Acute myeloid leukemia (AML) is a very heterogeneous type of blood cancer, which presents with a high rate of mortality especially in elderly patients. Better understanding of critical players, such as molecules with tumor suppressive properties, may help to fine-tune disease classification and thereby treatment modalities for this detrimental disease. Here, we summarize well-known and established tumor suppressors as well as emerging tumor suppressors, including transcription factors (TCFs) and other transcriptional regulators, such as epigenetic modulators. In addition, we look into the versatile field of miRNAs also interfering with tumorigenesis and progression, which offer new possibilities in AML diagnosis, prognosis, and therapy.
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http://dx.doi.org/10.1080/10428194.2021.1907372 | DOI Listing |
PLoS One
January 2025
Cancer Center, Kagoshima University Hospital, Kagoshima, Japan.
Kinase-related gene fusion and point mutations play pivotal roles as drivers in cancer, necessitating optimized, targeted therapy against these alterations. The efficacy of molecularly targeted therapeutics varies depending on the specific alteration, with great success reported for such therapeutics in the treatment of cancer with kinase fusion proteins. However, the involvement of actionable alterations in solid tumors, especially regarding kinase fusions, remains unclear.
View Article and Find Full Text PDFCell Rep
January 2025
Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA; Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455, USA. Electronic address:
Localized prostate cancer can be cured by radiation or surgery, but advanced prostate cancer continues to be a clinical challenge. Altered alternative polyadenylation occurs in numerous cancers and can downregulate tumor-suppressor genes and upregulate oncogenes. We found that the cleavage and polyadenylation specificity factor (CPSF) complex factor CPSF1 is upregulated in patients with advanced prostate cancer, with high CPSF1 expression correlating with worse progression-free survival.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.
Background: Differential DNA methylation in the promoter region of tumour suppressor genes leads to gene function silencing.
Materials And Methods: In this study, we aimed to evaluate the salivary promoter methylation of EDNRB, MGMT and TIMP3 genes in H&NC patients (n = 100), premalignant lesions patients (n = 25) and healthy controls (n = 50). Blood and saliva samples were collected from all three groups and 20 concomitant tumour tissues were collected from the H&NC patients.
Curr Drug Targets
January 2025
Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, 443002, China.
Metallothionein 1J pseudogene (MT1JP) is a long non-coding RNA (lncRNA) that functions as a tumor suppressor in various malignancies. Reduced MT1JP expression is associated with increased tumor proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and treatment resistance in nine cancers, such as gastric cancer, intrahepatic cholangiocarcinoma, hepatocellular carcinoma, and breast cancer. Mechanistically, MT1JP acts as a competitive endogenous RNA (ceRNA) to regulate oncogenic microRNAs (miRNAs), including miR-92a-3p, miR-214-3p, and miR-24-3p.
View Article and Find Full Text PDFCell Biochem Funct
January 2025
School of Medicine, Foshan University, Foshan, Guangdong, China.
With the rapid development of gene editing technology, its application in breast cancer has gradually become the focus of research. This article reviews the application of gene editing technology in the treatment of breast cancer, and discusses its challenges and future development directions. The key application areas of gene editing technology in the treatment of breast cancer will be outlined, including the discovery of new therapeutic targets and the development of drugs related to the pathway.
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