Explore the vast range of titles available.

The Oncology Nursing Society's Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) provides nurses with the tools to understand how medications are used in cancer treatment, the effect of medication-related toxicities, and evidence-based recommendations to manage and treat these toxicities. This edition features many new cancer therapies approved since the 2019 publication. Extensive drug tables provide nurses with categorical drug information based on treatment type and tips for managing patients receiving these treatments.

In our previous paper, we reported that amphiphilic Ir complex–peptide hybrids (IPHs) containing basic peptides such as KK(K)GG (K: lysine, G: glycine) (e.g., ASb-2) exhibited potent anticancer activity against Jurkat cells, with the dead cells showing a strong green emission. Our initial mechanistic studies of this cell death suggest that IPHs would bind to the calcium (Ca2+)–calmodulin (CaM) complex and induce an overload of intracellular Ca2+, resulting in the induction of non-apoptotic programmed cell death. In this work, we conduct a detailed mechanistic study of cell death induced by ASb-2, a typical example of IPHs, and describe how ASb-2 induces paraptotic programmed cell death in a manner similar to that of celastrol, a naturally occurring triterpenoid that is known to function as a paraptosis inducer in cancer cells. It is suggested that ASb-2 (50 µM) induces ER stress and decreases the mitochondrial membrane potential (ΔΨm), thus triggering intracellular signaling pathways and resulting in cytoplasmic vacuolization in Jurkat cells (which is a typical phenomenon of paraptosis), while the change in ΔΨm values is negligibly induced by celastrol and curcumin. Other experimental data imply that both ASb-2 and celastrol induce paraptotic cell death in Jurkat cells, but this induction occurs via different signaling pathways.

Annually, millions of new cancer cases are reported, leading to millions of deaths worldwide. Among the newly reported cases, breast and colon cancers prevail as the most frequently detected variations. To effectively counteract this rapid increase, the development of innovative therapies is crucial. Small molecules possessing pyridine and urea moieties have been reported in many of the currently available anticancer agents, especially VEGFR2 inhibitors. With this in mind, a rational design approach was employed to create hybrid small molecules combining urea and pyridine. These synthesized compounds underwent in vitro testing against breast and colon cancer cell lines, revealing potent submicromolar anticancer activity. Compound 8a, specifically, exhibited an impressive GI50 value of 0.06 μM against the MCF7 cancer cell line, while compound 8h displayed the highest cytotoxic activity against the HCT116 cell line, with a GI50 of 0.33 ± 0.042 μM. Notably, compounds 8a, 8h, and 8i demonstrated excellent safety profiles when tested on normal cells. Molecular docking, dynamic studies, and free energy calculations were employed to validate the affinity of these compounds as VEGFR2 inhibitors.

Membrane‐lytic peptides offer broad synthetic flexibilities and design potential to the arsenal of anticancer therapeutics, which can be limited by cytotoxicity to noncancerous cells and induction of drug resistance via stress‐induced mutagenesis. Despite continued research efforts on membrane‐perforating peptides for antimicrobial applications, success in anticancer peptide therapeutics remains elusive given the muted distinction between cancerous and normal cell membranes and the challenge of peptide degradation and neutralization upon intravenous delivery. Using triple‐negative breast cancer as a model, the authors report the development of a new class of anticancer peptides. Through function‐conserving mutations, the authors achieved cancer cell selective membrane perforation, with leads exhibiting a 200‐fold selectivity over non‐cancerogenic cells and superior cytotoxicity over doxorubicin against breast cancer tumorspheres. Upon continuous exposure to the anticancer peptides at growth‐arresting concentrations, cancer cells do not exhibit resistance phenotype, frequently observed under chemotherapeutic treatment. The authors further demonstrate efficient encapsulation of the anticancer peptides in 20 nm polymeric nanocarriers, which possess high tolerability and lead to effective tumor growth inhibition in a mouse model of MDA‐MB‐231 triple‐negative breast cancer. This work demonstrates a multidisciplinary approach for enabling translationally relevant membrane‐lytic peptides in oncology, opening up a vast chemical repertoire to the arms race against cancer. Schematic diagram of integrated design of peptide‐based nanomedicine in cancer treatment. The process of nanomedicine development involves peptide drug design, evaluation against both 2D and 3D cell cultures, and nanomedicine formulation for animal study.

