Cancer Biology

Introduction to Cancer

Cancer is a disease characterized by uncontrolled cell growth and division, resulting from genetic and molecular changes within cells. Understanding the mechanisms behind cancer development is essential for General Biology students.

• Unregulated proliferation: Excessive cell growth and division due to loss of normal regulatory controls.

• Unregulated apoptosis: Programmed cell death is disrupted, allowing abnormal cells to survive.

• Multiple mutations within somatic cells can lead to cancer.

• Cancers are genetically unstable, with various mutations and chromosomal aberrations.

• There are two main types of tumors:

  • Benign tumors: Abnormal proliferation, but remain localized.

  • Malignant tumors: Invade other tissues and metastasize to distant areas.

Example: Benign vs. Malignant tumor diagrams illustrate localized vs. invasive growth.

Tumorigenesis

Tumorigenesis is the process by which normal cells transform into malignant cancer cells, involving multiple genetic changes.

• Requires more than one mutation.

• Affects signal transduction pathways that regulate cell activities.

• Cancer is clonal: Derived from a single cell.

• Genetic aberrations are passed onto progeny cells.

• Cancer stem cells can proliferate and create more tumor cells.

Causes of Cancer

Cancerous mutations can arise from various sources, leading to activation of cancer-causing genes.

• Viruses: Can introduce mutations or aberrant genes.

  • Example: Human papillomavirus (HPV) E6 and E7 proteins.

• Epigenetic changes: Alterations to chromatin histone proteins can misregulate gene expression.

  • Can cause over-activation or under-activation of regulatory genes.

• Environmental substances: Exposure to mutagens (e.g., cigarette smoke) can induce mutations.

Cell Cycle Regulation in Cancer

The cell cycle is tightly regulated by proteins called cyclins and cyclin-dependent kinases (CDKs), which control progression through cell cycle checkpoints.

• Cell cycle checkpoints ensure proper DNA replication and division.

  • G1 to S transition: Controlled by retinoblastoma protein.

  • G2 to M transition: Controlled by CDC2 cyclin-dependent kinase and cyclin B.

• Checkpoints prevent damaged DNA from being replicated.

Example: Graph showing cyclin concentrations during cell cycle phases (G1, S, G2, Mitosis).

Genetic Mutations in Cancer

Cancer develops after multiple mutations accumulate in a single cell. These mutations can be classified as passenger or driver mutations.

• Passenger mutations: No direct contribution to cancer.

• Driver mutations: Provide growth advantages to cancer cells.

Classes of Cancer Mutations

• Oncogenes: Mutant alleles that act dominantly to promote cell division.

  • Proto-oncogenes: Wild-type alleles that become oncogenes when mutated. Examples: Ras GTPase, HPV E6 and E7 proteins.

• Tumor suppressors: Alleles whose normal function is to stop cell division.

  • Loss of function leads to uncontrolled growth. Examples: Retinoblastoma, p53 transcription factor.

Example: Diagram showing activation of oncogenes and loss of tumor suppressor function in cancer cells.

Review Questions

1. A mutation in a tumor suppressor gene causes what to happen?

   • a. The mutated tumor suppressor acts to suppress the tumor

   • b. The mutated tumor suppressor can no longer act to suppress the tumor, and allows tumor growth

   • c. The mutated tumor suppressor has no direct contribution to the cancer

2. True or False: Proto-oncogenes are mutated versions of oncogenes

   • a. True

   • b. False

3. Which of the following is a tumor suppressor?

   • a. Ras GTPase

   • b. HPV E6 protein

   • c. p53 transcription factor

Summary Table: Oncogenes vs. Tumor Suppressors

Additional info: The study notes expand on the original content by providing definitions, examples, and a summary table for clarity and completeness.