The Impact of Climate Change on Waterborne Microbial Diversity and Dysbiosis in Carcinogenesis of Indian Sundarbans Fisherpersons: A Review | Chapter 9 | Research Advances in Environment, Geography and Earth Science Vol. 2

Fishing is one of the employment-generating as well as fastest growing sectors and has an important role in socio-economic development in India. Approximately 4 lakh fishermen directly, and 6 lakhs indirectly engage and depend on this industry in West Bengal. Indian Sunderbans lies in North & South 24 Parganas districts and has faced major cyclone shocks of Amphan, Bulbul, Yaas, and Fani within a span of the last 5 years and huge cultivable and livable areas went into the water. Recent reports reveal that these 2 districts have the highest cancer registry in West Bengal. Fishing involves physical hazards, chemical hazards, and biological hazards and it is of national interest to estimate post-climate change chemical and biological effects on affected fisherpersons.
 
Our project would look into pre and post-climate change data from primary health centers and identify affected areas and fisherpersons following questionnaires and health checkups. Reported occupational health hazards and precancerous lesions from the affected population will be further analyzed along with the quality of water-in-use or contact, and residing pathogenic or carcinogenic microbes whether correlated with dysbiosis, direct or zoonotic pathogenesis, etc. This will be the first of a kind of work connecting affected fisherpersons, the quality of their used waterbodies affected by climate change, the rising cancer scenario, and occupational health hazards in Indian Sundarbans. Climate anomalies (salinity, anoxic conditions, and temperature) in waterbodies favor pathogens to grow rapidly that affect fisherperson’s health through opportunistic invasion directly or through zoonotic transmission resulting in waterborne diseases.  Such waterborne infection is linked to increased gastric and gynecological cancer risk by dysbiosis of gut microbiota (producing toxins and metabolites). The goal of this review paper is to suggest a baseline regarding the alteration of climate that may induce factors of dysfunction that may prevalence of cancer (skin, uterine, gastric) in fishermen who are in direct contact with saline water.

Author(s) Details:

Sanjib Saha,
Vidyasagar College for Women (University of Calcutta), 39, Sankar Ghosh Lane, Kolkata – 700009, West Bengal, India.

Biswarup Basu,
Department of Neuroendocrinology & Experimental Haematology, Chittaranjan National Cancer Institute, (Ministry of Health and Family Welfare, Govt of India), 37, S. P. Mukherjee Road, Kolkata-700 026, India.

Please see the link here: https://stm.bookpi.org/RAEGES-V2/article/view/14357

Keywords: Climatic change, Sunderbans, fisherpersons, occupational health hazards, microbial dysbiosis, zoonotic transmission, carcinogenesis

The Role of Cadmium Induced EGFR/STAT5 Pathway Activation in Epithelial to Mesenchymal Transition | Chapter 4 | Current Innovations in Disease and Health Research Vol. 7

 Cadmium (Cd) is a poisonous and carcinogenic heavy metal about cigarette fume, air and drinking water, due to land and industrial endeavors, posing a health risk to the inexact population. Prolonged, depressed-dose Cd exposure by way of inhalation or ingestion induces alveolus and kidney cancers in two together humans and animal models. While exposure to extreme-dose Cd is cytotoxic and is equated with the occupational background, low-dose Cd uncovering is carcinogenic and mainly correlated with the inexact population. Even though Cd is classification as a group 1 “human carcinogen” by IARC, the means by which Cd-unprotected cells overcome calcium chelation and induce diseased transformation remains imprecise. This study examines the system by which cells unprotected to low doses of Cd live the loss of E-cadherin cell-cell grip and induce epithelial-to-mesenchymal change (EMT). Two epithelial cell lines, BEAS-2B and HEK293, were exposed to 0.4 µM and 1.6 µM of Cadmium chloride hemipentahydrate (CdCl2.2.5H2O) for 24 hours (h) and 9 weeks (wks). The preferred doses are environmentally relevant to levels of Cd found in bread and cigarettes. A dose-helpless decrease in E-cadherin and an increase in N-cadherin protein expression was observed in containers treated accompanying low-dose Cd. Moreover, Cd medicated cells exhibited a faster increase rate when compared accompanying control cells. This observation surpassed to the examination of the EGFR/STAT5 road activation, which has again been noticed to be activated in studies exhausted cancer cells. Our results accompanied a dose-weak and time-dependent increase in two together total EGFR and phosphorylated EGFR (p-EGFR) protein. Similar results were observed accompanying STAT5 and phosphorylated STAT5 (pSTAT5) protein in both short-term and complete exposures, nevertheless the 0.4 µM dose had the highest verbalization at 24 h. EGFR/STAT5 inducible genes were also upregulated in Cd-medicated cells in just 24 h. These dossier demonstrate that epithelial cells can overcome Cd-intervened toxicity by activating the EGFR/STAT5 road to induce cell continuation and proliferation, chief to EMT.

