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Title: CANCER CHEMOTHERAPY (1)


1
CANCER CHEMOTHERAPY
2
Introduction
  • Cancer is a group of diseases in which there is
    uncontrolled multiplication and spread within the
    body of abnormal forms of the body's own cells,
    OR
  • A group of diseases that occur when malignant
    forms of abnormal cell growth develop in one or
    more body organs.
  • These cancer cells continue to divide to produce
    tumors

3
Tumors can be benign or malignant
4
  • Both benign and malignant tumours manifest
    uncontrolled proliferation.
  • The appearance of these abnormal characteristics
    reflects altered patterns of gene expression in
    the cancer cells, resulting from genetic
    mutations.

5
The pathogenesis of cancer.
6
Cont
  • Cancer cells manifest, to varying degrees
  • Four characteristics that distinguish them from
    normal cells
  • Uncontrolled proliferation,
  • Dedifferentiation and loss of function,
  • Invasiveness,
  • Metastasis.

7
The genesis of a cancer cell
  • A normal cell turns into a cancer cell because of
    one or more mutations in its DNA, which can be
    inherited or acquired.
  • The development of cancer is a complex multistage
    process, involving not only more than one genetic
    change but also other epigenetic factors
    (hormonal action, co-carcinogen and tumor
    promoter effects, etc)

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Cont.
  • There are two main categories of genetic change
    that lead to cancer
  • The activation of proto-oncogenes to oncogenes
  • 2. The inactivation of tumor suppressor genes

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Activation of proto-oncogenes to oncogenes
  • Proto-oncogenes are genes that normally control
  • cell division,
  • apoptosis
  • differentiation
  • But can be converted to oncogenes by viral or
    carcinogen action.

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Inactivation of tumor suppressor genes (TSG)
  • Normal cells contain tumor suppressor genes
    (anti-oncogenes) eg p53
  • TSG have the ability to suppress malignant
    changes
  • The loss of function of tumor suppressor genes
    can be the critical event in carcinogenesis

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The special characteristics of cancer cells
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Cancer treatment strategies
  • Cancer treatment strategies includes
  • 1. Goals of treatment
  • 2. Indication for treatment
  • 3. Tumor susceptibility and the growth cycle

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1. Goals of treatment
  • (A) The ultimate goal of cancer treatment is a
    CURE (Eradication of every neoplastic cells). If
    cure is not attainable, then the goal became
  • (B) CONTROL OF THE DISEASE (stop the cancer from
    enlarging and spreading) to extent survival and
    QoL of the patient.

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  • At this step, the cancer being treated as a
    chronic disease. The neoplastic cell burden is
    initially reduced (debulked), either by surgery
    and / or by radiation followed by chemotherapy,
    immunotherapy, or combination of these treatment
    modalities.
  • (C) In advanced stages of cancer, the likelihood
    of controlling the cancer is far from reality and
    the goal become PALLIATION (alleviation of
    symptoms)

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2. Indications for treatment
  • Treatment modalities depend on the extent of the
    cancer
  • For Localized cancer is mainly treated by surgery
  • For Loco-regional disease by radiotherapy
  • For widespread disease by chemotherapy, hormonal
    therapy, or biological therapy

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Indications for chemotherapy
  • Chemotherapy indicated when neoplasms are
    disseminated and are not responsive to surgery
  • Treatment modality with chemotherapy may be
  • Adjuvant chemotherapy
  • Neoadjuvant chemotherapy
  • Maintenance chemotherapy
  • Induction chemotherapy

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  • Adjuvant chemotherapy - Chemo is used as
    supplemental treatment to attack micrometastases
    following surgery radiation

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  • Neoadjuvant chemotherapy Chemotherapy given
    prior to the surgical procedure in an attempt to
    shrink the tumor
  • Induction chemotherapy is chemotherapy given
    before the initiation of another treatment (eg
    radiation, surgery, chemoradiation etc)
  • Maintenance chemotherapy Chemotherapy given in
    lower doses to assist in prolonging a remission

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3. Tumor susceptibility and the growth cycle
  • The fraction of tumor cells that are in the
    replicative cycle (growth fraction) influences
    their susceptibility to most cancer
    chemotherapeutic agents
  • Rapidly dividing cells are generally more
    sensitive to anticancer drugs while slowly
    proliferating cells are less sensitive to
    chemotherapy

