scholarly journals The Molecular Mechanisms of Tobacco in Cancer Pathogenesis

2017 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Elaheh Nooshinfar ◽  
Davood Bashash ◽  
Mahnaz Abbasalizadeh ◽  
Ava Safaroghli-Azar ◽  
Parisa Sadreazami ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Sergio Romera-Giner ◽  
Zoraida Andreu Martínez ◽  
Francisco García-García ◽  
Marta R. Hidalgo

Abstract Background Cancer is a major health problem which presents a high heterogeneity. In this work we explore omics data from Breast, Kidney and Lung cancers at different levels as signalling pathways, functions and miRNAs, as part of the CAMDA 2019 Hi-Res Cancer Data Integration Challenge. Our goal is to find common functional patterns which give rise to the generic microenvironment in these cancers and contribute to a better understanding of cancer pathogenesis and a possible clinical translation down further studies. Results After a tumor versus normal tissue comparison of the signaling pathways and cell functions, we found 828 subpathways, 912 Gene Ontology terms and 91 Uniprot keywords commonly significant to the three studied tumors. Such features interestingly show the power to classify tumor samples into subgroups with different survival times, and predict tumor state and tissue of origin through machine learning techniques. We also found cancer-specific alternative activation subpathways, such as the ones activating STAT5A in ErbB signaling pathway. miRNAs evaluation show the role of miRNAs, such as mir-184 and mir-206, as regulators of many cancer pathways and their value in prognoses. Conclusions The study of the common functional and pathway activities of different cancers is an interesting approach to understand molecular mechanisms of the tumoral process regardless of their tissue of origin. The existence of platforms as the CAMDA challenges provide the opportunity to share knowledge and improve future scientific research and clinical practice.



Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 389
Author(s):  
Marisol Miranda-Galvis ◽  
Reid Loveless ◽  
Luiz Paulo Kowalski ◽  
Yong Teng

Epidemiological and clinical studies over the past two decades have provided strong evidence that genetic elements interacting with environmental components can individually and collectively influence one’s susceptibility to cancer. In addition to tumorigenic properties, numerous environmental factors, such as nutrition, chemical carcinogens, and tobacco/alcohol consumption, possess pro-invasive and pro-metastatic cancer features. In contrast to traditional cancer treatment, modern therapeutics not only take into account an individual’s genetic makeup but also consider gene–environment interactions. The current review sharpens the focus by elaborating on the impact that environmental factors have on the pathogenesis and progression of head and neck cancer and the underlying molecular mechanisms involved. Recent advances, challenges, and future perspectives in this area of research are also discussed. Inhibiting key environmental drivers of tumor progression should yield survival benefits for patients at any stage of head and neck cancer.



2019 ◽  
Vol 3 (1) ◽  
pp. 105-130 ◽  
Author(s):  
Tyler G. Demarest ◽  
Mansi Babbar ◽  
Mustafa N. Okur ◽  
Xiuli Dan ◽  
Deborah L. Croteau ◽  
...  

Aging is a major risk factor for many types of cancer, and the molecular mechanisms implicated in aging, progeria syndromes, and cancer pathogenesis display considerable similarities. Maintaining redox homeostasis, efficient signal transduction, and mitochondrial metabolism is essential for genome integrity and for preventing progression to cellular senescence or tumorigenesis. NAD+is a central signaling molecule involved in these and other cellular processes implicated in age-related diseases and cancer. Growing evidence implicates NAD+decline as a major feature of accelerated aging progeria syndromes and normal aging. Administration of NAD+precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) offer promising therapeutic strategies to improve health, progeria comorbidities, and cancer therapies. This review summarizes insights from the study of aging and progeria syndromes and discusses the implications and therapeutic potential of the underlying molecular mechanisms involved in aging and how they may contribute to tumorigenesis.



Author(s):  
Vishal Sharma ◽  
Chhaya Bawa ◽  
Kuldeep Chand Vatsyan

Extensive efforts are going on to understand the molecular mechanisms behind tumor initiation, progression, and invasion and find novel targets for cancer treatment. The physiological state of the tumor microenvironment (TME) is crucial to every step of tumor cell growth and angiogenesis. Cancer cells are rarely in contact with each other. The intervening medium between the cancer cells, immune cells, and other cells become acidic, which significantly affects cancer pathogenesis. It could be a novel targeting marker and may help treat tumors. Even after extensive research in this area, the nature of molecular alterations and the basic mechanisms in the tumor microenvironment remains unclear. Based on recent studies of TME, this mini-review bids a more inclusive overview of the role of TME in cancer cell growth. Also, it helps to understand the potential of TME for therapeutic interventions.



2019 ◽  
Vol 45 (06) ◽  
pp. 559-568 ◽  
Author(s):  
Bal Krishan Sharma ◽  
Matthew J. Flick ◽  
Joseph S. Palumbo

AbstractPathological activation of the coagulation system occurs with virtually all forms of cancer, particularly epithelial malignancies. Accordingly, thrombosis is one of the most common comorbidities associated with cancer. Indeed, cancer-associated thromboembolism is the second leading cause of death for cancer patients, second only to the cancer itself. The identification of specific molecular mechanisms whereby tumor cells activate the coagulation system and drive thrombosis has been an active area of investigation for several decades. Studies in animal models and human trials have revealed that there is a bidirectional relationship between coagulation factor activity and cancer, whereby the pathological hemostatic system activation associated with cancer not only promotes thromboembolism but also drives progression of the malignancy. Numerous studies indicate that factors up and down the clotting cascade can contribute to various stages of cancer, including tumorigenesis, primary tumor growth, and metastasis. Although there are some mechanistic points of commonality, there are also clearly context-dependent contributions of coagulation components to cancer progression dependent on the type of cancer and stage of disease. It is also notable that in some instances, coagulation factors appear to contribute to cancer progression independently of their traditional roles in hemostasis and thrombosis. Here, the authors review the current state of the field with regard to hemostatic factor-driven cancer pathogenesis.



