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Toxic substances have a deleterious effect on biological systems if accrued in ecosystems beyond their acceptable limit. A natural ecosystem can become contaminated due to the excessive release of toxic substances by various anthropogenic and natural activities, which necessitates rehabilitation of the environmental contamination. Phytoremediation is an eco-friendly and cost-efficient method of biotechnological mitigation for the remediation of polluted ecosystems and revegetation of contaminated sites. The information provided in this review was collected by utilizing various sources of research information, such as ResearchGate, Google Scholar, the Scopus database and other relevant resources. In this review paper, we discuss (i) various organic and inorganic contaminants; (ii) sources of contamination and their adverse effects on terrestrial and aquatic life; (iii) approaches to the phytoremediation process, including phytoextraction, rhizoremediation, phytostabilization, phytovolatilization, rhizofiltration, phytodegradation, phytodesalination and phytohydraulics, and their underlying mechanisms; (iv) the functions of various microbes and plant enzymes in the biodegradation process and their potential applications; and (v) advantages and limitations of the phytoremediation technique. The reported research aimed to adequately appraise the efficacy of the phytoremediation treatment and facilitate a thorough understanding of specific contaminants and their underlying biodegradation pathways. Detailed procedures and information regarding characteristics of ideal plants, sources of heavy metal contamination, rhizodegradation techniques, suitable species and removal of these contaminants are put forward for further application. Scientists, planners and policymakers should focus on evaluating possible risk-free alternative techniques to restore polluted soil, air and water bodies by involving local inhabitants and concerned stakeholders. [ABSTRACT FROM AUTHOR]

Simple Summary: Around 15% of papillary thyroid carcinoma (PTC) patients are not cured using standard surgery followed by radioactive iodine (RAI) therapy, and instead develop refractory disease. The aim of this study was to help identify RAI-refractory PTC patients early and guide precision medicine by performing a clinical and genomic characterization of RAI-refractory and avid PTCs. RAI-refractory PTCs had a more aggressive clinical presentation, a higher number of mutations, harbored more TERT promoter (TERTp) mutations, and were enriched with APOBEC-related mutations. Notably, the APOBEC single-base substitution (SBS) mutational signature, SBS13, and TERTp mutations were revealed to be independent predictors of RAI refractoriness in PTC. Although SBS13 and TERTp mutations alone highly predicted RAI refractoriness, when combined, they formed a stronger predictor of RAI refractoriness in PTC. This study highlights the APOBEC SBS13 mutational signature as a novel independent predictor of RAI refractoriness in a distinct subgroup of PTC. Standard surgery followed by radioactive iodine (131I, RAI) therapy are not curative for 5–20% of papillary thyroid carcinoma (PTC) patients with RAI refractory disease. Early predictors indicating therapeutic response to RAI therapy in PTC are yet to be elucidated. Whole-exome sequencing was performed (at median depth 198x) on 66 RAI-refractory and 92 RAI-avid PTCs with patient-matched germline. RAI-refractory tumors were significantly associated with distinct aggressive clinicopathological features, including positive surgical margins (p = 0.016) and the presence of lymph node metastases at primary diagnosis (p = 0.012); higher nonsilent tumor mutation burden (p = 0.011); TERT promoter (TERTp) mutation (p < 0.0001); and the enrichment of the APOBEC-related single-base substitution (SBS) COSMIC mutational signatures 2 (p = 0.030) and 13 (p < 0.001). Notably, SBS13 (odds ratio [OR] 30.4, 95% confidence intervals [CI] 1.43–647.22) and TERTp mutation (OR 41.3, 95% CI 4.35–391.60) were revealed to be independent predictors of RAI refractoriness in PTC (p = 0.029 and 0.001, respectively). Although SBS13 and TERTp mutations alone highly predicted RAI refractoriness, when combined, they significantly increased the likelihood of predicting RAI refractoriness in PTC. This study highlights the APOBEC SBS13 mutational signature as a novel independent predictor of RAI refractoriness in a distinct subgroup of PTC. [ABSTRACT FROM AUTHOR]

Head and neck squamous cell carcinomas (HNSCCs) are aggressive diseases with a dismal patient prognosis. Despite significant advances in treatment modalities, the five-year survival rate in patients with HNSCC has improved marginally and therefore warrants a comprehensive understanding of the HNSCC biology. Alterations in the cellular and non-cellular components of the HNSCC tumor micro-environment (TME) play a critical role in regulating many hallmarks of cancer development including evasion of apoptosis, activation of invasion, metastasis, angiogenesis, response to therapy, immune escape mechanisms, deregulation of energetics, and therefore the development of an overall aggressive HNSCC phenotype. Cytokines and chemokines are small secretory proteins produced by neoplastic or stromal cells, controlling complex and dynamic cell–cell interactions in the TME to regulate many cancer hallmarks. This review summarizes the current understanding of the complex cytokine/chemokine networks in the HNSCC TME, their role in activating diverse signaling pathways and promoting tumor progression, metastasis, and therapeutic resistance development. [ABSTRACT FROM AUTHOR]

Simple Summary: Half of all colorectal cancer (CRC) patients develop metastasis, despite current management. The aim of this study was to help guide precision medicine in metastatic CRC patients, by performing genomic characterisation of primary CRC and metastatic tumours, and revealing the effects of therapy on the metastatic process. We confirmed common ancestry between paired primary CRC and metastatic tumours, with most metastases seemingly having disseminated late (after acquiring most genomic diversity) from their corresponding primary tumour, via either a single clone (monoclonal spread) or multiple clones (polyclonal spread). Treatment prompted the selection for distinct resistant clones, through monoclonal seeding to distant metastatic sites. Overall, this study supports the importance of early clinical detection and surgical removal of the CRC tumour, whilst further highlighting the challenges for treating and managing metastatic CRC with increased intratumour heterogeneity (either due to early dissemination or metastatic spread through multiple clones) and the underlying risk of future therapeutic resistance in treated patients. Colorectal cancer (CRC) is the third most frequently diagnosed cancer worldwide, where ~50% of patients develop metastasis, despite current improved management. Genomic characterisation of metastatic CRC, and elucidating the effects of therapy on the metastatic process, are essential to help guide precision medicine. Multi-region whole-exome sequencing was performed on 191 sampled tumour regions of patient-matched therapy-naïve and treated CRC primary tumours (n = 92 tumour regions) and metastases (n = 99 tumour regions), in 30 patients. Somatic variants were analysed to define the origin, composition, and timing of seeding in the metastatic progression of therapy-naïve and treated metastatic CRC. High concordance, with few genomic differences, was observed between primary CRC and metastases. Most cases supported a late dissemination model, via either monoclonal or polyclonal seeding. Polyclonal seeding appeared more common in therapy-naïve metastases than in treated metastases. Whereby, treatment prompted for the selection of distinct resistant clones, through monoclonal seeding to distant metastatic sites. Overall, this study reinforces the importance of early clinical detection and surgical excision of the CRC tumour, whilst further highlighting the clinical challenges for metastatic CRC with increased intratumour heterogeneity (either due to early dissemination or polyclonal metastatic spread) and the underlying risk of future therapeutic resistance in treated patients. [ABSTRACT FROM AUTHOR]