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  • In general, nonproliferating cells (those in G0
    phase) usually survive the toxic effects of many
    anticancer drugs

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Treatment protocols
  • Combination-drug chemotherapy is more successful
    than single-drug treatment in most of the cancer
  • Combined drugs should be based on
  • Qualitatively different toxicities
  • Different mechanism of action
  • Different molecular sites of action

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  • Advantage of drug combination
  • Provide maximal cell killing within the range of
    tolerated toxicity
  • Are effective against a broader range of cell
    lines in the heterogeneous tumor population
  • May delay of prevent the development of resistant
    cell lines .

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  • Many cancer treatment protocols have been
    developed
  • Each one is applicable to a particular neoplastic
    state
  • They are usually identified by an acronym
  • For example a common regimen called POMP, used
    for treatment of ALL consists of Prednisone,
    Oncovin (vincristine), Methotrexate, and
    Purinethol (mercaptopurine)
  • Therapy is scheduled intermittently (appr 21 days
    apart) to allow recovery of patients immune
    system.

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Problems associated with Chemo.
  • Narrow therapeutic index (highly toxic)
  • Resistant of tumor cells to anticancer agents
  • Multidrug resistance (MDR) eg P-gp
  • Treatment induced tumors

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Treatment approaches
  • Main approaches in cancer treatment
  • Surgery
  • Radiation
  • Chemotherapy
  • Immunotherapy
  • Targeted therapy
  • The role of each of these depends on the type of
    tumor and the stage of its development.
  • Chemotherapy can be used on its own or as an
    adjunct to other forms of therapy

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  • Chemotherapy of cancer, as compared with that of
    bacterial disease, presents a difficult problem.
  • In biochemical terms, microorganisms are both
    quantitatively and qualitatively different from
    human cells
  • However cancer cells and normal cells are so
    similar in many respects that it is more
    difficult to find general, exploitable,
    biochemical differences between them.

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General principles of action of cytotoxic
anticancer drugs
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  • One of the major difficulties in the use of
    cancer chemotherapy is that a tumor is usually
    far advanced before it is diagnosed.
  • Most currently used anticancer drugs, in
    particular those which are 'cytotoxic', affect
    only one characteristics of cancer cells i.e
    uncontrolled proliferation

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  • Thus, they are antiproliferative
  • They have no specific inhibitory effect on
  • Invasiveness,
  • Loss of differentiation or
  • The tendency to metastasize

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  • For many, their antiproliferative action results
    mainly from an action during S phase of the cell
    cycle, and the resultant damage to DNA initiates
    apoptosis
  • Furthermore, because their main effect is on cell
    division, they will affect all rapidly dividing
    normal tissues and thus they are likely to
    produce, to a greater or lesser extent, the
    following general toxic effects

34
Cont
  • Bone marrow toxicity (myelosuppression) with
    decreased leucocyte production and thus decreased
    resistance to infection
  • Impaired wound healing
  • Loss of hair (alopecia)
  • Damage to gastrointestinal epithelium
  • Depression of growth in children
  • Sterility
  • Teratogenicity

35
Cont
  • They can also, in certain circumstances, be
    carcinogenic (i.e. they may themselves cause
    cancer).
  • In addition, if there is rapid cell destruction
    with extensive purine catabolism, urates may
    precipitate in the renal tubules and cause kidney
    damage.

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  • Finally, virtually all cytotoxic drugs produce
    severe nausea vomiting, which has been called
    'the inbuilt deterrent' to patient compliance in
    completing a course of treatment with these
    agents.
  • Some compounds have particular toxic effects that
    are specific for them.

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Cell cycle and action of chemotherapeutic drugs
38
Cont.
  • Many chemotherapeutic drugs inhibit progression
    of cell cycle.
  • An understanding of cell cycle kinetics is
    essential for the proper use of anticancer drugs.
  • The cell division cycle is the fundamental
    mechanism to maintain tissue homeostasis.
  • The cell cycle can be divided into 4 phases

39
Cell cycle phases
  • (1) Growth phase 1 (G1- phase) a phase that
    precedes DNA synthesis
  • (2) Synthesis phase (S-Phase) a DNA synthesis
    phase
  • (3) growth phase 2 (G2-phase) an interval
    following the termination of DNA synthesis
  • (4) mitotic phase (M phase) the phase in which
    the cell, containing a double complement of DNA,
    divides into two daughter G1 cells.

