Cancer Statistics 2024 Overview

Cancer Statistics

• Cancer Incidence: Number of new cancer cases in a specific population during a particular year, typically per 100,000 people.
• Projected 2024 new cases: ~2 million, higher than 2016's ~1.6 million
• 2024 Breakdown (approx):
  • 16% Breast Cancer
  • 15% Prostate Cancer
  • 12% Lung & Bronchus Cancer
  • 8% Colon & Rectum Cancer
  • These four account for ~50% of new cases.
• Cancer Mortality: Number of cancer-related deaths in a specific year per 100,000.
• 2024 US Mortality: ~611,000 (similar to 2016's ~600,000), suggesting improved survival rates despite more new cases
• 2024 Breakdown (approx):
  • 20% Lung & Bronchus Cancer
  • 9% Colon & Rectum Cancer
  • 8% Pancreatic Cancer
  • 7% Breast Cancer
  • These four account for ~45% of cancer deaths.
• Cancer is the 2nd leading cause of death after cardiovascular diseases.
• ~18.1 million cancer survivors in 2022.

Cancer Incidence by Sex

• Breast cancer more prevalent in females.
• Prostate cancer specific to males.
• Lung & bronchus cancer remains a leading cause of death in both males and females.
• Colon & rectum cancer, melanoma are also significant.

Cancer Survival Trends

• Graph shows projected (red) vs. actual (blue) cancer deaths from 1975-2020; the difference illustrates reduced cancer deaths due to research since the 1980s.
• Significant improvement in 5-year survival rates from 1970-1977 to 2007-2013.
• 5-year survival rate: Percentage of patients who survive for 5 years after diagnosis.
• High survival rates for breast, melanoma, and prostate cancer (80-100%), but lung and pancreatic cancer survival rates remain low (single digits for pancreatic).
• 2018-2022: 16 of 19 common cancers in men and 16 of 20 in women showed lower death rates; a slight decrease in lung cancer, but increased pancreatic cancer.

Cell Growth Regulation and Dysregulation

What is Cancer?

• Uncontrolled proliferation of transformed cells.
• Proliferation: rapid growth.
• Transformation: change from normal to abnormal cell.
• Initiators and promoters (genetic, biological, chemical, physical) cause normal cells to transform into abnormal cells.
• Abnormal cells lose growth control; develop into benign or malignant tumors.

Benign vs. Malignant Tumors

• Benign: Normal but have lost growth control, remain localized, usually harmless.
• Malignant (Cancer): Abnormal cells with uncontrolled growth. Metastasize (spread) to secondary locations. Often causes death as cancer cells disrupt function of secondary tissue.

Cancer Diagnosis and Treatment

• Cancer diagnosis often occurs too late for optimal intervention.
• Treatments include chemotherapy, surgery, targeted therapy, and immunotherapy.

Cell Cycle Regulation

• Cell Cycle Phases:
  • G1: Cell growth, protein synthesis, nutrient acquisition.
  • S: DNA replication.
  • G2: DNA quality control.
  • M: Cell division (mitosis).
• Checkpoints: Control points for DNA damage, cell size, nutrient availability (G1), DNA replication integrity (G2), spindle attachment (M).
• Cell Cycle Regulators:
  • Cyclins: proteins synthesized in specific phases to drive the cell cycle.
  • CDKs: constant (inactive) until paired with appropriate cyclin for activation and phosphorylation of targeted proteins.

Cell Growth and Differentiation

• Mammalian development from fertilized eggs (stem cells). Differentiate into specialized cells (e.g., hepatocytes, neurons).
• Fully differentiated cells, like hepatocytes, have lost proliferation ability.
• Benign tumors less proliferative, stay in place; malignant tumors like cancer cells are stem-like, more proliferative, and resemble progenitor cells.

Cancer Risk Factors

• Genetic:
  • Oncogenes (e.g., RAS): Mutated proto-oncogenes promoting uncontrollable growth.
  • Tumor Suppressor Genes (e.g., Rb, p53): Prevent uncontrolled division of cells with damaged DNA; mutations lead to abnormal growth.
• Biological (e.g., Viruses):
  • HPV (Human Papillomavirus): DNA virus linked to cervical and other cancers. E7 and E6 proteins disrupt cell cycle and inhibit DNA damage responses.
• Physical (e.g., Radiation): UV and ionizing radiation damage DNA potentially leading to tumor formation.
• Chemical: Carcinogens form covalent adducts with DNA causing mutations; direct or indirect action.

Key Examples of Genetic Risk Factors

• RAS gene: Proto-oncogene, small G protein involved in signaling pathways. Mutations lead to constitutively active RAS, driving cell growth.
• Rb gene: Tumor suppressor, regulates G1 to S phase transition. Loss-of-function mutations lead to uncontrolled cell division.
• p53 gene: Tumor suppressor, “guardian of the genome.” Responds to DNA damage and either repair or apoptosis. Mutations hamper this function causing uncontrolled growth.