Radiation and Cancer Quiz
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Questions and Answers

Which type of cancer is primarily associated with ultraviolet radiation exposure?

  • Multiple myeloma
  • Basal cell carcinoma (correct)
  • Cervical cancer
  • Glioma

    • What is a known effect of ionizing radiation?

  • Eliminates chromosomal aberrations
  • Alters immune system cells (correct)
  • Causes glioma exclusively
  • Cures skin cancer

    • Which virus is linked to cervical cancer?

  • Epstein-Barr virus
  • Helicobacter pylori
  • Human papillomavirus (HPV) (correct)
  • Hepatitis B virus

    • What type of radiation includes microwaves and radar?

    <p>Electromagnetic radiation</p> Signup and view all the answers

    Which of the following is a long-term risk of ionizing radiation exposure?

    <p>Higher likelihood of leukemia</p> Signup and view all the answers

    Which cancer is associated with Helicobacter pylori infection?

    <p>Stomach cancer</p> Signup and view all the answers

    What is the primary source of ultraviolet radiation?

    <p>Sunlight</p> Signup and view all the answers

    Which virus is linked to both leukemia and lymphoma?

    <p>Human T-cell lymphotropic virus type 1</p> Signup and view all the answers

    Which type of cancer is most directly associated with tobacco use?

    <p>Esophageal cancer</p> Signup and view all the answers

    What is the primary substance involved in the activation of xenobiotic chemicals?

    <p>Cytochrome P-450 family</p> Signup and view all the answers

    Which dietary component is known to improve DNA repair?

    <p>Supplemental coenzyme Q10</p> Signup and view all the answers

    How does obesity contribute to cancer risk?

    <p>By producing hyperinsulinemia</p> Signup and view all the answers

    Which cancers are associated with higher body mass index (BMI)?

    <p>Endometrial and colorectal cancers</p> Signup and view all the answers

    What role do glutathione-S-transferases (GSTs) play in cancer risk?

    <p>They metabolize environmental carcinogens</p> Signup and view all the answers

    Which food items are described as primary dietary donors of DNA methylation?

    <p>Folate, choline, and B vitamins</p> Signup and view all the answers

    In terms of diet, which factor could suppress cancer stem cell renewal?

    <p>Altered micro-ribonucleic acid (miRNA)</p> Signup and view all the answers

    What type of mutation is referred to as a 'driver mutation'?

    <p>A mutation that contributes to the progression of cancer.</p> Signup and view all the answers

    What is the result of gene amplification?

    <p>Repeated duplication of a chromosome resulting in increased gene copies.</p> Signup and view all the answers

    What characterizes chromosome translocation?

    <p>The movement of a gene segment from one chromosome to another.</p> Signup and view all the answers

    What process describes the change of a normal cell into a cancer cell?

    <p>Malignant transformation.</p> Signup and view all the answers

    How does cancer heterogeneity arise?

    <p>Due to clonal proliferation and mutation variability.</p> Signup and view all the answers

    Which of the following best describes the concept of clonal proliferation?

    <p>Accumulation of cancer cell progeny outpacing nonmutant cells.</p> Signup and view all the answers

    What are epigenetic changes in cancer biology?

    <p>Alterations in gene function that do not involve changes in the DNA sequence.</p> Signup and view all the answers

    Which statement best reflects the relationship between cancer development and wound healing?

    <p>Both processes involve similar biological mechanisms.</p> Signup and view all the answers

    Which HPV types are primarily responsible for the majority of cancers?

    <p>HPV types 16 and 18</p> Signup and view all the answers

    What is a common cancer associated with asbestos exposure?

    <p>Mesothelioma</p> Signup and view all the answers

    What role do tumor-suppressor genes play in cancer development?

    <p>Negatively regulate proliferation</p> Signup and view all the answers

    What is the result of activating proto-oncogenes?

    <p>Hyperactivity of growth-related gene products</p> Signup and view all the answers

    Which of the following chemicals is linked to bladder cancer?