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Cont,,,
  • Each of these daughter cells may immediately
    re-enter the cell cycle or pass into a
    nonproliferative stage, referred to as G0.
  • Chemotherapeutic drugs can be divided into three
    classes based on their relationship with cell
    cycle
  • 1. Cell cycle specific
  • 2. Cell cycle non-specific
  • 3. Non-cell cycle active e.g. hormones.
  •  

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Characteristics of chemotherapeutic drugs
  • Most anticancer drugs are cytotoxic agents that
    inhibit the synthesis of new genetic material or
    cause irreparable damage to DNA itself.
  • Anticancer drugs often have a narrower
    therapeutic index and a greater potential for
    causing harmful side effects than other drugs.

44
Cont.
  • Anticancer Drugs are most effective when used in
    combination.
  • Most of the side effects of anticancer drugs are
    manageable

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Anticancer drug classification
  • Cell cycle specific
  • Cell cycle non-specific
  • None cell cycle active (e.g Hormones)

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Target of anticancer agents
  • There are three targets associated with the use
    of the most commonly-used anticancer agents.
  • Damage the DNA of the affected cancer cells
  • Inhibit the synthesis of new DNA strands to stop
    the cell from replicating
  • Stop mitosis or the actual splitting of the
    original cell into two new cells.

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DRUGS USED IN CANCER CHEMOTHERAPY
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Outline of mechanism of action
  • 1. Cytotoxic drugs
  • Alkylating agents and related compounds- act by
    forming covalent bonds with DNA and thus impeding
    DNA replication
  • Examples of alkylating agents are

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  • Cisplatin
  • Oxaliplatin
  • Carboplatin
  • Chlorambucil
  • Cyclophosphamide
  • Mechlorethamine,
  • Melphalan
  • Carmustine
  • Busulphan
  • Decarbazine
  • Procarbazine

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  • Antimetabolites - block or subvert one or more of
    the metabolic pathways involved in DNA synthesis

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  • Cytotoxic antibiotics, i.e. substances of
    microbial origin that prevent mammalian cell
    division
  • Plant derivatives (vinca alkaloids, taxanes,
    campothecins) most of these specifically affect
    microtubule function and hence the formation of
    the mitotic spindle.

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  • 2. Hormones
  • The most important are steroids, namely
  • Glucocorticoids,
  • Estrogens
  • Androgens
  • Ddrugs that suppress hormone secretion or
    antagonize hormone action

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I. CYTOTOXIC DRUGS
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1. Alkylating agents and related compounds
  • Cross-link 2 strands of DNA leading to impairment
    of DNA replication and RNA transcription.
  • Their principal effect occurs during DNA
    synthesis the resulting DNA damage triggers
    apoptosis.
  • Unwanted effects include myelosuppression,
    sterility and risk of non-lymphocytic leukaemia

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  • The main alkylating agents are
  • Nitrogen mustards, e.g. cyclophosphamide
  • Cyclophosphamide is probably the most commonly
    used alkylating agent.
  • It is inactive until metabolised in the liver by
    the P450 mixed function oxidases
  • It has a pronounced effect on lymphocytes and can
    be used as an immunosuppressant

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Cont
  • It is usually given p.o or by I/V injection but
    may also be given by I/M
  • Important toxic effects are
  • nausea and vomiting,
  • bone marrow depression
  • haemorrhagic cystitis

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  • This last effect (which also occurs with the
    related drug ifosfamide) is caused by the
    metabolite acrolein and can be ameliorated by
    increasing fluid intake and administering
    compounds that are sulfhydryl donors, such as
    N-acetylcysteine or mesna (sodium-2-mercaptoethane
    sulfonate).
  • These agents interact specifically with acrolein,
    forming a non-toxic compound.

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  • Cyclophosphamide is activated to give
    aldophosphamide, which is then converted to
    phosphoramide mustard (the cytotoxic molecule)
    and acrolein (which causes bladder damage that
    can be ameliorated by mesna)
  • Cyclophosphamide myelosuppression affects
    particularly the lymphocytes.

