Epithelial-mesenchymal transition (EMT) is a physiological program during which polarised, immobile epithelial cells lose connection with their neighbours and are converted to migratory mesenchymal phenotype. Mechanistically, EMT occurs via a series of genetic and cellular events leading to the repression of epithelial-associated markers and upregulation of mesenchymal-associated markers. EMT is very crucial for many biological processes such as embryogenesis and ontogenesis during human development, and again it plays a significant role in wound healing during a programmed replacement of the damaged tissues. However, this process is often hijacked in pathological conditions such as tumour metastasis, which constitutes the most significant drawback in the fight against cancer, accounting for about 90% of cancer-associated mortality globally. Worse still, metastatic tumours are not only challenging to treat with the available conventional radiotherapy and surgical interventions but also resistant to several cytotoxic agents during treatment, owing to their anatomically diffuse localisation in the body system. As the quest to find an effective method of addressing metastasis in cancer intervention heightens, understanding the molecular interplay involving the signalling pathways, downstream effectors, and their interactions with the EMT would be an important requisite while the challenges of metastasis continue to punctuate. Unfortunately, the molecular underpinnings that govern this process remain to be completely illuminated. However, it is becoming increasingly clear that EMT, which initiates every episode of metastasis, significantly requires some master regulators called EMT transcription factors (EMT-TFs). Thus, this review critically examines the roles of TFs as drivers of molecular rewiring that lead to tumour initiation, progression, EMT, metastasis, and colonisation. In addition, it discusses the interaction of various signalling molecules and effector proteins with these factors. It also provides insight into promising therapeutic targets that may inhibit the metastatic process to overcome the limitation of “undruggable” cancer targets in therapeutic design and upturn the current spate of drug resistance. More so, it extends the discussion from the basic understanding of the EMT binary switch model, and ultimately unveiling the E/M cellular plasticity along a phenotypic spectrum via multiple trans-differentiations. It wraps up on how this knowledge update shapes the diagnostic and clinical approaches that may demand a potential shift in investigative paradigm using novel technologies such as single-cell analyses to improve overall patient survival.

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Background: In low-and middle-income countries, high burden of cervical cancer is associated with human papillomavirus (HPV) due to poor screening and diagnostic methods at early stage. Reports showed that there are discrepancies in data correlating HPV-infection with development of cervical cancer while the functional roles of P53  oncogenic mutation are controversial. Furthermore, the molecular pathogenesis of multiple HPV-genotypes remains an open question. Thus, advancing investigations on HPV-associated cervical abnormalities would add to early diagnostic precision. Methods: Two hundred (n=200) cervical samples were collected from apparently healthy, active adult women following an ethical approval. Laboratory analyses were conducted through cytological assessment and histochemistry screening using the Papanicolaou smear. PCR methods were used to characterize HPV-DNA genotypes and P53  gene mutations. Positive cervical dysplasia cases were matched with HPV-DNA, and the HPV-genotypes were used to evaluate the prevalence of various HPV-subtypes and the risk of cervical cancer. Results:  Twenty-four (n=24) cervical dysplasia and fifty-one (n=51) HPV+ were identified comprising single and multiple genotypes. While nine cases (n=9) showed p53  gene mutation with concurrent multiple high-risk HPV (hrHPV) genotypes, none of the single hrHPV genotypes had p53  mutation. More so, individuals with coexisting p53  mutation and multiple hrHPV-genotypes already manifesting cervical dysplasia were 22.2% of the group, while 77.8% had normal cervical architecture, the fate of whom was unknown during investigation. There was a higher cervical dysplasia among those with HPV oncogenes; there were connections between the HPV positivity with some genotypes (hrHPV16,18,31 and 33, respectively) and p53 mutation. Conclusion: P53 gene mutation was independent of HPV-associated cervical abnormalities in single hrHPV-genotype, though other mechanistic drivers attributed to p53 dysfunction by E6 and E7 remain plausible. On the other hand, infection with multiple hrHPVs showed a concomitant predominance with the P53  mutation, implying a potential interplay and an increased risk of cervical cancer.

Background:Pneumocystis jirovecii, formerly known as P. carinii, is an opportunistic fungus causing Pneumocystis carinii pneumonia especially in immunocompromised patients.Aim:The aim of this study was to detect P. jirovecii in sputum samples from patients suspected of having respiratory tract infections.Materials and Methods:In this study, 230 acid fast bacilli negative sputum samples from 230 patients presenting with respiratory tract infections submitted to three teaching hospitals’ medical microbiology laboratories in Osun and Oyo States, Nigeria for routine investigation were examined for P. jirovecii by microscopical and polymerase chain reaction methods.Results:P. jirovecii cysts were observed in 15 (6.5%) samples and polymerase chain reaction was positive for 29 (12.6%) samples out of 230 samples examined. It was observed that the detection of P. jirovecii was associated with age (P < 0.05) while there were no associations between diagnosis, sex, and prevalence of P. jirovecii (P > 0.05). Polymerase chain reaction was showed to be a better method for the detection of P. jirovecii based on the 51.7% sensitivity and 100% specificity of the microscopy.Conclusion:The study concluded that P. jirovecii is prevalent in patients with respiratory tract infections in hospitals from the southwestern part of Nigeria and should be included in diagnosis of these infections in this part of the world.