-
Critical Reviews in Oncology/hematology Aug 2023Lynch syndrome (LS) is a genetic predisposition leading to colorectal and non-colorectal tumors such as endometrial, upper urinary tract, small intestine, ovarian,... (Review)
Review
Lynch syndrome (LS) is a genetic predisposition leading to colorectal and non-colorectal tumors such as endometrial, upper urinary tract, small intestine, ovarian, gastric, biliary duct cancers and glioblastoma. Though not classically associated with LS, growing literature suggests that sarcomas might develop in patients with LS. This systematic review of literature identified 44 studies (N = 95) of LS patients who developed sarcomas. It seems that most sarcomas developed in patients with a germline mutation of MSH2 (57 %) exhibit a dMMR (81 %) or MSI (77 %) phenotype, as in other LS-tumors. Although undifferentiated pleomorphic sarcoma (UPS), leiomyosarcoma, and liposarcoma remain the most represented histologic subtype, a higher proportion of rhabdomyosarcoma (10 %, especially pleomorphic rhabdomyosarcoma) is reported. Further studies are required to better characterize this sub-population.
Topics: Humans; Colorectal Neoplasms, Hereditary Nonpolyposis; Colorectal Neoplasms; Genetic Predisposition to Disease; Germ-Line Mutation; Sarcoma; Rhabdomyosarcoma; DNA Mismatch Repair; Microsatellite Instability
PubMed: 37301271
DOI: 10.1016/j.critrevonc.2023.104055 -
Briefings in Bioinformatics Jul 2023In only a few years, as a breakthrough technology, clustered regularly interspaced short palindromic repeats/CRISPR-associated protein (CRISPR/Cas) gene-editing systems...
In only a few years, as a breakthrough technology, clustered regularly interspaced short palindromic repeats/CRISPR-associated protein (CRISPR/Cas) gene-editing systems have ushered in the era of genome engineering with a plethora of applications. One of the most promising CRISPR tools, so-called base editors, opened an exciting avenue for exploring new therapeutic approaches through controlled mutagenesis. However, the efficiency of a base editor guide varies depending on several biological determinants, such as chromatin accessibility, DNA repair proteins, transcriptional activity, factors related to local sequence context and so on. Thus, the success of genetic perturbation directed by CRISPR/Cas base-editing systems relies on an optimal single guide RNA (sgRNA) design, taking those determinants into account. Although there is 11 commonly used software to design guides specifically for base editors, only three of them investigated and implemented those biological determinants into their models. This review presents the key features, capabilities and limitations of all currently available software with a particular focus on predictive model-based algorithms. Here, we summarize existing software for sgRNA design and provide a base for improving the efficiency of existing available software suites for precise target base editing.
Topics: RNA, Guide, CRISPR-Cas Systems; Gene Editing; CRISPR-Cas Systems; Software; DNA
PubMed: 37287132
DOI: 10.1093/bib/bbad205 -
Chemico-biological Interactions Aug 2023Citrinin (CIT) is a polyketide-derived mycotoxin, which is produced by many fungal strains belonging to the gerena Monascus, Aspergillus, and Penicillium. It has been... (Review)
Review
Citrinin (CIT) is a polyketide-derived mycotoxin, which is produced by many fungal strains belonging to the gerena Monascus, Aspergillus, and Penicillium. It has been postulated that mycotoxins have several toxic mechanisms and are potentially used as antineoplastic agents. Therefore, the present study carried out a systematic review, including articles from 1978 to 2022, by collecting evidence in experimental studies of CIT antiplorifactive activity in cancer. The Data indicate that CIT intervenes in important mediators and cell signaling pathways, including MAPKs, ERK1/2, JNK, Bcl-2, BAX, caspases 3,6,7 and 9, p53, p21, PARP cleavage, MDA, reactive oxygen species (ROS) and antioxidant defenses (SOD, CAT, GST and GPX). These factors demonstrate the potential antitumor drug CIT in inducing cell death, reducing DNA repair capacity and inducing cytotoxic and genotoxic effects in cancer cells.
Topics: Antineoplastic Agents; Citrinin; Neoplasms; Humans; Animals; Cell Lineage; Cell Death
PubMed: 37230156
DOI: 10.1016/j.cbi.2023.110561 -
Journal of Cancer Research and Clinical... Aug 2023The existence of cancer stem cells (CSCs) is closely related to tumor recurrence, metastasis, and resistance to chemoradiotherapy. In addition, given the unique physical... (Review)
Review
PURPOSE
The existence of cancer stem cells (CSCs) is closely related to tumor recurrence, metastasis, and resistance to chemoradiotherapy. In addition, given the unique physical and biological advantages of charged particle, we hypothesized that charged particle irradiation would produce strong killing effects on CSCs. The purpose of our systematic review is to evaluate the biological effects of CSCs irradiated by charged particle, including proliferation, invasion, migration, and changes in the molecular level.
METHODS
We searched PubMed, EMBASE, and Web of Science until 17 march 2022 according to the key words. Included studies have to be vitro studies of CSCs irradiated by charged particle. Outcomes included one or more of radiation sensitivity, proliferation, metastasis, invasion, and molecular level changes, like DNA damage after been irradiated.
RESULTS
Eighteen studies were included in the final analysis. The 18 articles include 12-carbon ion irradiation, 4-proton irradiation, 1 α-particle irradiation, 1-carbon ion combine proton irradiation.
CONCLUSION
Through the extraction and analysis of data, we came to this conclusion: CSCs have obvious radio-resistance compared with non-CSCs, and charged particle irradiation or in combination with drugs could overcome this resistance, specifically manifested in inhibiting CSCs' proliferation, invasion, migration, and causing more and harder to repair DNA double-stranded breaks (DSB) of CSCs.
Topics: Humans; Protons; Neoplasm Recurrence, Local; DNA Damage; Neoplastic Stem Cells; Carbon
PubMed: 36611110
DOI: 10.1007/s00432-022-04561-6