Cancer is caused by genetic alterations that lead to uncontrolled cell growth. Anticancer therapies include chemotherapy, radiotherapy, immunotherapy, and surgery. Chemotherapies work by killing cancer cells or stopping their growth. Major classes of chemotherapies discussed were alkylating agents, antimetabolites, microtubule-targeting drugs, topoisomerase inhibitors, and antibiotics. Each class has specific mechanisms of action and side effects that were outlined. The presentation provided an overview of different anticancer drug classes and their mechanisms and uses for treating cancer.

1. ANTICANCER THERAPY
Presented by
Anitta Augustine
Mpharm
Department of pharamcology
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2. • Cancer is a disease in which normal cells are
transformed into neoplastic cells through
alteration of their genetic material,leading to
expression of oncogenes, inhibition of tumor
suppressor genes, and uncontrolled growth.
• Oncogenes typically encode growth factors,
many of which are kinases that activate
cellular regulatory proteins that promote cell
division.
• For example, the cyclins are proteins that
activate cyclindependent
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3. • Cancer
– Uncontrolled multiplication and spread within
the body of abnormal forms of body's own cells
• Neoplasm
– A mass of tissue formed as a result of
• Abnormal
• Excessive
• Uncoordinated
• Autonomous and
• purposeless
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4. • The anticancer drug either kill cancer cells or
modify their growth.
• Cancer treatment:
Chemotherapy
Radiotherapy
Immunotherapy
surgery
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11. DNA alkylating drugs
• These compounds produce highly reactive
carbonium ion intermediates which transfer
alkyl groups to cellular macromolecules by
forming covalent bonds.
• Alkylating agents have cytotoxic and
radiomimetic (like ionizing radiation) actions
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12. Mechanism
Alkaylating agents produces reactive carbonium ion
Transfer the alkyl group to N7 guanine of DNA
Alkylation results in cross linking/abnormal base
pairing/ scission of DNA strand
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13. ADR
• Bone marrow toxicity
Suppersion of cellular and humoral immunity
Myelosuppression
• Lukemogenesis
• Female and male reproductive toxicity
• Alpoceia
• Nausea and vomitting 30-60 min after
administration of mechlorethamine,
cyclophosphamide, or carmustine.
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14. Cyclophosphamide
• Cyclophosphamide is a prodrug that must be
converted to active metabolites by hepatic
mixed-function oxidase (cytochrome P450)
enzymes.
• The active alkylating metabolite of
cyclophosphamide is thought to be
phosphoramide mustard.
• Cyclophosphamide is partly converted to acrolein,
which is probably responsible for hemorrhagic
cystitis,an adverse effect that sometimes occurs
with use of drugs.
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16. Pharmacological actions
• Cytotoxic action
– Hemopoetic system highly susceptible
• Chlorambucil – more against lymphoid series
• Busulfan
– more against myeloid series
– Epithelial tissues, hair follicles
– Spermatogenesis , fetopathic effect
• Immunosupressant action
• Miscellaneous
– Severe nausea & vomiting
• Known as radiomimetic drugs
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17. Platinum coordination complexes
• It is a platinum coordination complex that is
hydrolysed intracellularly to produce a highly
reactive moiety which causes cross linking of
DNA.
• The favoured site is N7 of guanine residue.
• It can also react with –SH groups in proteins
and has radiomimetic property.
• Cisplatin is very effective in metastatic
testicular and ovarian carcinoma.
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18. Cisplatin enters cells
Forms highly reactive platinum complexes
Intra strand & interstrand cross link
DNA damage
Inhibits cell proliferation
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19. ADR
• Emesis
• Nephrotoxicity
(The use of mannitol and sodium thiosulfate will decrease
the severity of nephrotoxicity, an adverse effect
associated with loss of potassium and magnesium,
reducedglomerular filtration, and renal failure.)
• Peripheral neuropathy
• Ototoxicity (Tinnitus, deafness, neuropathy
• and hyperuricaemia are other problems)
• thrombocytopenia
• Leukopenia
• mild myelosuppression
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20. Indications
• It is given intravenously as a first-line drug
fortreating testicular, ovarian, cervical, and
bladder cancers,
• it is also useful in the treatment of melanoma
and a number of other solid tumors
• Carboplatin has a similar spectrum of activity,
but it is approved only for ovarian cancer.
• Oxaliplatin is used in treating advanced colon
cancer.
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21. Antimetabolites
• Antimetabolites generally interfere with the
availabilty of normal purine or pyrimidine
nucleotide precurssor,either by inhibiting their
synthesis or by competing with them in DNA
or RNA synthesis.
• Their maximal cytotoxic effect are in s- phase.