2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hadis Fathizadeh ◽  
Zatollah Asemi

AbstractLung cancer is one of very important malignancies which are related to high mobility and mortality in the world. Despite several efforts for improving diagnosis and treatment strategies of lung cancer, finding and developing new and effective therapeutic and diagnostic are needed. A variety of internal and external factors could be involved in lung cancer pathogenesis. Among internal factors, epigenetic mechanisms have been emerged as very important players in the lung cancer. Non-coding RNAs is known as one of epigenetic regulators which exert their effects on a sequence of cellular and molecular mechanisms. P-element induced wimpy testis (PIWI)-interacting RNAs (piRNAs or piR) is one of small non-coding RNAs that the deregulation of these molecules is associated with initiation and progression of different cancers such as lung cancer. Several activities are related to PIWI/piRNA pathway such as suppression of transposons and mobile genetic elements. In vitro and in vivo studies demonstrated the upregulation or downregulation of PIWI proteins and piRNAs could lead to the increasing of cell proliferation, apoptosis reduction and promoting tumor growth in the lung cancer. Hence, PIWI proteins and piRNA could be introduced as new diagnostic and therapeutic biomarkers in the lung cancer therapy. Herein, we have focused on PIWI proteins and piRNA functions and their impact on the progression of lung cancer.



Author(s):  
Eduarda Leite-Gomes ◽  
Ana M Dias ◽  
Catarina M Azevedo ◽  
Beatriz Santos-Pereira ◽  
Mariana Magalhães ◽  
...  

Abstract Colitis-associated cancer is a major complication of inflammatory bowel disease remaining an important clinical challenge in terms of diagnosis, screening, and prognosis. Inflammation is a driving factor both in inflammatory bowel disease and cancer, but the mechanism underlying the transition from colon inflammation to cancer remains to be defined. Dysregulation of mucosal glycosylation has been described as a key regulatory mechanism associated both with colon inflammation and colorectal cancer development. In this review, we discuss the major molecular mechanisms of colitis-associated cancer pathogenesis, highlighting the role of glycans expressed at gut epithelial cells, at lamina propria T cells, and in serum proteins in the regulation of intestinal inflammation and its progression to colon cancer, further discussing its potential clinical and therapeutic applications.



Author(s):  
Hans Lehrach ◽  
Thomas Kessler ◽  
Lesley Ogilvie ◽  
Moritz Schütte ◽  
Christoph Wierling


2019 ◽  
Vol 20 (14) ◽  
pp. 3590 ◽  
Author(s):  
Michael A. Moses ◽  
Andrea L. George ◽  
Nozomi Sakakibara ◽  
Kanwal Mahmood ◽  
Roshini M. Ponnamperuma ◽  
...  

The p63 gene is a member of the p53/p63/p73 family of transcription factors and plays a critical role in development and homeostasis of squamous epithelium. p63 is transcribed as multiple isoforms; ΔNp63α, the predominant p63 isoform in stratified squamous epithelium, is localized to the basal cells and is overexpressed in squamous cell cancers of multiple organ sites, including skin, head and neck, and lung. Further, p63 is considered a stem cell marker, and within the epidermis, ΔNp63α directs lineage commitment. ΔNp63α has been implicated in numerous processes of skin biology that impact normal epidermal homeostasis and can contribute to squamous cancer pathogenesis by supporting proliferation and survival with roles in blocking terminal differentiation, apoptosis, and senescence, and influencing adhesion and migration. ΔNp63α overexpression may also influence the tissue microenvironment through remodeling of the extracellular matrix and vasculature, as well as by enhancing cytokine and chemokine secretion to recruit pro-inflammatory infiltrate. This review focuses on the role of ΔNp63α in normal epidermal biology and how dysregulation can contribute to cutaneous squamous cancer development, drawing from knowledge also gained by squamous cancers from other organ sites that share p63 overexpression as a defining feature.



Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3264
Author(s):  
Hossein Tabatabaeian ◽  
Samantha Peiling Yang ◽  
Yvonne Tay

Thyroid cancer is the most prevalent malignancy of the endocrine system and the ninth most common cancer globally. Despite the advances in the management of thyroid cancer, there are critical issues with the diagnosis and treatment of thyroid cancer that result in the poor overall survival of undifferentiated and metastatic thyroid cancer patients. Recent studies have revealed the role of different non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) that are dysregulated during thyroid cancer development or the acquisition of resistance to therapeutics, and may play key roles in treatment failure and poor prognosis of the thyroid cancer patients. Here, we systematically review the emerging roles and molecular mechanisms of ncRNAs that regulate thyroid tumorigenesis and drug response. We then propose the potential clinical implications of ncRNAs as novel diagnostic and prognostic biomarkers for thyroid cancer.



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