cancer
CANCER
Understanding Cancer
Hundreds of genes involved: Genes and the proteins produced by them regulate DNA replication and cell division.
Tight regulation: DNA replication and cell division are closely monitored processes.
Mutation implications: If a mutation occurs in genes that manage these processes, it can lead to serious cellular problems.
Uncontrolled Cell Division
Definition: Uncontrolled cell division results in a mass of unspecialized cells, often referred to as a tumor.
Tumors:
Benign Tumor:
Characteristics: Non-cancerous, does not invade neighboring tissues.
Malignant Tumor:
Characteristics: Cancerous, exhibits continuous growth, undergoes angiogenesis (formation of new blood vessels), and can metastasize, thus impairing organ function.
Characteristics of Cancer Cells
Key Features:
Uncontrolled cell division: Cells divide without regulation.
Deranged metabolism: Cancer cells often exhibit abnormal metabolic pathways.
Loss of attachment: Cancer cells may lose their ability to adhere to neighboring cells.
Chromosomal changes: Abnormalities in chromosome structure and number.
Example: Chronic Myeloid Leukemia (CML).
Mechanisms for Cancer
Normal defense: The immune system typically recognizes and destroys cancer cells.
Evasion of immune response: Some cancer cells develop mechanisms to evade detection.
Role of p53 Protein:
Function: Stops the cell cycle and activates DNA repair mechanisms.
If repairs fail: P53 triggers apoptosis (programmed cell death).
Mutations impact:
Defective mutations can impair DNA repair pathways and control of mitosis, leading to cancer.
The Cell Cycle and Cancer
Cell Cycle Checkpoints: Ensure accurate cell division by regulating a cell’s progress through the cell cycle.
If checkpoints identify problems (e.g., DNA damage), they prevent progression to further stages (G₁, S, G₂, Mitosis).
Apoptosis in response to damage: Cells with irreparable damage undergo apoptosis to prevent the proliferation of damaged cells.
Gene Mutations in Cancer
Proto-oncogenes: These promote mitosis ("GO" signals).
Mutation can result in overactivity, leading to excessive cell division (oncogene).
Tumor suppressor genes: These stop cell division ("STOP" signals).
Mutation can inactivate these genes, removing the inhibitory mechanism on cell division.
Component of cancer development: An accumulation of multiple mutations is necessary for cancer development.
Examples of Mutations and Their Effects
Proto-oncogenes vs oncogenes:
Normal proto-oncogenes respond to growth signals, while mutated oncogenes promote division regardless of external signals.
Tumor suppressor genes: Normal functions include recognizing damage and pausing the cycle; mutations lead to unregulated division.
Example: Effect of BRCA1/BRCA2 mutations on cancer predisposition.
Inherited vs Acquired Mutations
Inherited Mutations: Associated with higher risks of specific cancers, such as breast and ovarian cancers via BRCA gene mutations.
Genetic testing can identify high-risk mutations.
Acquired Mutations:
Causes: Chemicals (carcinogens), radiation (UV light, x-rays), and viruses (e.g., HPV).
Example: UV radiation leads to DNA bonding errors that can initiate mutations.
Data on risk factors: Acquired mutations contribute significantly to cancer risk due to environmental exposure and lifestyle choices.
Cancer Screening Recommendations
Breast Screenings: Mammograms recommended every two years starting at age 40.
Cervical Screenings: Pap smears recommended every three years for women aged 21-30 and every five years for ages 30-65.
Prostate Screenings: First prostate exam by age 50.
Colon Screenings: Begin at age 45, recommended every ten years.
Cancer Treatments
Categories of Treatments:
Surgery: Removal of tumors or at-risk tissues.
Chemotherapy: Destroys rapidly dividing cells throughout the body.
Radiation Therapy: Kills cells by damaging DNA in targeted areas.
Targeted Therapy: Specifically attacks cancer cells by exploiting their specific weaknesses (e.g., PARP inhibitors).
Immunotherapy: Enhances the immune system's ability to recognize and destroy cancer cells.
Targeted Therapy Example: CML
Targeting Specific Mutations: Imatinib is used to inhibit the BCR-ABL tyrosine kinase activity in CML, preventing cancer cell division.
Cancer Survival Statistics (1977-2013)
Five-Year Survival Rates: Varies by cancer type; for example:
Prostate cancer: 80% survival rate.
Lung cancer: low survival rate.
Preventive Strategies for Reducing Cancer Risk
Lifestyle Modifications:
Avoid tobacco: Reduces risk of multiple cancers.
Healthy diet and exercise: Maintain a balanced diet, manage weight to reduce cancer risk.
Screen regularly: Early detection through screenings improves treatment outcomes.
Vaccination: Protect against cancers caused by viral infections (e.g., HPV).
Genetic testing: For individuals with family histories of cancer, plan ahead with screening and potentially prophylactic surgery.