This paper discusses the integration of artificial intelligence (AI) tools in education, delineating their potential to transform pedagogical practices alongside the challenges they present. Generative AI models like ChatGPT, had a disruptive impact on teaching and learning, due to their ability to create text, images, and sound, revolutionizing educational content creation and modification. However, nowadays the educational community is polarized, with some embracing AI for its accessibility and efficiency thus advocating it as an indispensable tool, while others cautioning against risks to academic integrity and intellectual development. This document is designed to raise awareness about AI tools and provide some examples of how they can be used to improve education and learning. From an educator’s perspective, AI is an asset for curriculum development, course material preparation, instructional design and student assessment, while reducing bias and workload. For students, AI tools offer personalized learning experiences, timely feedback, and support in various academic activities. The Turkish Biochemical Society (TBS) Academy recommends educators to embrace and utilize AI tools to enhance educational processes, and engage in peer learning for better adaptation while maintaining a critical perspective on their utility and limitations. The transfer of AI knowledge and methods to the teaching experiences should complement and not replace the educator’s creativity and critical thinking. The paper advocates for an informed embrace of AI, AI fluency among educators and students, ethical application of AI in academic settings, and continuous engagement with the evolving AI technologies, ensuring that AI tools are used to augment critical thinking and contribute positively to education and society.

Tyrosine kinase inhibitor (TKI) resistance is a major problem in chronic myeloid leukemia (CML). We generated a TKI-resistant K562 sub-population, K562-IR, under selective imatinib-mesylate pressure. K562-IR cells are CD34^-/CD38^-, BCR-Abl-independent, proliferate slowly, highly adherent and form intact tumor spheroids. Loss of CD45 and other hematopoietic markers reveal these cells have diverged from their hematopoietic origin. CD34 negativity, high expression of E-cadherin and CD44; decreased levels of CD45 and β-catenin do not fully confer with the leukemic stem cell (LSC) phenotype. Expression analyses reveal that K562-IR cells differentially express tissue/organ development and differentiation genes. Our data suggest that the observed phenotypic shift is an adaptive process rendering cells under TKI stress to become oncogene independent. Cells develop transcriptional instability in search for a gene expression framework suitable for new environmental stresses, resulting in an adaptive phenotypic shift in which some cells partially display LSC-like properties. With leukemic/cancer stem cell targeted therapies underway, the difference between treating an entity and a spectrum of dynamic cellular states will have conclusive effects on the outcome.

Cancer remains a deadly disease, and its treatment desperately needs to be managed through novel, rapidly advancing strategies. Most cancer cases eventually develop into recurrences, for which cancer stem cells (CSCs) are thought to be responsible. These cells are considered a subpopulation of all tumor cancer cells, with aberrant regulation of self-renewal, unbalanced proliferation, and cell death properties. CSCs show a marked degree of resistance to chemotherapy or radiotherapy and immune surveillance. To combat CSCs, new drugs are flooding the market each year, increasing the cost of therapy dramatically. Natural products are becoming a new research area, presenting a diverse chemical library to suppress CSCs and some natural products show great promise in this regard. In the near future, the introduction of natural products as a source of new chemotherapy modalities may result in the development of novel anticancer drugs that could be reasonably-priced alternatives to expensive current treatments. Lately preclinical and clinical research has focused on natural compounds’ effects on targeting surface markers, signaling pathways, apoptosis, and escape from immunosurveillance. In this review, we present research on the mechanisms through which natural compounds kill CSCs and the potential use of natural compounds in the inhibition of CSCs.

Tetraploidy, or whole-genome duplication, is a common phenomenon in cancer and preludes chromosome instability, which strongly correlates with disease progression, metastasis, and treatment failure. Therefore, it is reasonable to hypothesize that tetraploidization confers multidrug resistance. Nevertheless, the contribution of whole-genome duplication to chemo-radiotherapy resistance remains unclear. Here, using isogenic diploid and near-tetraploid clones from three colorectal cancer cell lines and one non-transformed human epithelial cell line, we show a consistent growth impairment but a divergent tumorigenic potential of near-tetraploid cells. Next, we assessed the effects of first-line chemotherapeutic drugs, other commonly used agents and ionizing radiation, and found that whole-genome duplication promoted increased chemotherapy resistance and also conferred protection against irradiation. When testing the activation of apoptosis, we observed that tetraploid cells were less prone to caspase 3 activation after treatment with first-line chemotherapeutic agents. Furthermore, we found that pre-treatment with ataxia telangiectasia and Rad3 related (ATR) inhibitors, which targets response to replication stress, significantly enhanced the sensitivity of tetraploid cells to first-line chemotherapeutic agents as well as to ionizing radiation. Our findings provide further insight into how tetraploidy results in greater levels of tolerance to chemo-radiotherapeutic agents and, moreover, we show that ATR inhibitors can sensitize near-tetraploid cells to commonly used chemo-radiotherapy regimens.

Ganoderma lucidum is a medicinal higher Basidiomycetes mushroom that exerts anticancer effects through several different mechanisms. This study investigated the effects of G. lucidum on the telomerase activity and microRNA (miRNA) profiles of MCF-7 cells. According to the cytotoxicity results, the G. lucidum ether extract exhibits the highest cytotoxic potency; therefore it was chosen for the subsequent telomerase activity assay and miRNA profiling. The telomerase activity observed in the cells treated with a half-maximal inhibitory concentration of G. lucidum ether extract (100 µg/mL in dimethyl sulfoxide) was 32.2% lower than that of the control cells treated with 1% dimethyl sulfoxide. Among 1066 miRNAs, the most downregulated miRNA was hsa-miR-27a* (4.469-fold), and the most upregulated miRNA was hsa-miR-1285 (10.462-fold). A database search revealed the predicted miRNAs that target the catalytic subunit of the telomerase enzyme telomerase reverse transcriptase, and only miR-3687 (upregulated 2.153-fold) and miR-1207-5p (upregulated 2.895-fold) were changed by at least 2-fold. The miRNA profile changes demonstrated in this study provide a data set regarding their effects on the pathways that regulate telomerase activity in MCF-7 breast cancer cells treated with G. lucidum. These data should aid the development of novel cancer treatment strategies.

Cholangiocarcinoma (CCA) is a poorly treatable type of cancer and its incidence is dramatically increasing. The lack of understanding of the biology of this tumor has slowed down the identification of novel targets and the development of effective treatments. Based on next generation sequencing profiling, alterations in DNA damage response (DDR)-related genes are paving the way for DDR-targeting strategies in CCA. Based on the notion of synthetic lethality, several DDR-inhibitors (DDRi) have been developed with the aim of accumulating enough DNA damage to induce cell death in tumor cells. Observing that DDRi alone could be insufficient for clinical use in CCA patients, the combination of DNA-damaging regimens with targeted approaches has started to be considered, as evidenced by many emerging clinical trials. Hence, novel therapeutic strategies combining DDRi with patient-specific targeted drugs could be the next level for treating cholangiocarcinoma.