Kamoru ADEDOKUN

Kamoru ADEDOKUN

Immunology, Roswell Park Cancer Institute, Buffalo, Minnesota, USA
orcid

Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 July 2020 in Journal of Infection and Public Health
Verified
Journal Article
Open access
RKRamat Toyin Kamorudeen
Ramat Toyin Kamorudeen
Kamoru ADEDOKUNKamoru ADEDOKUN
Kamoru ADEDOKUN
Ayodeji OlarinmoyeAyodeji Olarinmoye
Ayodeji Olarinmoye
The outbreak of Ebola virus disease (EVD) that raged between 2014 and 2016 in the West African sub-region was one of the global epidemics that spiked international public health concern in the last decade. Since the discovery of ebolavirus in 1976, the 2014-2016 epidemics have been the worst with significant case fatality rates and socioeconomic impact in the affected countries. This review looks at important health determinants that directly accounted for the spatial events of rapid spread and severity of EVD in West Africa, with consequent high fatality rates. It also brings up a time-point health determinant model to conceptualize understanding of this important outbreak with a view to enlightening the public andproviding valuable recommendations that may be crucial to preventing or curtailing any future outbreak of the disease.

18 November 2021 in Frontiers in Oncology
Verified
Journal Article
Open access
SISikiru O. Imodoye
Sikiru O. Imodoye
Kamoru ADEDOKUNKamoru ADEDOKUN
Kamoru ADEDOKUN
AMAbdurrasheed Ola Muhammed
Abdurrasheed Ola Muhammed
IBIbrahim O. Bello
Ibrahim O. Bello
MMMusa A. Muhibi
Musa A. Muhibi
MOMusiliu A. Oyenike
Musiliu A. Oyenike
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.


7 May 2025 in Journal of Rare Diseases
Verified
Journal Article
Open access
PDF file
Kamoru ADEDOKUNKamoru ADEDOKUN
Kamoru ADEDOKUN
SASaheed A. Adekola
Saheed A. Adekola
ATAdebisi Tajudeen
Adebisi Tajudeen
ABAbdulraheem A. Bello-Ibiyemi
Abdulraheem A. Bello-Ibiyemi
MBMusa Muhammad Babandina
Musa Muhammad Babandina
ABAminah Bello
Aminah Bello
Human metapneumovirus (hMPV), a prominent respiratory pathogen with a history of global circulation spanning over seven decades, has re-emerged as a critical public health concern. Since late 2024, there has been a significant global surge in hMPV cases, first reported in China and subsequently spreading to countries such as the USA, India, and Pakistan. Although the World Health Organization (WHO) and Chinese authorities have downplayed the severity of this increase, attributing it to expected seasonal trends, the growing prevalence of hMPV raises alarm due to its potential to cause severe respiratory illness. Particularly at risk are vulnerable populations, including children, the elderly, and immunocompromised individuals. Recent epidemiological data indicate a 17% increase in pediatric hMPV-related hospital admissions in the first quarter of 2025 compared to the same period in 2023 in both the USA and China, with similar trends observed among elderly and immunocompromised patients. These findings highlight the urgent need for enhanced surveillance and public health preparedness. This study explores the immunopathogenesis of hMPV, which is marked by its immune evasion strategies, including inhibition of interferon signaling pathways and suppression of key antiviral cytokines. These mechanisms enable persistent viral replication and contribute to severe respiratory pathologies. Moreover, dysregulated cytokine production, particularly the overexpression of pro-inflammatory cytokines, exacerbates immune responses and leads to tissue damage, further worsening clinical outcomes in vulnerable populations. This review delves into the complex immune dynamics of hMPV infection, highlighting impaired dendritic cell activation and suboptimal T-cell responses, which hinder long-lasting immunity, especially in immunocompromised individuals. The virus's high mutation rate (6.95 to 7.12 × 10−4 substitutions/site/year), along with its immune evasion mechanisms and significant cytopathic effects, further enhances its pathogenicity. The global spread of hMPV underscores its resilience and adaptability, making it a growing threat to public health. As hMPV-related immunology becomes increasingly relevant amid this new outbreak, this review emphasizes the need for robust genomic surveillance, targeted antiviral therapies, and vaccine development. Drawing on lessons from COVID-19 and Ebola, the importance of early detection systems, antiviral research, and targeted immunization strategies is paramount to mitigating the impact of this emerging viral threat. With insights from the current study, future immunological approaches should prioritize the development of novel vaccine candidates, enhancement of monoclonal antibody therapies, and improvement of host-directed immunomodulatory treatments. By integrating these strategies, global health systems can effectively respond to future hMPV outbreaks and safeguard vulnerable populations.

26 June 2020 in Infectious Diseases of Poverty
Verified
Journal Article
Open access
PDF file
Kamoru ADEDOKUNKamoru ADEDOKUN
Kamoru ADEDOKUN
Ayodeji OlarinmoyeAyodeji Olarinmoye
Ayodeji Olarinmoye
JMJelili O. Mustapha
Jelili O. Mustapha
RKRamat T. Kamorudeen
Ramat T. Kamorudeen
Background: There is sufficient epidemiological and biological evidence of increased human susceptibility to viral pathogens such as Middle East respiratory syndrome coronavirus, respiratory syncytial virus, human metapneumovirus and influenza virus, in cold weather. The pattern of outbreak of the coronavirus disease 2019 (COVID-19) in China during the flu season is further proof that meteorological conditions may potentially influence the susceptibility of human populations to coronaviruses, a situation that may become increasingly evident as the current global pandemic of COVID-19 unfolds. Main body: A very rapid spread and high mortality rates have characterized the COVID-19 pandemic in countries north of the equator where air temperatures have been seasonally low. It is unclear if the currently high rates of COVID-19 infections in countries of the northern hemisphere will wane during the summer months, or if fewer people overall will become infected with COVID-19 in countries south of the equator where warmer weather conditions prevail through most of the year. However, apart from the influence of seasons, evidence based on the structural biology and biochemical properties of many enveloped viruses similar to the novel severe acute respiratory syndrome coronavirus 2 or SARS-CoV-2 (aetiology of COVID-19), support the higher likelihood of the latter of the two outcomes. Other factors that may potentially impact the rate of virus spread include the effectiveness of infection control practices, individual and herd immunity, and emergency preparedness levels of countries. Conclusion: This report highlights the potential influence of weather conditions, seasons and non-climatological factors on the geographical spread of cases of COVID-19 across the globe.

1 January 2020 in Asian Pacific Journal of Tropical Medicine
Verified
Journal Article
Closed access
PDF file
JMJelili Olaide Mustapha
Jelili Olaide Mustapha
Kamoru ADEDOKUNKamoru ADEDOKUN
Kamoru ADEDOKUN
INIdris Abdullahi Nasir
Idris Abdullahi Nasir
Asian Pacific Journal of Tropical Medicine, Editorial office of Hainan Medical University