    <p>Dyes and aromatic amines</p> Signup and view all the answers

    What is typically the result of mutations in tumor-suppressor genes?

    <p>Loss of inhibitory function</p> Signup and view all the answers

    What characteristic defines oncogenes?

    <p>Mutant genes that enhance growth</p> Signup and view all the answers

    Which types of cancer have been recently associated with HPV infections?

    <p>Oropharyngeal and throat cancers</p> Signup and view all the answers

    What role do caretaker genes play in the genome?

    <p>They are responsible for the maintenance of genomic integrity.</p> Signup and view all the answers

    What can result from the loss of function of caretaker genes?

    <p>Increased mutation rates.</p> Signup and view all the answers

    What is an example of a hereditary condition related to genomic instability?

    <p>Hereditary Nonpolyposis colorectal cancer.</p> Signup and view all the answers

    Which of the following can lead to genomic instability?

    <p>Mutations in caretaker genes.</p> Signup and view all the answers

    What process contributes to epigenetic silencing in gene expression?

    <p>DNA methylation.</p> Signup and view all the answers

    What are oncomirs?

    <p>miRs that stimulate cancer development.</p> Signup and view all the answers

    How do mutations in caretaker genes affect cancer transmission in families?

    <p>They increase the risk of specific cancers being passed down.</p> Signup and view all the answers

    What is a potential consequence of gene expression alterations due to changes in miRNAs?

    <p>Higher risk of cancer development.</p> Signup and view all the answers

    Which of the following is NOT a cause of fatigue in cancer patients?

    <p>Increased physical activity</p> Signup and view all the answers

    What is the primary consequence of cachexia in cancer patients?

    <p>Protein-calorie malnutrition</p> Signup and view all the answers

    Which symptom is associated with gastrointestinal complications from cancer treatment?

    <p>Malabsorption</p> Signup and view all the answers

    Which type of hair loss is commonly experienced by cancer patients undergoing treatment?

    <p>Alopecia</p> Signup and view all the answers

    What is a major risk factor for infections in cancer patients?

    <p>Immunosuppression</p> Signup and view all the answers

    What strategies might be employed to address infertility caused by cancer treatments?

    <p>Freezing eggs or embryos</p> Signup and view all the answers

    Which symptom is NOT typically associated with cachexia?

    <p>Increased energy levels</p> Signup and view all the answers

    What are the possible consequences of inadequate wound care in cancer patients?

    <p>Increased nosocomial infections</p> Signup and view all the answers

    Study Notes

    Cancer Pathophysiology

    • Cancer is derived from the Greek word for "crab" - karkinoma.
    • Cancer is another name for a malignant tumor.
    • A tumor is not a cancer.
    • Cancer is an abnormal growth resulting from uncontrolled proliferation, serving no physiologic function.
    • It is also referred to as a neoplasm: New growth.

    Benign vs. Malignant Tumors

    • Benign:
      • Slow growth
      • Well-defined capsule
      • Not invasive
      • Well differentiated
      • Low mitotic index
      • Does not metastasize
    • Malignant:
      • Rapid growth
      • Not encapsulated
      • Invasive
      • Poorly differentiated: Anaplasia
      • High mitotic index
      • Can spread distantly (metastasis)

    Classification and Nomenclature

    • Benign tumors: Named according to the tissue of origin.
      • Lipoma: Fat
      • Leiomyoma: Smooth muscle
      • Colonic or Gastric polyps: colon or stomach
      • Nevi: Melanocytes
    • Malignant tumors: Named according to the tissue of origin.
      • Carcinomas: Malignant epithelial tumors (ducts or glands)
      • Adenocarcinoma: A type of carcinoma.
      • Sarcomas: Malignant connective tissue tumors
      • Lymphomas: Cancers of lymphatic tissue
      • Leukemias: Cancers of blood-forming cells
    • Carcinoma in situ (CIS):
      • Preinvasive epithelial malignant tumors.
      • Have not broken through the basement membrane.
      • Are not malignant.
      • Three possible prognoses:
        • Can remain stable.
        • Can progress to invasive cancer.
        • Can regress and disappear.