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  • Nitrosoureas, e.g. Lomustine,
  • they are lipid soluble and can, therefore, cross
    the blood-brain barrier, may be used against
    tumors of the brain and meninges.
  • However, most nitrosoureas have a severe
    cumulative depressive effect on the bone marrow
    that starts 3-6 weeks after initiation of
    treatment.

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  • Busulphan
  • Busulphan has a selective effect on the bone
    marrow, depressing the formation of granulocytes
    and platelets in low dosage and red cells in
    higher dosage.
  • It has little or no effect on lymphoid tissue or
    the gastrointestinal tract.
  • It is used in chronic granulocytic leukemia.

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  • Cisplatin
  • Cisplatin is a water-soluble compound
  • Its action is analogous to that of the alkylating
    agents
  • Cisplatin is given by slow intravenous injection
    or infusion.
  • It is seriously nephrotoxic unless regimens of
    hydration and diuresis are instituted.
  • It has low myelotoxicity but causes very severe
    nausea and vomiting

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  • The 5-HT3-receptor antagonists (e.g. ondansetron,
    granisetron, dolasetron, and palonosetron are
    very effective in preventing this and have
    transformed cancer chemotherapy with cisplatin.
  • Tinnitus and hearing loss in the high frequency
    range may occur, as may peripheral neuropathies,
    hyperuricaemia and anaphylactic reactions
  • It has revolutionized the treatment of solid
    tumors of the testes and ovary.

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  • Carboplatin is a derivative of cisplatin.
  • It causes less nephrotoxicity, neurotoxicity and
    ototoxicity, and less severe nausea and vomiting
    than cisplatin, but is more myelotoxic.
  • Dacarbazine
  • Dacarbazine, a pro-drug, is activated in the
    liver, and the resulting compound is subsequently
    cleaved in the target cell to release an
    alkylating derivative.
  • Unwanted effects include myelotoxicity and severe
    nausea and vomiting.

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ii. Antimetabolites
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Folate antagonists
  • The main folate antagonist is methotrexate
  • it is one of the most widely used antimetabolites
    in cancer chemotherapy.
  • Methotrexate inhibits dihydrofolate reductase,
    preventing generation of tetrahydrofolate the
    main result is interference with thymidylate
    synthesis

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  • Methotrexate is usually given p.o but can also be
    given I/M, I/V or intrathecally.
  • The drug has low lipid solubility and thus does
    not readily cross the blood-brain barrier.
  • It is actively taken up into cells by the
    transport system used by folate and is
    metabolized to polyglutamate derivatives, which
    are retained in the cell for weeks (months in
    some tissues) in the absence of extracellular
    drug.

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  • Unwanted effects are
  • depression of the bone marrow and damage to the
    epithelium of the gastrointestinal tract.
  • Pneumonitis can occur
  • In addition, when high-dose regimens are used,
    there may be nephrotoxicity, caused by
    precipitation of the drug or a metabolite in the
    renal tubules

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Cont
  • High-dose regimens (doses 10 times greater than
    the standard doses), sometimes used in patients
    with methotrexate resistance, must be followed by
    'rescue' with folinic acid

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Pyrimidine analogues
  • Eg, of pyridine analogue is 5-fluorouracil
  • Fluorouracil is converted to a fraudulent
    nucleotide and inhibits thymidylate synthesis.
  • Fluorouracil is usually given parenterally
  • 5-FU is employed primarily in the treatment of
    slowly growing solid tumors e.g Colorectal,
    breast, ovarian, pancreatic, and gastric
    carcinomas.
  • Topically for treatment of basal cell carcinomas

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  • Rapidly metabolized in liver, lung kidney
  • The dose of 5-FU MUST be adjusted in case of
    impaired hepatic function
  • Metabolized by dihydropyrimidine dehydrogenase
    (DPD), a polymorphic enzyme
  • The main unwanted effects are nausea, vomiting,
    diarrhea, alopecia, ulceration of oral GI
    mucosa, myelotoxicity and anorexia.
  • Cerebellar disturbances can occur.

