Apoptosis in cancer therapy (original) (raw)
Related papers
Oral Oncology, 2004
Oral cancer is one of the most disfiguring types of cancer, since the surgical removal of the tumor may result in facial distortion. Oral cancer is also known to exhibit "field cancerization", resulting in the development of a second primary tumor. Furthermore, the five-year survival rate of this disease has remained approximately 50% during the past 30 years. Prevention and early detection/ treatment of oral cancer could significantly improve the quality of life for individuals at risk. Recently, the targeted elimination of oral squamous cell carcinoma cells by inducing apoptosis has emerged as a valued strategy to combat oral cancer. Studies utilizing a variety of chemical or biological interventions demonstrated promising results for induction of apoptosis in oral malignant cells. This review summarizes the results of a number of investigations focused specifically on induction of apoptosis in oral cancer cells by synthetic compounds and naturally occurring chemopreventive agents with apoptotic potential.
Apoptosis and genes involved in oral cancer - a comprehensive review
Oncology Reviews, 2020
Oral cancers needs relentless research due to high mortality and morbidity associated with it. Despite of the comparable ease in accessibility to these sites, more than 2/3rd cases are diagnosed in advanced stages. Molecular/genetic studies augment clinical assessment, classification and prediction of malignant potential of oral lesions, thereby reducing its incidence and increasing the scope for early diagnosis and treatment of oral cancers. Herein we aim to review the role of apoptosis and genes associated with it in oral cancer development in order to aid in early diagnosis, prediction of malignant potential and evaluation of possible treatment targets in oral cancer. An internet-based search was done with key words apoptosis, genes, mutations, targets and analysis to extract 72 articles after considering inclusion and exclusion criteria. The knowledge of genetics and genomics of oral cancer is of utmost need in order to stop the rising prevalence of oral cancer. Translational ap...
Apoptosis in malignant diseases
Archive of Oncology, 2005
Apoptosis is a special type of cell death essentially different from necrosis in nature and biological significance. It is an active process of genetically regulated cell autodestruction and in most cases has a homeostatic function. Apoptotic cells may be characterized by specific morphological and biochemical changes. A great number of genes are known today, whose protein products take part in regulation of the apoptotic process. Apoptosis or programmed cell death has been implicated in a wide range of pathological conditions. Studies of the correlation of programmed cell death with proliferation and the multistage carcinogenesis process are in the focus of modern research. Mutations and deletions of apoptotic genes play important roles in carcinogenesis, tumor growth, and tumor regression. This article reviews the current knowledge on mutations of apoptosis genes involved in pathogenesis of human cancers. Finally, we have recently summarized achievements in cancer therapy with a focus on the apoptotic genes.
Apoptosis in Cancer - An Update
Asian Pacific Journal of Cancer Prevention, 2012
Apoptosis is programmed cell death which is essential for development and survival of living organisms. It is a sequentially regulated suicidal programme where cells activate certain enzymes which dissolute their own nuclear component and various protein component of nucleus and cytoplasm. Disturbance of this regulatory pathway may lead to various diseases like autoimmune diseases, neurodegenerative diseases and cancers. The potential mechanisms of apoptosis and its role in cancer are discussed. The ability of apoptosis to modulate the life or death of a cell is also recognized for its immense therapeutic potential. Understanding the mechanisms from this review will give us better insight to the pathogenesis of various diseases including cancer and will open new horizons to therapeutic approaches.