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22. Folate antagonist
• MTX is actively transported into mammalian
cells and inhibits dihydrofolate reductase,
the enzyme that normally converts dietary
folate to the tetrahydrofolate form required for
thymidine and purine synthesis
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23. Mechanism
• The structures of MTX and folic acid are similar.
MTX, however, has an amino group substituted
for a hydroxyl group on the pteridine ring, and it
also has an additional methyl group.
• MTX is actively transported into mammalian cells
and inhibits dihydrofolate reductase, the
enzyme that normally converts dietary folate to
the tetrahydrofolate form required for thymidine
and purine synthesis
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25. Indications
• The use of MTX in the treatment of
choriocarcinoma, a trophoblastic tumor, was
the first demonstration of curative
chemotherapy.
• Used for the treatment of trophoblastic tumors,
breast cancer, and osteosarcoma. It is routinely
given by intrathecal administration to prevent
meningeal metastases during chemotherapy
of acute lymphocytic leukemia
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26. ADR
• It exerts major toxicity on bone marrow
• —low doses given repeatedly cause megaloblastic
anaemia, but high doses produce pancytopenia.
• Mucositis anddiarrhoea are common side effects.
• Desquamation and bleeding may occur in g.i.t.
Megaloblastic anemia
• Thrombocytopenia, leukopenia, aplasia
• Alopecia , liver damage, nephrpathy
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27. Purine antagonists
• The first purine analogue to be used in cancer chemotherapy
was mercaptopurine,a drug introduced almost 60 years ago for
the treatment of acute lymphocytic leukemia.
• Mercaptopurine and thioguanine are the this analogues of
the urine bases hypoxanthine and guanine, respectively.
• The active metabolites of mercaptopurine and thioguanine
inhibit several steps in the biosynthesis of purine bases
(adenine and guanine) and in purine recycling pathways that
supply purine precursors, thereby impairing DNA synthesis.
• Mercaptopurine is metabolized by xanthine oxidase, whereas
thioguanine is degraded by other enzymes.
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28. (HGPRT): hypoxanthine-guanine phosphoribosyl transferase
IMPDH:inosine monophosphate dehydrogenase
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29. ADR
• The main toxic effect of antipurines is bone
marrow depression, which develops slowly.
• Mercaptopurine causes more nausea and
vomiting than 6-TG. It also produces a high
incidence of reversible jaundice.
• Cancer chemotherapy places patients at risk
for these problems because the destruction of
cancer cells increases purine catabolism and
uric acid formation, called tumor lysis
syndrome.
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30. • Doses of mercaptopurine must be reduced by
at least 50% in patients who are taking
allopurinol, which inhibits xanthine oxidase
and thereby elevates plasma levels of
mercaptopurine.
• Allopurinol is often given to patients
undergoing cancer chemotherapy because it
inhibits the synthesis of uric acid and thereby
prevents hyperuricemia and gout.
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31. Pyrimidine Analogues
• 5-fluro uracil is converted into 5-fluro 2 deoxy
uridine monophosphate,it inhibits thymidylate
synthase and blocks the conversion of deoxy
uridilic acid to deoxy thymidiylic acid
• 5-FU produces anticancer effect in the s phase
of the cell cycle.
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33. ADR
• Nausea,vomiting diarrhea and alopecia
• Severe ulceration of the oral and GI mucosa
,bone marrow depression and anorexia
• Hand foot syndrome
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34. Indications
• Cancers of Colon, Breast, Ovary, Liver,
Pancreas, Rectum, Stomach
• Glioblastoma Multiforme (Orphan)
• Advanced Colorectal Carcinoma (Orphan)
• Esophageal Carcinoma (Orphan)
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35. Microtuble damaging agents
Obtained from periwinkle plant ( Vinca Rosea)
• Vincristine, vinblastine, vindesine, vinorelbine
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36. • Paclitaxel & docetaxel
• Plant product obtained from bark of Pacific
Yew ( Taxus Brevifolia) & European Yew
(Taxus Buccata)
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38. A, In normal mitosis, the mitotic spindle is formed
by microtubules that continuously undergo
assembly and disassembly as a result of tubulin
polymerization and depolymerization,
respectively.
B, Vincristine and other vinca alkaloids bind to
tubulin and prevent the polymerization of tubulin
dimers.
C, Paclitaxel and other taxanes bind to tubulin,
stabilize the tubulin polymer, and thereby prevent
depolymerization. As with vinca alkaloids,
taxanes cause metaphase arrest.
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39. Indications
• Vincristine is often used to treat hematologic
cancers, including acute lymphocytic leukemia,
Hodgkin and non-Hodgkin lymphomas, and
multiple myeloma.
• It also is used in the treatment of some solid
tumors (e.g., small cell lung cancer,
neuroblastoma, and sarcoma).
• Vinblastine is used for lymphomas and for
bladder, breast, ovarian, and testicular cancers.