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Cytarabine
  • Is an analog of 2-deoxycytidine
  • in its trisphosphate form inhibits DNA
    polymerase
  • Major clinical use is in acute nonlymphocytic
    leukemia in combination with 6-TG and
    daunorubicin
  • Adverse effect includes nausea, vomiting,
    diarrhea myelosuppression

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Purine analogues
  • The main anticancer purine analogues include
  • Fludarabine
  • Pentostatin
  • Cladribine
  • 6-Mercaptopurine (6-MP)
  • 6-Tioguanine (6-TG)

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  • Mercaptopurine
  • is converted into fraudulent nucleotide.
  • Fludarabine in its trisphosphate form inhibits
    DNA polymerase
  • Is used principally in the maintenance of
    remission in ALL
  • Its bioavailability can be reduced by FPM in the
    liver
  • In the liver, 6-MP is converted to 6-methyl-MP
    derivative or to thiouric acid (an inactive
    metabolites)

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  • Note the latter reaction is catalyzed by
    Xanthine oxidase (XO).
  • Because the XO inhibitor, allopurinal, is
    frequently used to reduce hyperuricemia in Cancer
    patients receiving chemotherapy, it is important
    to decrease the dose of 6-MP by 75 in these
    patients to avoid accumulation of the drug
  • The principal toxicity of 6-MP is
    myelosuppression. Also N, V, D jaundice.

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iii. Cytotoxic antibiotics
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Cont.
  • Antitumour antibiotics produce their effects
    mainly by direct action on DNA
  • They include
  • Doxorubicin
  • Dactinomycin
  • Bleomycins
  • Mitomycin
  • Procarbazine
  • Hydroxycarbamide

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Doxorubicin
  • Doxorubicin inhibits DNA and RNA synthesis the
    DNA effect is mainly through interference with
    topoisomerase II action.
  • It is used in combination with other agents for
    treatment of sarcomas and a variety of carcinomas
    e.g breast and lung Ca as well as for treatment
    of ALL and lymphomas.

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  • Must be administered by I/V inactivated in the
    GI tract
  • Do not penetrate BBB or testes
  • Undergo extensive hepatic metabolism bile is
    the major route of excretion
  • Dose adjustment is required in hepatic impairment
  • Due to dark red color of anthracycline drugs, the
    drug also impart a red color to the urine.

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  • Unwanted effects include
  • Irreversible, dose-dependent cardiotoxicity is
    the most serious adverse reaction (more common
    with doxorubicin daunorubicin than with
    idarubicin epirubicin)
  • Irradiation of the thorax increase the risk of
    cardiotoxicity
  • Addition of trastuzumab to protocols with
    doxorubicin or epirubicin increases CHF.

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Other adverse effects includes
  • nausea and vomiting,
  • myelosuppression
  • severe hair loss (alopecia)
  • Increased skin pigmentation
  • Stomatitis

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Bleomycin
  • Bleomycin causes fragmentation of DNA chains.
  • It is cell cycle specific acting on G2 phase
  • It is primarily in the treatment of testicular
    cancers in combination with vinblastine or
    etoposide
  • Response rates are close to 100 if cisplatin is
    added to the regimen.

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  • Most of the parent drug is excreted unchanged
    into the urine by GF dose adjustment in RF.
  • Unwanted effects include
  • fever,
  • allergies,
  • mucocutaneous reactions
  • pulmonary fibrosis
  • There is virtually no myelosuppression.

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Dactinomycin
  • Dactinomycin intercalates in DNA, interfering
    with RNA polymerase and inhibiting transcription.
  • It also interferes with the action of
    topoisomerase II.
  • It is used in combination with surgery and
    vincristine for the treatment of Wilms tumors
    (nephroblastoma)

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  • Used in combination with MTX for treatment of
    gestational choriocarcinoma
  • Unwanted effects include nausea, vomiting
    myelosuppression.

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iv. plant derivatives
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Vinca alkaloids
  • The main vinca alkaloids are
  • vincristine,
  • vinblastine
  • Venorelbine
  • They act by binding to tubulin and inhibiting its
    polymerisation into microtubules, which prevents
    spindle formation in mitosing cells and causes
    arrest at metaphase.