Purpose We analyzed the prevalence and severity of potential drug-drug interactions (PDDIs) in Korean patients receiving oral anticancer agents (OAAs) during two different periods. Methods A cross-sectional study was conducted using the national insurance reimbursement database. The subjects were adult outpatients diagnosed with cancer and prescribed OAAs at least once in 2010 or 2014. PDDIs were identified using a database and the PDDI severity was categorized as category X (contraindications) or D (consideration of therapy modification). The associated factors for the occurrence of PDDIs were also analyzed. Results Among the 118,258 patients prescribed OAAs in 2014, approximately 59% were middle-aged, and approximately half were diagnosed with breast cancer. The number of comorbidities increased over time, and majority were diagnosed with gastrointestinal disorders, hyperlipidemia, and psychonervous disorders. The PDDIs due to protein kinase inhibitors (PKIs) with gastrointestinal/metabolic and neurological drugs increased 3.1- and 4.9-fold, respectively, over the 5 years, and 24.0% of the PDDIs fell into category X. Tamoxifen, the most commonly prescribed OAAs, caused the PDDIs with antidepressants through QTc prolongation or pharmacokinetic interaction. The PKIs prescription, cancer type like breast or hematologic cancer, and number of comorbidities or co-prescribing drugs were independently associated with the occurrence of PDDIs. Conclusions The risk of PDDIs in patients receiving OAAs increases, particularly with the concomitant use of PKIs with gastrointestinal or psychiatric drugs and endocrine agents with antidepressants. Considering the potential risk of chronic concomitant use of these drug classes in outpatients, healthcare professionals should be made aware of the potential interactions.

Platinum-based anticancer drugs, including cisplatin and carboplatin, have been cornerstones in the treatment of solid tumors. We report here that these DNA-damaging agents, particularly cisplatin, induce apoptosis through plasma membrane disruption, triggering FAS death receptor via mitochondrial ( intrinsic ) pathways. Our objectives were to: quantify the composition of membrane metabolites; and determine the potential involvement of acid sphingomyelinase (ASMase) in the FAS-mediated apoptosis in ovarian cancer after cisplatin treatment. The resulting analysis revealed enhanced apoptosis as measured by: increased phosphocholine, and glycerophosphocholine; elevated cellular energetics; and phosphocreatine and nucleoside triphosphate concentrations. The plasma membrane alterations were accompanied by increased ASMase activity, leading to the upregulation of FAS , FASL and related pro-apoptotic BAX and PUMA genes. Moreover FAS, FASL, BAX, PUMA, CASPASE-3 and -9 proteins were upregulated. Our findings implicate ASMase activity and the intrinsic pathways in cisplatin-mediated membrane demise, and contribute to our understanding of the mechanisms by which ovarian tumors may become resistant to cisplatin.

DNA is believed to be the molecular target for the cytotoxic activities of platinum (Pt) anticancer drugs. We report here a class of platinum(II)- and platinum(IV)-pyrophosphato complexes that exhibit cytotoxicity comparable with and, in some cases, better than cisplatin in ovarian cell lines (A2780, A2780/C30, and CHO), yet they do not show any evidence of covalent binding to DNA. Moreover, some of these compounds are quite effective in cisplatin- and carboplatin-resistant cell line A2780/C30. The lack of DNA binding was demonstrated by the absence of a detectable Pt signal by atomic absorption spectroscopy using isolated DNA from human ovarian cells treated with a platinum(II)-pyrophosphato complex, (trans-1,2-cyclohexanediamine)(dihydrogen pyrophosphato) platinum(II), (pyrodach-2) and from NMR experiments using a variety of nucleotides including single- and double-stranded DNA. Furthermore, pyrodach-2 exhibited reduced cellular accumulations compared with cisplatin in cisplatin- and carboplatin-resistant human ovarian cells, yet the IC₅₀ value for the pyrophosphato complex was much less than that of cisplatin. Moreover, unlike cisplatin, pyrodach-2 treated cells overexpressed fas and fas-related transcription factors and some proapoptotic genes such as Bak and Bax. Data presented in this report collectively indicate that pyrodach-2 follows different cytotoxic mechanisms than does cisplatin. Unlike cisplatin, pyrodach-2 does not undergo aquation during 1 week and is quite soluble and stable in aqueous solutions. Results presented in this article represent a clear paradigm shift not only in expanding the molecular targets for Pt anticancer drugs but also in strategic development for more effective anticancer drugs.