    Biology of Cancer Cells

    • Cancer is predominantly a disease of aging.
    • Clonal proliferation or expansion occurs.
    • A mutation causes a cell to acquire advantageous characteristics over its neighbors.
      • Increased growth rate or decreased apoptosis
    • Cancer development requires multiple mutations.

    Biology of Cancer Cells (Continued)

    • Mutation: Alteration in DNA sequence.
      • Point mutations: Small-scale changes
      • Driver mutations: Drive cancer progression
      • Passenger mutations: Random events
    • Gene amplification: Repeated duplication of chromosomes.
      • 10s or 100s of gene copies are made.
    • Epigenetic changes: DNA methylation, histone acetylation, or altered expression of non-coding RNA.
    • Chromosome translocations: Large changes in chromosome structure.
      • Piece of one chromosome is moved to another.
        • Burkitt's Lymphoma - t(8:14)
        • Chronic Myeloid Leukemia - Philadelphia Chromosome - t(9:22)
    • Malignant transformation: Normal cell becomes a cancer cell.
      • Heterogeneous mixture of cancer cells
      • Stroma: Tumor microenvironment
    • Cancer development is similar to wound healing.

    Genetics, Epigenetics, and Tissue

    • Environmental-lifestyle behaviors and genetic factors contribute to cancers.
    • Cancer is driven by genetic alterations and changes in epigenetic regulation.
    • Cancer development involves tissue microenvironment or stroma.
    • Immune cells cause chronic inflammation leading to tumor progression.

    Genetics, Epigenetics, and Tissue (Continued)

    • Epigenetic processes influence cancer initiation, progression, and treatment.
    • Factors influencing cancer risk:
      • Detoxifying enzymes
      • DNA repair genes
      • Immune/inflammatory systems
      • Cell's immediate environment
      • Metabolic/hormonal factors
    • Key associations and causes of cancer include:
      • Tobacco, alcohol
      • Sun exposure
      • Reproduction
      • Occupational hazards
      • Ionizing radiation
      • Infections
      • Post-menopause
      • Lack of physical exercise
      • Overweight
      • Indoor and outdoor air pollution
      • Lack of fruit & vegetables
      • Processed/red meat
      • Lack of fiber
      • Hyperglycemia/Hyperinsulinemia, diabetes
    • Overall cancer rates are higher in men than women.
    • Highest cancer rates are in Denmark.
    • Decline in lung cancer correlates to decrease in tobacco use.
    • Cancer rates increased for ages 0-19.
    • Cancer deaths have decreased in men, women, and children.
    • Liver cancer is the most predominant cancer in mortality rates.
    • Male liver cancer mortality is more than double the rate for women.

    In Utero and Early Life Conditions

    • Conditions increasing cancer susceptibility include:
      • Prenatal and early life exposure
      • Parental exposures before conception
      • Nutrition
      • DES exposure
    • Gene and environment interactions
      • Developmental plasticity: Degree to which development is contingent on its environment.
    • Reduce risk by starting early
      • Avoid peak sun hours, cover skin
      • Increase physical exercise
      • Avoid high-risk sexual practices

    Environmental-Lifestyle Factors

    • Tobacco use: Carcinogenic and the most important risk factor.

      • Linked to various cancers (lung, mouth, larynx, etc.).
      • Secondhand smoke (ETS) increases lung cancer risk.

    • Alcohol consumption:

      • Classified as a carcinogen.
      • Increases risk of oral cavity, throat, esophageal, liver, colorectal, and breast cancers.
      • Combined with smoking increases risk of malignant tumors.

