Simon Ngigi Mbugua

The structural versatility, excellent sensitivity and bio-compatibility of organic fluorophores and responsive luminescent materials have made them essential detection and bio-imaging tools in the recent past.

Photoactivation is the stimulation or regulation of a chemical or a chemical process by utilizing light of specific wavelength that corresponds to an absorbance optimum of the agent being used and can penetrate into tissues. In cancer therapy, photoactivatable drugs utilize this phenomenon by allowing the temporal and spatial regulation of their cytotoxicity using irradiation. Therefore, in order to reduce the adverse effects of platinum medications, photoactivatable anticancer pharmaceuticals, which might be site‐activated in the tumour region, are a viable option. This paper summarizes different types of photoactivatable anticancer compounds that would produce an active version of a drug by the process of photouncaging. The mode of photoactivation and rationale for drug design are summarized. The effects of typical complexes on cellular pathways, photocytotoxicity and dark cytotoxicity are explored. When compared to traditional Pt(II) anticancer medications, photoactivatable anticancer compounds provide a number of benefits, including ability to overcome drug resistance, and in situ monitoring of drug accumulation and activation inside cells. This review also covers the design approaches, synthesis techniques, photoresponsiveness and antitumour effectiveness of various photochemotherapeutic compounds. Future developments and challenges in incorporating photoresponsive metal complexes are also covered. This detailed review aims at encouraging further thorough investigation into this intriguing area of study by offering a summary of current developments in the design and development of photoresponsive compounds for cancer treatment and future clinical prospects.

Correction for ‘Addressing the gaps in homeostatic mechanisms of copper and copper dithiocarbamate complexes in cancer therapy: a shift from classical platinum-drug mechanisms’ by Lydia W. Njenga et al., Dalton Trans., 2023, 52, 5823–5847, https://doi.org/10.1039/D3DT00366C.

This review will focus on copper homeostasis in mammalian cells and on our current understanding of copper dysregulation in cancer and recent therapeutic breakthroughs using copper coordination complexes as anticancer drugs.

Solid tumors have a unique tumor microenvironment (TME), which includes hypoxia, low acidity, and high hydrogen peroxide and glutathione (GSH) levels, among others. These unique factors, which offer favourable microenvironments and nourishment for tumor development and spread, also serve as a gateway for specific and successful cancer therapies. A good example is metal peroxide structures which have been synthesized and utilized to enhance oxygen supply and they have shown great promise in the alleviation of hypoxia. In a hypoxic environment, certain oxygen‐dependent treatments such as photodynamic therapy and radiotherapy fail to respond and therefore modulating the hypoxic tumor microenvironment has been found to enhance the antitumor impact of certain drugs. Under acidic environments, the hydrogen peroxide produced by the reaction of metal peroxides with water not only induces oxidative stress but also produces additional oxygen. This is achieved since hydrogen peroxide acts as a reactive substrate for molecules such as catalyse enzymes, alleviating tumor hypoxia observed in the tumor microenvironment. Metal ions released in the process can also offer distinct bioactivity in their own right. Metal peroxides used in anticancer therapy are a rapidly evolving field, and there is good evidence that they are a good option for regulating the tumor microenvironment in cancer therapy. In this regard, the synthesis and mechanisms behind the successful application of metal peroxides to specifically target the tumor microenvironment are highlighted in this review. Various characteristics of TME such as angiogenesis, inflammation, hypoxia, acidity levels, and metal ion homeostasis are addressed in this regard, together with certain forms of synergistic combination treatments.

The COVID-19 global epidemic poses this generations biggest worldwide public health challenge probably since the 1918 influenza epidemic. Recent reports on two new variants have triggered a dramatic upsurge in research to understand the pandemic, primarily focussing on the virology, triggers, clinical characteristics, and diagnostic tests including the prevention and management of the novel coronavirus. Whilst such studies are important in managing the present medical emergency, there is a need for further work to include interdependencies between the epidemic and other illnesses. This will help in developing effective approaches to treat and manage associated diseases in both the short and the long term. In this regard, people living with cancer are a subgroup that is highly vulnerable to respiratory infections and acute pneumonitis similar to the one caused by the COVID-19 virus. This is because the state of their immunity is compromised due to malignancy and the adverse effects of anticancer treatments. With annual cancer projections rising globally and an estimated 70 percent of all cancer-related deaths occurring in low- and middle-income countries, the patient population with impaired immune systems that could be adversely impacted by COVID-19 is only anticipated to rise. In this review, we delve into the challenges and health risks facing cancer patients and cancer treatment in the COVID-19 context, with suggestions into viable measures which can be taken to minimize exposure to the risk of contracting COVID-19 for this vulnerable subgroup. New mutations and the prospects offered by vaccines development and how they relate to this class of patients are also discussed.

In a bid to come up with potential anticancer agents, a class of thiosemicarbazone ligands bearing substituted thiophene were synthesized followed by complexation with various Pd(II) and Pt(II) metal precursors. The ligands (E)-1-((thiophen-2-yl)methylene)thiosemicarbazide (L1), (E)-1-((4-bromothiophen-2-yl)methylene)thiosemicarbazide (L2), and (E)-1-((5-bromothiophen-2-yl)methylene)thiosemicarbazide (L3) were synthesized by condensation reactions and obtained in good yields. Complexation of L1 and L2 with Pd(cod)Cl₂ gave C1 (C₆H₇Cl₂N₃PdS₂) and C2 (C₆H₆BrCl₂N₃PdS₂), respectively. Complexation of L1 with K₂PtCl₄ gave C3 (C₆H₇Cl₂N₃PtS₂), while L3 with K₂PtCl₂[(PPh)₃]₂ gave C4 (C₂₄H₂₁BrClN₃PPtS₂). The structures and coordination for all compounds were established by FTIR, ¹H-NMR, ¹³C-NMR, UV-Vis, elemental analysis, and single-crystal X-ray diffraction studies for ligand L1. Tuning of the spectral and anticancer activity of the compounds was investigated by changing the position of the bromide substituent, metal center, and the σ or π-donor/acceptor strength of the groups surrounding the metal center. The compounds had low to moderate anticancer potency with their spectral and structural properties correlating with the corresponding anticancer activity profiles. DNA binding modes were studied by spectroscopy and were comparable to known DNA intercalators. Structure-activity profiles were evident especially between C1 and C2 differing by the presence of a Br in position 5 of thiophene ring, which caused a remarkable increase in IC₅₀ values, from 14.71 ± 0.016 (C1) to 43.08 ± 0.001(C2) in Caco-2 cells, 1.973 ± 0.048 (C1) to 59.56 ± 0.010 (C2) in MCF-7 cells, 16.65 ± 0.051 (C1) to 72.25 ± 0.003 (C2) in HeLa cells, 14.64 ± 0.037 (C1) to 94.34 ± 0.003 (C2) in HepG2, and 14.05 ± 0.042 (C1) to >100(C2) in PC-3 cells.