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40. Topoisomers 2 inhibitor
• It is a semisynthetic derivative of
podophyllotoxin, a plant glycoside.
• It is not a mitotic inhibitor, but arrests cells in the
G2 phase and causes DNA breaks by affecting
DNA topoisomerase-2 function.
• While the cleaving of double stranded DNA is not
interfered, the subsequent resealing of the strand
is prevented.
• Alopecia, leucopenia
• and g.i.t. disturbances are the main toxicity
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42. INDICATIONS
• Etoposide is used in testicular tumours, lung
cancer, Hodgkin’s and other lymphomas,
carcinoma bladder and stomach
ADR
• Alopecia
• Mild nausea and vomiting
• Dose-limiting myelosuppression.
• They have also been associated with a low
incidence of secondary nonlymphocytic
leukemias.
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43. Topoisomerase 1 inhibitor
Camptothecin analogues
• Irinotecan is approved for the treatment of colorectal
cancer that has recurred or progressed after fluorouracil
therapy.
• It is also active against lymphomas and breast, cervical,
gastric, lung, and other tumors.
• Topotecan is active against glioma, sarcoma, and lung and
ovarian tumors.
• The dose-limiting toxicity of both camptothecin analogues
is myelosuppression.
• Irinotecan produces diarrhea in a significant percentage
of patients, and both drugs can cause alopecia and mild
nausea and vomiting.
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45. ADR
• The major toxicity is bone marrow depression,
especially neutropenia.
• Other adverse effects are pain abdomen,
vomiting ,anorexia and diarrhoea.
• thrombocytpenia
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46. ANTIBIOTICS
• These are products obtained from
microorganisms and have prominent
antitumour activity.
• Practically all of them intercalate between
DNA strands and interfere with its template
function.
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47. Anthracyclines
• Daunorubicin and doxorubicin are antibiotics
obtained from a Streptomyces species, and
idarubicin is a semisynthetic derivative.
• These drugs have a four-member anthracene ring
with attached sugars.
• Two of the four rings are quinone and
hydroquinone moieties that enable the compounds
to accept and donate electrons and thereby
promote the formation of free radicals.
• The anthracene ring accounts for the intense red
color of the drug compounds.
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48. mechanism
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49. • Doxorubicin and other anthracycline drugs
intercalate between DNA base pairs.
• Anthracyclines are reduced to intermediates
that donate electrons to oxygen to form
superoxide.
• Superoxide then reacts with itself to make
hydrogen peroxide, which is cleaved in the
presence of iron to form the destructive
hydroxyl radical that cleaves DNA.
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50. ADR
• myelosuppression
• nausea and vomiting
• alopecia; and mucosal ulcerations.
• The anthracyclines cause both acute and chronic
cardiotoxicity.
• Manifestations of acute toxicity include sinus tachycardia and
ventricular premature beats.
• These cardiac rhythm disturbances often occur during the first
24 hours and are self-limited.
• Chronic toxicity leads to congestive cardiomyopathy and
limits the cumulative dose of anthracycline that can be given
to any patient.
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51. INDICATION
• Daunorubicin and idarubicin are agents used in
induction and consolidation therapy for acute
myeloid leukemia.
• Doxorubicin has a broader spectrum of
activity.
• It is one of the most active drugs against breast
cancer, and it is also useful in the treatment of
Hodgkin disease, bladder cancer, ovarian
cancer, and other hematologic cancers and
solid tumors
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52. Bleomycin
• Bleomycin is a mixture of two peptides obtained
from Streptomyces verticillus.
• The drug has its greatest effect on neoplastic cells
in the G2 phase of the cell replication cycle.
• Although bleomycin intercalates DNA, the major
cytotoxicity is believed to result from
ironcatalyzed free radical formation and DNA
strand breakage.
• The iron-bleomycin complex binds to DNA,
which reduces molecular oxygen to oxygen free
radicals that cause single strands of DNA to break
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54. MISCELLANEOUS CYTOTOXIC
DRUGS
Hydroxyurea
• It blocks the conversion of ribonucleotides to
deoxyribonucleotides by inhibiting the enzyme
ribonucleoside diphosphate reductase—thus
interferes with DNA synthesis;exerts S-phase
specific action.
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56. • Hydroxyurea is well absorbed orally and is
eliminated in urine with a plasma t½ of ~ 4
hours.
• Myelosuppression is the major toxicity.
• Gastrointestinal disturbances and cutaneous
reactions including pigmentation also occur
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57. INDICATIONS
• Its primary therapeutic value is in chronic
myeloid leukaemia,psoriasis, polycythaemia
vera and occasionally in some solid tumours.
• It is also employed as a radiosensitizer before
radiotherapy, and is a first-line drug for sickle
cell disease in adults.