    • Diet:

      • Nutrigenomics: Study of nutrition on individual variability based on genomic differences.
      • Primary dietary donors: Folate, choline, B vitamins
      • Altered miRNA: Predisposes to cancer
      • Suppresses cancer stem cell renewal: Decreases cancer risk.
      • Consuming kiwi, cooked carrots, or supplemental coenzyme Q10 improves DNA repair.
      • Decrease cancer risk.

    • Xenobiotic chemicals (diet cont.):

    • Toxic, mutagenic, carcinogenic chemicals in food.

    • Activated by phase 1 activation enzymes.

    • Primary substance: Cytochrome P-450 family

    • Defense mechanisms: Phase II detoxification enzymes (liver) and antioxidants

    • Glutathione-S-transferases (GSTs) metabolize environmental carcinogens and ROS.

    • High consumption of red meats & processed meats increase colorectal cancer risk.

    • Obesity:

      • Associated with endometrial, colorectal, kidney, esophageal, breast (postmenopausal), pancreatic, and other cancers.
      • Correlates to body mass index (BMI)
      • Energy expenditure involves resting metabolic rate, thermic food effects, and physical activity
      • Can cause a poorer outcome for some cancers. Increased insulin resistance → hyperinsulinemia. Insulin↑ promotes insulin-like growth factor 1. Adipose tissue secretes adipokines. Circadian disruptions may affect cancer growth.

    • Air pollution: Linked to lung cancer.

      • Outdoor pollution (smog, particles): Increases daily mortality, inflammation, oxidative stress
      • Indoor pollution (e.g., cigarette smoke): Worse than outdoor, associated with lung cancer.

    • Ionizing radiation:

      • Emitted from x-rays, radioisotopes, radioactive sources.
      • Associated with acute leukemias; increased thyroid and breast carcinomas
      • Enters cells and randomly deposits energy in tissues.

    • Ultraviolet radiation: Causes basal cell carcinoma, squamous cell carcinoma, and melanoma. Major skin cancers. Main source is sunlight.

    • Infections contribute to cancer development include:

      • Human papillomavirus (HPV): Cervical cancer
      • Hepatitis B and C: Liver cancer
      • Helicobacter pylori: Stomach cancers
      • Epstein-Barr virus (EBV): Nasopharynx, stomach cancers; Hodgkin and non-Hodgkin lymphoma
      • Human herpes virus type 8: Kaposi sarcoma
      • Human T-cell lymphotropic virus type 1: Leukemia and lymphoma

    • Sexual and reproductive behaviors and HPVs:

      • HPV is the most common sexually transmitted virus. Types 16 and 18 cause most cancers.
      • Associated with cervical, anal, vaginal, vulvar, and penile cancers.
      • Recently associated with oropharynx cancers. HPV infects epithelial cells. Mutations lead to cancer.

    • Chemicals and occupational hazards: Substantial number of occupational carcinogens exist.

    Oncogenes and Tumor-Suppressor Genes

    • Three key genetic mechanisms in human carcinogenesis.
      • Activation of proto-oncogenes resulting in hyperactivity of growth related gene products (oncogenes).
      • Mutation inactivation of gene products that would normally inhibit growth (tumor suppressor genes).
    • Mutation inactivation of genes that prevent normal cell death or apoptosis(apoptosis)

    Oncogenes and Tumor-Suppressor Genes (Continued)

    • Oncogenes: Normal nonmutant genes coding for cellular growth. Mutated genes direct protein synthesis and cellular growth.
    • Tumor-suppressor genes: Encode proteins that negatively regulate proliferation in their normal state. Also known as anti-oncogenes.

