Proto-oncogenes act as central regulators of the growth in normal cells that code for proteins involved in growth and repair processes in the body. Proteins such as growth factors or transcription factors are necessary for normal growth.

Genetic mutations in proto-oncogenes produce oncogenes. Oncogene activation causes the overexpression of growth- promoting proteins, resulting in hypercellular proliferation and tumorigenesis. Tumor suppressor genes normally counteract proto-oncogenes by encoding proteins that prevent cellular differentiation. When mutations in tumor suppressor genes cause loss of function, the expressed tumor suppressor proteins are no longer able to suppress cellular growth.

For example, the activation of proto-oncogenes (e.g., ras) involved in the growth process or inactivation of suppressor genes (e.g., p53), which keeps growth in check by binding and activating genes that put the brakes on cell division, is responsible for neoplastic transformation of a cell. Defects in the gene for p53 cause about 50% of all cancers.

p53 Protein

The p53 gene (tumor suppressor gene) is located on chromo some 17 and produces a protein that downregulates the cell cycle. A mutation of p53 is associated with an increased incidence of many types of cancer. The p53 tumor suppressor protein is dysfunctional in most human cancers. Even when p53 is not itself mutant, its regulators (e.g., p14^ARF, a p53-stabilizing protein) are often altered. The p53 protein is a key responder to various stresses, including DNA damage, hypoxia, and cell cycle aberrations. Specific molecular pathways that activate p53 depend on the nature of the stress and the cell type. Consequently, these determine the specific downstream effectors and cellular response—apoptosis, growth arrest, or senescence.

It is widely believed that the central role of p53 in tumor suppression is to mediate the response to DNA damage. If p53 is missing when damage occurs, cells do not undergo p53 mediated arrest or apoptosis. Cells that have sustained mutations in oncogenes or tumor suppressor genes because of the damage obtain a growth advantage that fuels the development of cancer.

Apparently, DNA damage itself is not the critical event that leads to cancer, as long as the oncogenic stress pathways that activate p53 are intact. For any given cancer type, p53 dysfunction generally correlates with poor treatment response and poor prognosis; therefore, restoration of p53 function is a potential avenue for therapeutic development. Drugs currently being developed will enhance the function of kinases that activate p53 in response to DNA damage.

اخر الاخبار

اخبار العتبة العباسية المقدسة

سماحة السيد الصافي يكرم عددًا من عوائل الشهداء ضمن فعاليات مهرجان روح النبوة النسوي العالمي الثامن

إحدى أمهات الشهداء: نعتز بتضحيات أبنائنا ونفتخر بشهادتهم دفاعًا عن الدين والمقدسات

ضمن فعاليات مهرجان روح النبوة… عرض فيلم يوثق نشاطات الشعب النسوية في العتبة العباسية المقدسة

فعاليات مهرجان روح النبوة الثقافي تشهد تقديم أوبريت الثقلين القرآني

المزيد

الآخبار الصحية

ماذا يحدث لجسمك عند تناول الوجبات السريعة يوميا؟

لصحة عظام المرأة.. الشاي أفضل أم القهوة؟

لبناء العضلات وإنقاص الوزن.. ما أفضل توقيت لتناول البيض؟

أطعمة صحية تساعد على التعافي من "الإنفلونزا الخارقة"

المزيد

الآخبار التكنلوجية

دراسة تكشف قدرة الحيتان على سماع الأصوات منخفضة وعالية التردد من مسافة بعيدة

تجربة جديدة: الأسفلت المدعوم بالطحالب يقاوم الحفر ويقلل الانبعاثات الكربونية

تسريبات تكشف ملامح أول هاتف قابل للطي من "أبل"

رصد نوع نادر من القطط في تايلاند للمرة الأولى منذ عقود

المزيد

مواضيع ذات صلة

Application of Liquid Biopsy to Non-small- Cell Lung Cancer Lung

Circulating Tumor DNA

Biomarkers in the Blood and in Tissues: A Complementary Approach

Biomarkers in Oncology: An Evolving Concept

Clinical Development of Venetoclax for Acute Myeloid Leukemia

Clinical Development of Oblimersen for Acute Myeloid Leukemia

Modalities for treating cancer

Tumor markers

Cancer-Predisposing Genes

Stages of Carcinogenesis

Causative Factors in Human Cancer

Types of Tumors