Chemotherapy

 

 

Biotherapy

Biotherapy is also called:

  • Immunotherapy
  • Biological therapy
  • Biological response modifier therapy

These treatments try to use the body's immune system, either directly or indirectly, to destroy the cancer cells and alleviate some of the side effects secondary to chemotherapy.

 

History of Biotherapy

  • Early in the 20th century, Dr. William B. Coley observed that patients who suffered severe infections after surgery to remove a malignancy seemed to have longer tumour-free intervals.
  • He went on to use bacterial toxins to induce an immune response  in patients with the hope of reducing tumour burden.
  • 1950s theory of immune surveillance: tumour cells express abnormal tumour antigens on their surfaces that can be recognized and destroyed by the immune system.
  • Early 1970s discovery of recombinant DNA and development of hybridoma technology
  • Recombinant DNA technology allows for the production of large quantities of purified proteins by placing human genes inside bacteria or yeast cells.

 

Mechanism of Action:

  • Augment, modulate, or restore the host’s immune responses
  • Direct anti-tumour effect
    • Cytotoxic - immune system recognizes surface antigens (or markers) on cancer cells.
    • Anti-proliferation mechanism
    • Affects differentiation/maturation of tumor cells
    • Prevent metastasis
  • Other biological effects (including supportive treatment).

 

Drug Classification

Mechanism of Action

Interferons
  • Modulates immune response and has direct antitumour activity
  • Slows tumour cell growth
  • Antiviral

Interleukins
  • Stimulate growth of early bone marrow precursors
  • Augment T-cell cytotoxicity and B-cell differentiation

Monoclonal antibodies
  • Very specific immunoglobulins produced from a single clone
  • Recognize and react with tumour associated antigens on the surface of cells

Hematopoietic Growth Factors
  • Stimulate or regulate hematopoiesis
  • Used primarily to expedite bone marrow recovery following chemotherapy

 

Toxicities

  • Capillary–leak syndrome
  • Flu-like syndrome/fever/chills/bone pain
  • Dependent on agent and dose

 

Interferons

Normal cells will produce interferons which can damage cancer cells and prevent their spread and growth.

AGENT CLINICAL USE

Alpha Interferon (a-IFN)

  • Modulate immune responses
  • Used in the treatment of some forms of adult cancer such as hairy cell leukemia, AIDs related Kaposi's sarcoma and melanoma.

 

 

Interleukins

  • Hormone-like substance produced by certain normal blood cells.
  • Stimulate the immune system.
  • Regulate inflammatory and immune responses.
  • Dependent on agent and dose

AGENT CLINICAL USE
Interleukin-2 (IL-2)
  • Supports growth/maturation of T-cells
  • Enhances T-cell function and Natural Killer (NK) cell function.
  • Can be effective for melanoma if given with lymphocytes treated with IL-2.

Major toxicities include

  • Capillary–leak syndrome
  • Flu-like syndrome/fever/chills/bone pain

 

Monoclonal Antibodies/Targeted Therapy

Use the development of specific antibodies (protein molecules produced by B cells as a primary immune defense), which are directed against antigens (substances that are capable of inducing a specific immune response) located on the surface of tumor cells.

See Targeted Therapy

      AGENT CLINICAL USE
      Monoclonal Antibodies Cause cell death through interaction with immune responses/recognize tumor-associated antigens

     

Hematopoietic Growth Factors (HGFs).

  • Support hematopoietic (blood cell) colony formation in vitro.
  • Includes erythropoietin, interleukin-3 and colony-stimulating factors (CSFs).

 

      AGENT CLINICAL USE
      Granulocyte-colony stimulating factor (G-CSF)

      Stimulates proliferation/ differentiation of neutrophils

      Granulocyte-macrophage colony stimulating factor (GM-CSF) Enhances function of granulocyte and macrophage lineages
      Erythropoietin (EPO) Stimulates production/differentiation of RBCs (erythrocytes).

 

 

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