    Hallmarks of Cancer

    • Genomic instability (mutator phenotype)
    • Enabling replicative immortality
    • Tumor-promoting inflammation
    • Avoiding immune destruction
    • Deregulatory cellular energetics
    • Inducing angiogenesis
    • Activating invasion and metastasis

    Sustained Proliferative Signaling

    • Increased growth factor receptors
    • Mutation of the signal from cell surface receptor.
      • Ras intracellular signaling protein
      • Activation of protein kinases for cell cycle Single genetic event for oncogene activation.
    • Point mutations -e.g. RAS
    • Chromosomal translocations -e.g. BCR:ABL
    • Gene amplifications -e.g. N-myc

    Evading Growth Suppressors

    • Two gene mutations to allow cancer to occur.
    • Mutation in RB (retinoblastoma) gene; leads to persistent cell growth.
      • Loss of RB function with hyperphosphorylation.
    • Mutation in the TP53 gene (tumor-suppressor gene); suppressing normal apoptosis.
    • Monitors intracellular signals to induce stress-activated kinases, activating caretaker genes.

    Caretaker Genes

    • Responsible for maintaining genomic integrity.
    • Encode proteins for repairing damaged DNA.
    • Loss of function results in increased mutation rates.

    Genomic Instability

    • Increased tendency for alterations in the genome.
    • Mutations protect genome and DNA repair, increasing instability and cancer risk.
      • Hereditary Nonpolyposis colorectal cancer (HNPCC)-DNA base pair mismatch repair defect.
    • Epigenetic silencing (DNA methylation, histone modifications) leads to gene function changes.
    • Altered gene expression.

    Genomic Instability (Continued)

    • Gene expression networks regulated by miRNA.
    • Oncomirs stimulate cancer development.
    • Chromosome instability in malignant cells.

    Genomic Instability (Continued)

    • Chromosome instability (CIN) may be increased in malignant cells.
      • Caused by malfunctions in the cellular machinery that regulate chromosomal segregation at mitosis.
    • Results in a high rate of chromosomal loss and heterozygosity, and chromosomal amplification. These events accelerate the loss of tumor suppressor genes, and overexpression of oncogenes.

    Angiogenesis

    • Growth of new blood vessels.
    • Neovascularization: New blood vessels form.
    • Essential for the growth and spread of cancer.
    • Advanced cancers secrete angiogenic factors to feed the tumor.
      • Vascular endothelial growth factor (VEGF) – induced by oxygen sensitive HIF1alpha
      • Basic fibroblast growth factor (bFGF).

    Reprogramming Energy Metabolism (Cancer Metabolism)

    • Allows use of lactate and its metabolites for the efficient production of lipids and other molecular building blocks.
    • This process is activated by oncogene overexpression or loss-of-function of the tumor suppressor gene.
    • Reverse Warburg effect: Cancer cells produce large amounts of ATP.
      • CAFs using aerobic glycolysis to secrete metabolites cancer cells can use in OXPHOS to produce ATP.
      • Autophagy of CAFs to provide materials needed for new organelles.

    Resisting Cell Death

    • Apoptosis occurs as a mechanism for tissue remodeling, and as protection during aberrant cell growth.
    • Extrinsic and intrinsic pathways trigger apoptosis.
      • Both pathways are often dysregulated in cancer cells.
    • Most common loss-of-function mutation in cancer cells is TP53 leading to imbalance between pro- and anti-apoptotic molecules.
      • Expression of Bcl-2 in B-cell lymphomas.
    • Down-regulation of caspases.

    Inflammation as a Cause for Cancer

    • Chronic inflammation is an important factor in cancer development.
    • Active inflammation increases susceptibility to cancer by stimulating wound healing.
      • Including cell proliferation and blood vessel growth.
    • Causes include solar radiation, asbestos, pancreatitis and infection.
    • Susceptible organs: Gastrointestinal tract, pancreas, thyroid gland, prostate, urinary bladder, pleura and skin.

    Inflammation as a Cause of Cancer (Continued)

    • Examples of inflammation and cancer linked include:
      • Ulcerative colitis for 10+ years, 30-fold increased risk of colon cancer.
      • HBV and HCV increase liver cancer.
      • H. pylori increases stomach cancer risk.
    • Tumor-associated macrophages (TAMs) are key for tumor survival.
      • Block cytotoxic T cells and NK cells
      • Produce advantageous cytokines promoting tumor growth.
      • Secrete angiogenesis factors, further boosting tumor progression.

