
Genetic and Cancer Understanding the Genetic Basis of Cancer
Published 9/2026
MP4 | Video: h264, 3840x2160 | Audio: AAC, 44.1 KHz, 2 Ch
Language: English | Duration: 11h 25m | Size: 23.93 GB
Explore DNA Mutations, Oncogenes, Tumor Suppressor Genes, Cancer Development, and the Molecular Basis of Cancer
What you'll learn
Explain the fundamental principles of genetics, DNA structure, genes, chromosomes, and genetic variation.
Describe how genetic mutations and alterations in DNA can contribute to the development of cancer.
Identify the roles of oncogenes, tumor suppressor genes, and DNA repair genes in cancer development.
Explain how genetic and molecular changes can affect normal cell growth, division, and survival.
Requirements
Understanding these mechanisms helps explain why cancer is fundamentally a genetic and molecular disease and why modern cancer treatments often target specific abnormal pathways or genetic alterations.
Description
"This course contains the use of artificial intelligence."
Welcome toGenetics and Cancer: Understanding the Genetic Basis of Cancer, a comprehensive and beginner-friendly course designed to help you understand how genetic and molecular changes contribute to the development and progression of cancer.
Cancer is fundamentally a disease of abnormal cellular growth and regulation, and genetics plays a central role in understanding why these changes occur. In this course, you will explore the relationship betweenDNA, genes, mutations, cellular regulation, and cancer development in a clear and structured way.
You will begin by building a foundation in genetics, includingDNA structure, genes, chromosomes, genetic variation, and mutations. From there, the course introduces the major genetic and molecular mechanisms that can transform a normal cell into a cancer cell.
You will learn about the important roles ofoncogenes, tumor suppressor genes, and DNA repair genes, and understand how alterations in these genes can affect normal cell growth, division, survival, and programmed cell death. The course also explores how abnormal molecular signaling pathways can contribute to uncontrolled cell proliferation and cancer progression.
Key topics covered includegenetic mutations, cancer-causing genes, cell-cycle regulation, apoptosis, DNA damage and repair, hereditary cancer, cancer risk, and molecular mechanisms of tumor development. You will also gain an introduction to genetic testing, molecular profiling, targeted therapies, and the emerging role of personalized medicine in cancer care.
This course is particularly suitable formedical, nursing, pharmacy, biomedical science, biotechnology, genetics, biology, and life-science students, as well as healthcare professionals, laboratory professionals, researchers, and anyone interested in understanding cancer genetics.
The content is presented in aclear, accessible, and learner-friendly manner, making it suitable for beginners and learners who want to strengthen their foundational knowledge.
By the end of this course, you will have a solid understanding of
- The fundamentals of genetics and molecular biology
- DNA, genes, chromosomes, and genetic mutations
- How genetic alterations contribute to cancer
- Oncogenes and tumor suppressor genes
- DNA repair mechanisms and genomic instability
- Cell-cycle regulation and programmed cell death
- Molecular pathways involved in cancer development
- Inherited genetic changes and hereditary cancer
- The basics of cancer genetic testing and molecular profiling
- The role of targeted therapy and personalized medicine
Whether you are studying for an examination, building your foundation in cancer biology, or simply interested in understanding the genetic basis of cancer, this course will provide you with a structured introduction to this important and rapidly developing field.
Enroll today and begin your journey into the fascinating world of Genetics and Cancer!
Who this course is for
This course is designed for students, healthcare learners, and anyone interested in understanding the relationship between genetics and cancer.
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