Author(s) Details:

Aikaterini Stavrou,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Angelica Ortiz,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Max Costa,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Please see the link here: https://stm.bookpi.org/CIDHR-V7/article/view/12042

Oral Microbiota: As a Cause of Head and Neck Cancers | Chapter 9 | Perspective of Recent Advances in Medical Research Vol. 11

 Head and narrow connector squamous cell cancers are a meaningful source of cancer-accompanying morbidity and humanness worldwide (HNSCC). Risk factors like terrestrial differences, ancestral predisposition, gender, age, type of diet, hot and/or alcohol devouring habits, and intercourse preferences may imitate in the etiology of HNSCC, contingent upon the site that is troubled. Another hypothesis for the cause of HNSCC is dysbiosis. Over 700 symbionts and pathogenic microbial variety can be found in the spoken microbiota. By causing never-ending inflammation and creating an invulnerable-suppressed microenvironment that advances cell increase and inhibits apoptosis, disruption of the active balance of the oral microbiota compensate the carcinogenic mechanisms (Fig. 1). With traditional links between the spoken microbiota and chronic inflammation and container proliferation, current studies have discovered that things with the human microbiome are linked to a type of cancer types. The bacterial genome, poisons, and metabolites have also been projected as additional causes or enablers of carcinogenesis and allure progression in the head and neck domain in addition to incessant inflammation. But it's still not completely clear what the exact mechanisms are. However, a deeper comprehension of the latent mechanisms ability result in the creation of new preventive or specific therapies that can be used in standard clinical practice. A current and well-received topic in the oncological and dental societies is the connection 'tween oral dysbiosis and the rise of HNSCC. As a result, this chapter aims to present a thorough survey of the information that is to say currently available on the potential mechanistic relates between alterations in the spoken microbiota and the emergence of HNSCC, which is still in the research time.

Author(s) Details:

Efsun Somay,
Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Baskent University, Ankara, Turkey.

Busra Yilmaz,
Department of Oral and Maxillofacial Radiology, Faculty of Dentistry, Baskent University, Ankara, Turkey.

Erkan Topkan,
Department of Radiation Oncology, Faculty of Medicine, Baskent University, Adana, Turkey.

Ahmet Kucuk,
Department of Radiation Oncology, Mersin City Hospital, Mersin, Turkey.

Berrin Pehlivan,
Department of Radiation Oncology, Bahcesehir University, Istanbul, Turkey.

Ugur Selek,
Department of Radiation Oncology, School of Medicine, Koc University, Istanbul, Turkey and Department of Radiation Oncology, MD Anderson Cancer Center, The University of Texas, Houston, TX, USA.

Please see the link here: https://stm.bookpi.org/PRAMR-V11/article/view/9516

Post-Translational Modification of SUMOylation and Cancer: A Brief Review | Chapter 09 | New Horizons in Medicine and Medical Research Vol. 3

 SUMOylation is a reversible post-translational modification that plays a role in DNA damage repair, immunological responses, carcinogenesis, cell cycle progression, and apoptosis. SUMO1, SUMO2/3, and SUMO4 are the four SUMO isoforms that have been identified. In complicated protein regulatory networks, many levels of regulation or SUMOylation may play a crucial role. SUMOylation dysfunction can lead to the development of illnesses and malignancies. As a result, SUMO could be employed as a cancer treatment target. The small ubiquitin-like modifier (SUMO) pathway is found in all eukaryotes and is involved in gene regulation, cellular signalling, and the preservation of genomic integrity. Maturation, activation, conjugation, ligation, and de-modification are all part of the SUMO catalytic cycle. The SUMO system has been related to a number of disorders, the most prominent of which being cancer. Carcinogenesis, DNA damage response, cancer cell proliferation, metastasis, and apoptosis are all affected by SUMOylation. SUMO has the potential to be a cancer treatment target. To better comprehend the role of SUMO in human disease, we present the basic concepts of the SUMO system and summarise the involvement of SUMO proteins in cancer cells in this review.

Author(S) Details

ZhI-Jian Han
Key Laboratory of the Digestive System Tumors of Gansu Province, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Yan-Hu Feng
Key Laboratory of the Digestive System Tumors of Gansu Province, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Bao-Hong Gu
Department of General Surgery, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Yu-Min Li
Department of General Surgery, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Hao Chen
Department of General Surgery, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

View Book:- https://stm.bookpi.org/NHMMR-V3/article/view/6338

An Overview on Pathogenesis of Cancer: Cancer Reparative Trap | Chapter 1 | Research Trends and Challenges in Medical Science Vol. 2

Cancer is one of the leading causes of death in the world, and the long-term prognosis is still unfavorable, despite the enormous efforts in the search for effective anti-cancer drugs. We think that the obstacle to creating the effective anti-cancer drugs is the existing idea that the basis of cancer is the damage of the genetic apparatus of the cell. In this paper we present the pathogenesis of cancer which is based on the formation of the special sustainable pathophysiological state of the organism – the state of "cancer reparative trap". The essence of this pathophysiological state of the organism is in the reparative orientation of the immune system of cancer patients, when constant tissue repair is accompanied by systemic suppression of the anti-tumor immunity. Specifically, during the long-term exposure to carcinogens (exogenous and/or endogenous) the continuous tissue damage occurs which induces permanent stimulation of cell proliferation (imbalanced Th1<Th2 lymphocytes, M1<M2 macrophages, inflammation, angiogenesis, etc.) in order to repair the tissues damaged. At the same time, tissue repair is necessarily accompanied by the suppression of anti-tumor immunity (increase in T regulatory cell (Treg), imbalanced Th1<Th2 lymphocytes, M1<M2 macrophages et al.), which creates the necessary conditions for the survival of the malignantly transformed cells, formed by the action of carcinogens. The determining role of the imbalance in the autonomous nervous system (simpathetic/hypersympathetic dominance) in the development, maintenance and generalization of the cancer process has been shown. The explanation of a number of phenomena has been presented: the cell resistance to chemotherapy and the phenomenon of cancer cell dormancy. The promising approaches for the cancer management in clinical practice has been proposed.

Author(s) Details

Dr. Oleg V. Bukhtoyarov,
Medical Center 39, LLC, Kaliningrad, Russia

Dr. Denis M. Samarin,
Laboratory of Psychoimmunology, Medical Center 39, LLC, Kaliningrad, Russia.

View Book :- http://bp.bookpi.org/index.php/bpi/catalog/book/190