    Evading Immune Destruction

    • Tumor cells avoid immune systems, as antigens form oncogenes, antigens form oncogenic viruses, oncofetal antigens and altered glycoproteins.
    • Immune surveillance hypothesis: The immune system successfully suppresses most developing malignancies.
    • Immunotherapy hypothesis: Immune system used to target tumor-associated antigens; leading to tumor destruction clinically.

    Immune System & Viral-Associated Cancers

    • Immunotherapy = Active or Passive.
      • Active: Immunization with tumor antigens to boost immune response towards a particular cancer type.
      • Passive: Injecting a patient with antibodies or lymphocytes directed against tumor antigens.
    • Examples of cancers associated with viruses include:
      • HPV (16, 18, 35, 41) – cervical cancer
      • EBV (Epstein-Barr virus) – Burkitt's lymphoma (t(8:14)), nasopharynx, and stomach cancers.
      • Kaposi sarcoma herpesvirus (KSHV or HHV8) - skin and mucosal surfaces (lungs, nasal and oral cavities).
      • HTLV-1- Adult T-cell Leukemia.
      • HBV, HCV - liver cancers.
    • Tumor-infiltrating lymphocytes (T-reg cells) and decreased natural killer cells prevent the immune response from being destructive to the tumor.

    Invasion and Metastasis

    • Metastasis = Spread of cancer cells from the original site.

    • Spread involves the following steps:

      • Survive
      • Proliferate
      • Spread to distant locations (using lymph vessels, blood stream, or other pathways).

    • Epithelial-mesenchymal transition (EMT): Many epithelial-like characteristics of cancer cells are lost during metastasis

      • Migratory capacity of cancer cells increases.
      • Resistance to apoptotic cell death increases.
      • Dedifferentiation into a stem cell-like state improves cancer cell growth, survival in foreign microenvironments, and creation of metastatic disease.

    • Invasion: Local spread as a prerequisite for metastasis. Cancer frequently spreads first to regional lymph nodes (lymphatic system) and then to other distant organs via blood vessels.

    • Cancer invasion requires the cancer cells to survive while they attach to specific receptors in the new environment.

    • Cancer cells (via TAMs and CAFs) secrete protease and protease activators. -Proteases digest ECM (extracellular matrix) and basement membranes to create pathways for cancer cell migration. -Metastatic cells need strength to withstand the pressures of travel/circulation (blood and lymphatic). -Cancer cells need platelets and clotting factors, and myeloid derived suppressor cells (MDSCs).

    • Metastatic cells need to survive in the new environment

    Clinical Manifestations of Cancer

    • Paraneoplastic syndromes: Symptom complexes are triggered by a cancer but are not by direct local effects. Causes include hormones, immune response. Can be life-threatening (e.g., Small Cell Lung Cancer – Cushing's disease).

    • Anemia: Due to factors like chronic bleeding, malnutrition, chemotherapy, or cancer in blood-forming organs. Examples include colorectal cancer or genitourinary cancers and iron malabsorption.

    • Bone Density Loss: Due to osteoporosis or osteopenia due to secondary hormone or steroid treatment.

    • Fatigue: Most frequent, persistent symptom with causes including sleep issues, chronic inflammation, anemia, depression, physical activity, nutritional status, and environmental factors.

    • Gastrointestinal Tract: Sensitivity to radiation and chemotherapy, as well as causing malabsorption, diarrhea, and infection risk.

    • Hair loss (alopecia) and skin: Temporary hair loss or skin breakdown and dryness, due to treatment side effects.

    • Cachexia: Most severe form of malnutrition or protein calorie malnutrition, due to wasting or progressive decline of body tissues and strength.

