Cytology in COVID-19 and Laryngopharyngeal Reflux Disease| Book Publisher International

 

Introduction: SARS-CoV-2 infection and laryngopharyngeal reflux (LPR) both expose the upper aerodigestive tract to injurious biological agents—viral particles and gastric refluxate, respectively. These exposures can trigger mucosal inflammation, oxidative stress, and genotoxic changes detectable through cytological and immunohistochemical evaluation.

 

Aim: This study aimed to assess genotoxicity and oxidative DNA damage in exfoliated mucosal cells of individuals with suspected COVID-19 and patients with LPR, and to evaluate epithelial–mesenchymal transition (EMT)–related markers to understand early mucosal remodelling.

 

Settings and Design: A cross-sectional study conducted at AIIMS, Mangalagiri, between August 2022 and February 2024.

 

Methods: Exfoliated buccal or pharyngeal mucosal samples were collected from 86 COVID-19-suspected individuals (18–45 years) undergoing RT-PCR testing and from clinically diagnosed LPR patients with healthy controls. Smears were stained using the Papanicolaou technique for cytological analysis, and immunohistochemistry was performed to evaluate oxidative DNA damage (8-OHdG) and EMT markers (E-cadherin, N-cadherin). Micronucleated cells, inflammatory infiltrates, and oxidative marker expression were quantified. Statistical analysis was done using independent t-tests and ANOVA, with significance set at p < 0.05.

 

Results: COVID-19 RT-PCR–positive subjects showed significantly elevated micronucleated cells, total micronuclei, and inflammatory cell counts compared to RT-PCR–negative individuals, along with intense 8-OHdG expression indicating marked oxidative DNA damage. LPR patients similarly demonstrated increased oxidative stress with strong 8-OHdG staining and higher micronucleated cell frequencies than healthy controls. While E-cadherin expression remained largely preserved, N-cadherin showed moderate upregulation in LPR patients, suggesting an early EMT-related cadherin shift. Both conditions exhibited a reduced epithelial-to-inflammatory cell ratio, reflecting ongoing mucosal injury and remodelling.

 

Conclusion: Both SARS-CoV-2 infection and chronic laryngopharyngeal reflux exert measurable genotoxic and oxidative effects on mucosal epithelial cells. The increased micronuclei formation, heightened 8-OHdG expression, and early EMT-associated changes indicate genomic instability and mucosal remodelling driven by persistent inflammation and oxidative stress. These findings underscore the importance of early detection and targeted interventions to prevent progression toward long-term mucosal damage and potential malignant transformation.

Author(s) Details

Yogita Poojari
All India Institute of Medical Sciences, Mangalagiri, India.

 

Ambati Gowtham Sai
All India Institute of Medical Sciences, Mangalagiri, India.

 

B Vishnu
All India Institute of Medical Sciences, Mangalagiri, India.

 

Pranav Donkada
All India Institute of Medical Sciences, Mangalagiri, India.

 

Hemanth Bonamsetty
All India Institute of Medical Sciences, Mangalagiri, India.

 

Senthil Murugan
Department of Antomy, All India Institute of Medical Sciences, Mangalagiri, India.

 

P K Sankaran
Department of Antomy, All India Institute of Medical Sciences, Mangalagiri, India.

 

Please see the book here :- https://doi.org/10.9734/bpi/mono/978-93-47485-50-3

Cell Cycle Regulators in Cancer: A Review | Chapter 11 | Achievements and Challenges of Medicine and Medical Science Vol. 4

A recent in-depth view of cell cycle regulation and cancer has provided novel samples of research at the “Frontiers of Science.” However, the number of foremost revealing information about both topics has been derived from the intersection of these two fields. Genomic integrity is required to maintain long life and prevent diseases associated with genomic instability such as “cancer.” The cell cycle is a compilation of well-organized, sequential molecular events, that lead to succession of DNA replication and segregation of replicated chromosomes. Checkpoint is an important control point present in the cell cycle where stop and start signals can regulate the cell cycle. Cell cycle checkpoints are the strict regulatory mechanisms that monitor the order, integrity, and fidelity of the main events of the cell cycle. These include growth up to the acceptable cell size, replication, and integrity of the chromosomes, and their accurate segregation in due course of mitosis. Many of these mechanisms are highly conserved, while other studies on higher organisms have shown to control alternative cell fates with a significant impact on tumor suppression. Here, these different checkpoint pathways in a cell cycle and the consequences of their dysfunction on the fate of a cell has been taken into consideration. Undoubtedly, the hidden aspects of checkpoint signaling can be further explored with the help of an ever-growing arsenal of highly sophisticated experimental tools and techniques, which will enable us to get a more clear and complete picture of the remarkable fidelity of the cell cycle.

 

Author (s) Details

Swarup K Panda
Department of Biochemistry, IMS & SUM Hospital III, Sitalapalli, Ganjam, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Subhashree Ray
Department of Biochemistry, IMS & SUM Hospital, K8, Kalinga Nagar, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Sarthak R Nayak
Department of Biochemistry, IMS and SUM Hospital II, Phulnakhara, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Sudeshna Behera
Department of Biochemistry, IMS & SUM Hospital, K8, Kalinga Nagar, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Sangeeta S Bhanja
Department of Biochemistry, IMS & SUM Hospital, K8, Kalinga Nagar, Siksha ‘O’ Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India.

 

Viyatprajna Acharya
Department of Biochemistry, KIMS, KIIT (Deemed to be University), Bhubaneswar, Odisha, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v4/3165 

Genetic Disorder Fanconi Anemia: A Model for Understand the Genomic Instability and Cancer Development | Chapter 18 | Socio-Scientific Interaction in Diabetes and Cancer and Its Management

 “Genomic instability” is the hall mark of cancer. It has long been a debate whether the genomic instability is the causes of cancer or consequence of cancer. Significant amount of work has generated in the area of cell cycle and DNA damage repair for understanding the genomic instability, but how genomic instability transforms the normal cell into cancer cell is not well known. Studying rare human genetic diseases often leads to a better understanding of normal cellular functions. Fanconi anemia rare model disease cause genomic instability and cancer susceptibility syndrome. Fanconi kids are born normal except some kinds of congenital defects like bone marrow failure and other developmental defects, but when they are getting older (teen age) they become susceptible to all kinds of cancer.

Author(s) Details:

Ram Balak Mahto,
Department of Zoology, VSJ College Rajnagar, Madhubani (Bihar), India.

Please see the link here: https://stm.bookpi.org/SSIDCIM/article/view/12736