DPP8/9 inhibition induces either pyroptotic or apoptotic cell death in hematological malignancies. We previously reported that treatment with the DPP8/9 inhibitor 1G244 resulted in apoptotic cell death in myeloma, and our current study further evaluates the mechanism of action of 1G244 in different blood cancer cell lines. Specifically, 1G244 inhibited DPP9 to induce GSDMD-mediated-pyroptosis at low concentrations and inhibited DPP8 to cause caspase-3-mediated-apoptosis at high concentrations. HCK expression is necessary to induce susceptibility to pyroptosis but does not participate in the induction of apoptosis. To further characterize this DPP8-dependent broad-spectrum apoptosis induction effect, we evaluated the potential antineoplastic role for an analog of 1G244 with higher DPP8 selectivity, tominostat (also known as 12 m). In vitro studies demonstrated that the cytotoxic effect of 1G244 at high concentrations was enhanced in tominostat. Meanwhile, in vivo work showed tominostat exhibited antitumor activity that was more effective on a cell line sensitive to 1G244, and at higher doses, it was also effective on a cell line resistant to 1G244. Importantly, the weight loss morbidity associated with increasing doses of 1G244 was not observed with tominostat. These results suggest the possible development of novel drugs with antineoplastic activity against selected hematological malignancies by refining and increasing the DPP8 selectivity of tominostat.

Chitin is the second most abundant biopolymer consisting of N-acetylglucosamine units and is primarily derived from the shells of marine crustaceans and the cell walls of organisms (such as bacteria, fungi, and algae). Being a biopolymer, its materialistic properties, such as biodegradability, and biocompatibility, make it a suitable choice for biomedical applications. Similarly, its deacetylated derivative, chitosan, exhibits similar biocompatibility and biodegradability properties, making it a suitable support material for biomedical applications. Furthermore, it has intrinsic material properties such as antioxidant, antibacterial, and antitumor. Population studies have projected nearly 12 million cancer patients across the globe, where most will be suffering from solid tumors. One of the shortcomings of potent anticancer drugs is finding a suitable cellular delivery material or system. Therefore, identifying new drug carriers to achieve effective anticancer therapy is becoming essential. This paper focuses on the strategies implemented using chitin and chitosan biopolymers in drug delivery for cancer treatment.

Nanotechnology has been actively integrated as drug carriers over the last few years to treat various cancers. The main hurdle in the clinical management of cancer is the development of multidrug resistance against chemotherapeutic agents. To overcome the limitations of chemotherapy, the researchers have been developing technological advances for significant progress in the oncotherapy by enabling the delivery of chemotherapeutic agents at increased drug content levels to the targeted spots. Several nano-drug delivery systems designed for tumor-targeting are evaluated in preclinical and clinical trials and showed promising outcomes in cancerous tumors' clinical management. This review describes nanocarrier's importance in managing different types of cancers and emphasizing nanocarriers for drug delivery and cancer nanotherapeutics. It also highlights the recent advances in nanocarriers-based delivery systems, including polymeric nanocarriers, micelles, nanotubes, dendrimers, magnetic nanoparticles, solid lipid nanoparticles, and quantum dots (QDs). The nanocarrier-based composites are discussed in terms of their structure, characteristics, and therapeutic applications in oncology. To conclude, the challenges and future exploration opportunities of nanocarriers in chemotherapeutics are also presented.