    • Infection: Can increase risk of complications and death (e.g., opportunistic infections due to chemotherapy/malignancy).

      • Risk increased related to immunosuppression (lymphopenia etc.)
      • Increased prevalence of nosocomial (hospital-acquired) infections.

    • Infertility: Risk increases secondary to cancer, treatments (surgery, radiation, chemotherapy).

      • Freezing of eggs or embryos can help preserve fertility.

    • Leukopenia and Thrombocytopenia: Low WBC count and platelet count due to chemotherapy; leading to possible hemorrhage.

      • Fluid accumulation in lymphatic system can result from damage (lymphedema). Can increase with progression of disease.
      • Nerve damage from complications with surgery, chemotherapy, or radiation therapy can result in chronic pain.

    • Diagnosing and staging: Assess tumor size, degree/extent of invasion, spread (stages 1-4). Use the World Health Organization TNM system for staging (T = tumor, N = Nodes, M = metastasis).

    Tumor Markers

    • Substances produced by benign or malignant cells.
    • Found in blood, spinal fluid, urine. Includes hormones, enzymes, genes, antigens, and antibodies, that can indicate disease progression.
    • Examples of tumor markers include alpha fetoprotein (AFP) and prostate-specific antigen (PSA).

    Tumor Markers (Continued)

    • Used for cancer screening
      • Identify individuals at high risk. Diagnose specific types of tumors. Monitor clinical cancer course and evaluate response to treatment

    Surgery

    • Definitive treatment of cancers confined to the surgical margins.
    • Palliative surgery may be performed to reduce symptom severity.
    • In some high-risk cases, surgery can be preventative.
    • Mutations of the APC gene almost certainly lead to colon cancer.
    • Women with BRCA1/2 mutations have an increased risk for breast and ovarian cancer.

    Radiation Therapy

    • Used to kill cancer cells, minimizing damage to normal tissues
      • Direct DNA damage with ionizing radiation Causes irreversible damage to normal cells Uses include: Brachytherapy (seeds implanted).

    Chemotherapy

    • Uses drugs to kill cancer cells or enable body's natural defenses to eliminate remaining cancer cells.
    • Types of chemotherapy include: single agent; combination
    • Treatment goals include: induction chemotherapy, adjuvant chemotherapy, or neoadjuvant chemotherapy.
      • Induction: Shrink or destroy tumors.
      • Adjuvant: Eliminate micrometastases.
      • Neoadjuvant: Administered before localized treatment.

    Cell Cycle-Specific Drugs

    • These drugs target specific phases of the cell cycle, impacting rapidly-dividing cancer cells.
    • Include antibiotic, epipodophyllotoxin, camptothecin, and antimetabolites. -Most effective against cancers with high growth fraction (fast-growing cells).

    Cell Cycle Non-Specific Drugs

    • These drugs target DNA synthesis, but are not tied to a specific stage of cell cycle. -Examples include alkylating agents, nitrosoureas, antimetabolites, cisplatin, and dacarbazine.

    Immunotherapy

    • Immunomodulatory drugs targeting the immune system. -Examples of drugs include ipilimumab, nivolumab, pembrolizumab, atezolizumab
    • Immunomodulators include interferons, interleukins.
    • Example therapies include: Cancer vaccines, cell therapies (car-t), oncolytic viruses (e.g. oncolytic adenoviruses).

    Targeted Therapies

    • These therapies use medications to specifically target the underlying causes of cancer. Examples include: -CDKs (cyclin-dependent kinases) inhibitors; examples are abemaciclib, palbociclib, ribociclib. -PI3K inhibitors (for mutated or defective PI3K); examples are alpelisib, and others. -PARP (poly (ADP-ribose) polymerase) inhibitors for use in certain inherited cancers with germline BRCA1/2 mutations. Tyrosine kinase inhibitors: Examples include tucatinib for breast cancer. Immuno-checkpoint inhibitors to reduce immunosuppressive factors. Examples include atezolizumab.

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