Apoptosis and Predisposition To Oral Cancer
Critical Reviews in Oral Biology & Medicine, 1999
The term apoptosis, also known as programmed cell death (PCD), was coined by developmental biologists a number of years ago to describe a form of cell death characterized by several unique morphological and biochemical features. Genetic studies of the round worm Caeneorhabditis elegans, a simple multicellular organism, first revealed apoptosis to be an integral part of the developmental program. Subsequently, the importance of apoptosis in higher organisms was demonstrated in several eukaryotic systems. In mammals, apoptosis is widespread during embryogenesis and in adult tissues. It is required for normal tissue homeostasis and for clonal selection in the immune system. In both developing and adult organisms, apoptosis plays a central role in reinforcing appropriate cellular patterns and in regulating cell number by eliminating cells that are harmful or no longer needed. It is becoming increasingly clear that disruption in the apoptosis pathway can contribute to the development of a number of developmental, inflammatory, degenerative, and neoplastic diseases. The effector arm of the apoptotic program includes members of the Bcl-2 gene family that function as either death agonists or death antagonists. These proteins participate in an elaborate genetically controlled biochemical pathway that functions to maintain tissue and organ homeostasis and serve as a critical defense mechanism to guard against malignant transformation. Cancer is the result of a series of genetic lesions that include activation of oncogenes and inactivation or loss of tumor suppressor genes. Several groups of investigators have observed that deregulated expression of oncogenes can subvert apoptotic pathways, resulting in prolonged cell survival. In pathological settings such as cancer, members of the Bcl-2 gene family are able to synergize with oncogenes and tumor suppressor genes to transform cells. In this review, we describe the process of apoptosis in mammalian cells and define the role and biochemical pathways through which the Bcl-2 gene family induce and/or protect cells from apoptosis. Last, we will discuss the evidence which suggests that alterations in this pathway may play a central role in tumorigenesis by allowing genetically damaged cells normally destined for elimination to persist, predisposing them to additional mutations and driving them to malignancy.
Studia Ecologiae et Bioethicae, 2020
Apoptosis is a genetically programmed process that affects all multicellular organisms. This mechanism of programmed cell death is designed to protect the body against uncontrolled proliferation of cells with impaired functions. Apoptosis can occur through two major pathways. The extrinsic, initiated by signals from the death receptor, and the intrinsic one, resulting from a change in the permeability of the external mitochondrial membrane due to stress factors promoting the initiation of programmed cell death. Apoptosis may be influenced by many factors that may lead to suppressing the initiation of apoptotic pathways, and the damaged cell will develop, divide, and over time transform into a cancerous cell. As a result, cancer cells will be resistant to the applied chemo- and radiotherapy. The mechanisms responsible for apoptosis regulation are impaired, what eliminates the effects of therapies aimed at initiating this type of cell death. New types of molecular therapies provide an...
Apoptosis and cancer: insights molecular mechanisms and treatments
2015
Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment, but it is also involved in a wide range of pathological processes, including cancer. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer by acting in the extrinsic/intrinsic pathway. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. In particular, this review provides references concerning the apoptotic molecules, their interactions, the mechanisms involved in apoptosis resistance, and also the modulation of apoptosis for the treatment of cancer. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies.
Apoptosis in Cancer-An Update S
2012
Homeostatic balance between proliferation of cells and its death is essential for development and maintenance of biological system of a living being. Apoptosis is programmed cell death. It is a widespread phenomenon that plays a vital role in a myriad of physiological and pathological processes. The word apoptosis came from Greek origin; meaning “falling off or dropping off”. (Gewies, 2003) It resembles leaves falling off trees or petals dropping off flowers. This analogy emphasizes that the death of living matter is an integral and necessary part of the life cycle of organisms. The mechanism involved in the process of apoptosis in mammalian cells was first studied in a nematode Caenorhabditis elegans during its development phase (Horvitz, 1999). In this organism 1090 somatic cells are generated in the formation of the adult worm, of which 131 of these cells undergo apoptosis or “programmed cell death”. These 131 cells die at particular points during the development process, demonst...
Apoptosis: a relevant tool for anticancer therapy
Annals of Oncology, 2006
Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Resistance to standard chemotherapeutic strategies also seems to be due to alterations in the apoptotic pathway of cancer cells. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer. These new target include those acting in the extrinsic/intrinsic pathway, proteins that control the apoptosis machinery such as the p53 and proteosome pathway. Most of these forms of therapy are still in preclinical development because of their low specifity and susceptibility to drug resistance, but several of them have shown promising results. In particular, this review specifically aims at providing an update of certain molecular players that are already in use in order to target apoptosis (such as bortezomib) or which are still being clinically evaluated (such ONYX-015, survivin and exisulind/aptosyn) or which, following preclinical studies, might have the necessary requirements for becoming part of the anticancer drug programs (such as TRAIL/ Apo2L, apoptin/VP3).