The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.
Ibolya CzegleChelsea HuangPriscilla Geraldine SoriaDylan Wesley PurkissAndrea ShieldsEdina Amalia Wappler-GuzzettaPublished in: Life (Basel, Switzerland) (2023)
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.
Keyphrases
- papillary thyroid
- cell death
- oxidative stress
- reactive oxygen species
- squamous cell
- fatty acid
- clinical practice
- squamous cell carcinoma
- gene expression
- lymph node metastasis
- blood pressure
- copy number
- transcription factor
- signaling pathway
- drug delivery
- dna methylation
- replacement therapy
- cancer therapy
- skeletal muscle
- endometrial cancer
- wild type