Utilizing real-time qPCR assay and Pearson’s correlation test, we highlighted the correlation between PDLIM7 and Let-7g gene expression in the same tissues. The results showed the differential upregulations of the Enigma protein in different stages of PTCs compared to benign tissues along with AKT, VDR, BMP-1, and MDM2 proteins. Loss of DBP was observed in a subset of PTCs. Strong interactions of the Enigma with PI3K/AKT and MDM2 were noted, along with a weaker BMP-1 interaction. Pearson’s correlation coefficient analysis between PDLIM7 and let-7g gene expression was significant (p < 0.05); however, there was a weak inverse correlation (r = −0.27). The study suggests the potential utility of the PDLIM7-qPCR assay as a biomarker for thyroid cancer. The Enigma’s interactions with key signaling pathways may provide valuable insights into the development of thyroid cancer. The study contributes to understanding the molecular mechanisms involving the Enigma protein in thyroid cancer and highlights its potential as a biomarker.