How cancer stem cells cause disease recurrence in recovered patients

Many tumors contain phenotypic and functionally diverse populations of cancer cells that differ in terms of metastatic and angiogenic potential,as well as medication resistance.Tumor recurrence and metastasis are two of the most difficult aspects of cancer treatment and even with conventional therapies(such as chemotherapy and radio-therapy),satisfactory results have not been obtained.The main source of cancer stem cell tumorigenesis is CSCs,which,by dividing cells,produce the same daughter cells and differentiate into different types and can create tumor tissue from a single cell.They are responsible for the development of cancer,progression,metastasis,recurrence,and treatment resistance,and are recognized to have a role in the failure of conventional therapy and tumor recurrence.To resolve this quandary,careful identification of CSC molecular targets and comprehensive disclosure of the underlying processes of CSC immune system properties are required.Traditional cancer therapies are insufficient to kill all intracellular cells,particularly those with great resistance to therapy,such as CSC.Targeting CSC metabolism has been proposed as a novel treatment strategy for preventing the development of different malignancies.In this study,the identification of cancer stem cell populations,the role of CSCs in drug resistance,metastasis,hypoxia,and the role of Nrf2 in CSC tumorigenesis has been reviewed.

The mechanism of DDR genes in tumor progression

DNA is constantly exposed to damaging factors that require DNA repair processes to maintain its natural structure and maintain genomic integrity.Spot mutations,chromosomal shifts,and the expansion or destruction of chromosomal regions or entire chromosomes.It can be one of the consequences of not repairing DNA damage in time.Cell cycle halt,DNA repair,cellular aging,and apoptosis are all possible outcomes of DDR in injured somatic cells.DDR has been linked to a variety of illnesses in the clinic,including premature aging,tissue malfunction,immunological insufficiency,neurological disorders,and cancer.Defects in DDR genes promote cancer cell development by committing driving mutations,producing tumor heterogeneity,and allowing cancer cells to escape apoptosis.The discovery of the many functions of DDR pathways has led to the identification of critical targets for inhibition in the fight against cancer.The susceptibility of tumor cells to the efficacy of typical genotoxic therapies can be used to exploit this inhibition.Furthermore,employing the notion of artificial lethality,DDR faults in tumors can be used as a targeted weakness.In general,we discuss DDR pathways,mutations,and DNA damage in this article.DDR inhibitors in conjunction with other anti-cancer medicines such as immunotherapy,radiation,and epigenetic agents seem to be promising.Changes in DDR pathways are critical in the development of cancer and might lead to new anticancer therapies.We must insist on a logical rather than an empirical approach to the clinical development of DDR inhibitors through stronger collaboration between scientists and clinicians.