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  • Their effects only become manifest during
    mitosis.
  • They also inhibit other cellular activities that
    involve the microtubules, such as leucocyte
    phagocytosis and chemotaxis as well as axonal
    transport in neurons.
  • They are generally administered in combination
    with other drugs
  • Although similar in structure, their therapeutic
    indications are different

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  • Vincristine is used in treatment of ALL in
    children, Wilms tumors, and Hodgkin and
    non-Hodgkin lymphomas
  • Vinblastine in combination with bleomycin and
    cisplatin is used in treatment of metastatic
    testicular carcinoma
  • Venorelbine is beneficial in the treatment of
    advanced non-small cell lung cancer, either as a
    single agent or in combination with cisplatin.

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  • The vinca alkaloids are relatively non-toxic.
  • Vincristine has very mild myelosuppressive
    activity but causes paraesthesias (sensory
    changes) and muscle weakness fairly frequently.
  • Vinblastine is less neurotoxic but causes
    leucopenia, while vindesine has both moderate
    myelotoxicity and neurotoxicity.
  • Hyperuricemia is common administer XO inhibitors

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Taxanes
  • The taxanes paclitaxel and docetaxel act on
    microtubules, stabilising them (in effect
    'freezing' them) in the polymerised state.
  • This has repercussions similar to those described
    above for the vinca alkaloids.
  • Paclitaxel is given by intravenous infusion and
    docetaxel by mouth.

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  • Both have a place in the treatment of breast
    cancers
  • paclitaxel, given with carboplatin, is the
    treatment of choice for ovarian cancer.
  • Paclitaxel in combination with cisplatin have
    favourable results in treatment of non-small cell
    lung cancer

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Unwanted effects
  • Unwanted effects, which can be serious, include
    bone marrow suppression (neutropenia) and
    cumulative neurotoxicity.
  • Resistant fluid retention (particularly oedema
    of the legs) can occur with docetaxel.
  • Hypersensitivity to both compounds is liable to
    occur and requires pretreatment with
    corticosteroids and antihistamines.

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Etoposide
  • Etoposide is derived from mandrake root.
  • Its mode of action is not clearly known but it
    may act by inhibiting mitochondrial function and
    nucleoside transport, as well as having an effect
    on topoisomerase II similar to that seen with
    doxorubicin.
  • Unwanted effects include nausea and vomiting,
    myelosuppression hair loss.

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Campothecins
  • The campothecins irinotecan and topotecan bind to
    and inhibit topoisomerase I, high levels of which
    occur throughout the cell cycle.
  • Diarrhoea and reversible bone marrow depression
    occur but, in general, these drugs have fewer
    unwanted effects than most other anticancer
    agents.

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Clinical uses
  • First-line therapy (with 5-FU and leucovorin) for
    metastatic colorectal cancer (CRC)
  • It is also indicated for CRC that has recurred or
    progressed following initial fluorouracil-based
    therapy
  • Off-label advanced ovarian cancer, glioblastoma
    multiforme, NSCLC

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Enzyme (L-asparaginase)
  • Asparaginase is an enzyme that catalyzes the
    hydrolysis of l-asparagine to l-aspartic acid
    and ammonia.
  • Isolated from different types of bacteria,
    including E. coli
  • They inhibit protein synthesis in tumor cells by
    depriving them of the amino acid asparagine

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  • This drug is phase specific, with the greatest
    activity in the G1 phase of the cell cycle.
  • Clinical use is confined presently to acute
    lymphocytic leukemia
  • Asparaginase products may produce
  • Acute hypersensitivity reactions
  • Hypotension,
  • Sweating, 
  • Bronchospasm, and 
  • Urticaria.

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2. HORMONES
  • Tumors that are steroid hormone-sensitive may be
  • Hormone responsive regresses following
    treatment with a specific hormone
  • Hormone dependent regresses following removal
    of hormone stimulus
  • Both hormone responsive and dependent

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Overview of Targeted therapy
  • Targeted therapy is a type of cancer treatment
    that uses drugs or other substances to precisely
    identify and attack certain types of cancer cells
  • A targeted therapy can be used by itself or in
    combination with other treatments,

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Targeted therapy includes
  • Hormone therapies, 
  • Signal transduction inhibitors,
  • Gene expression modulators,
  • Apoptosis inducers,
  • Angiogenesis inhibitors,
  • Immunotherapies,
  • Toxin delivery molecules

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