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58. • L-Asparaginase (L-ASPase)
• The enzyme L-ASPase (from E. coli.) degrades L-
asparagine to L-aspartic acid, depriving the
leukaemic cells of an essential metabolite, and
causes cell death.
• L-asparaginase is a component of regimen for
inducing remission in acute lymphoblastic
leukaemia along with Mtx., prednisolone,
vincristine,etc.
• Moreover, L-ASPase is antigenic, produces
neutralizing antibodies which inactivate and clear
the enzyme rapidly.
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60. ADR
• Many of the typical adverse effects of
anticancerdrugs are not seen with L-ASPase
(no leukopenia, alopecia, or mucosal damage), but
it produces effects due to defective protein
synthesis—hyperglycaemia, raised
triglyceridelevels, pancreatitis, liver damage,
clotting defects and CNS symptoms.
• develop allergic reactions (urticaria, chills, fever,
rash), including anaphylaxis; deaths are reported.
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61. TARGETED DRUGS
Tyrosine-protein kinase inhibitors
• protein kinase inhibitors have been among the
most successful of the targeted anticancer drugs.
• These agents inhibit various kinases that
phosphorylate tyrosine or serine and threonine
residues of growth factor receptors and other
regulatory proteins, and thereby impede pathways
promotingmalignant cell transformation and
proliferation.
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62. • Imatinib, dasatinib, and nilotinib inhibit the BCR-ABL
tyrosine kinase expressed by the Philadelphia chromosome in
CML cells .
• BCR-ABL tyrosine kinase invokes malignant transformation
and proliferation by activating small cytoplasmic GTPases
(Ras and Raf ) and various serine/threonine kinases, including
the Jun kinase and sarcoma family kinases.
• The activated kinases stimulate transcription factors, including
c-Jun, NF-κB (nuclear factor–kappa B), and STAT5 (signal
transducer and activator of transcription 5).
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BCR-ABL signal transduction

63. • Some of these factors increase expression of cyclins
and other positive regulators of the cell cycle
• The activated kinases and transcription factors also
modulate mitochondrial apoptotic regulators, including
a proapoptotic caspase (BAD) and the antiapoptotic
BCL-XL.
• Together, these effects lead to inhibition of apoptosis
(programmed cell death) and promotion of cell
replication.
• BCR-ABL also activates cytoskeletal regulators,
leading to altered cell adhesion and motility .
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65. ADR
• abdominal pain
• Vomiting
• thrombocytopenia
• fluid retention
• periorbital edema
• pleural effusion
• Myalgia
• liver damage and CHF
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66. EGF receptor inhibitors
• Epidermal growth factor (EGF) receptor is a
transmembrane receptor-tyrosinekinase which
regulates growth and differentiation of epitheilal
cells.
• Binding of ligand (EGF) to the extracellular
domain of the receptor induces dimerization
leading to activation of tyrosine kinase activity of
the intracellular domain → autophosphorylation
of the kinase and phosphorylation of several
cytoplasmic regulatory proteins which modify
gene transcription to regulate growth
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68. Indication
• For the continued treatment of patients with
locally advanced or metastatic non-small cell
lung cancer after failure of either platinum-
based or docetaxel chemotherapies.
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69. Angiogenesis inhibitors
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•Angiogenesis
(proliferation of new
blood vessels)
is essential for growth
and metastasis of cancers.

70. • The vascular endothelial growth factor(VEGF) is
the most important stimulus for
neovascularization and increase in microvessel
density within solid tumours.
• VEGF interacts with cell surface VEGF receptor,
that is another receptor tyrosine kinase, which
promotes angiogenesis by phosphorylating
intracellular regulatory proteins.
• Several cancers over express VEGF receptor and
inhibitors of this receptor have been developed as
antitumour drugs.
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72. Adverse effects
• rise in BP,
• arterial thromboembolism leading to
hearattack and stroke
• vessel injury and haemorrhages
• proteinurea
• gastrointestinal perforations
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73. Proteasome inhibitors
• Proteasomes are packaged complexes of
proteolytic enzymes which degrade several
intracellular signalling proteins that control cell
cycle,apoptosis and survival response.
• drugs that target apoptosis inhibiting proteins,
such as the X-linked inhibitor of apoptosis
protein and the B-cell lymphoma gene–2 (Bcl-2)
protein.
• The proteasome inhibitor bortezomib has
recently been approved for treating multiple
myeloma.
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74. Bortezomib
• It is a unique boron containing compound that covalently
binds to proteasome and inhibits its proteolytic activity
disrupting many intracellular signalling pathways.
• The most important of these is nuclear factor-κB (NF-
κB)mediated signalling.
• NF-κB is a transcription factor that normally resides in the
cytoplasm bound to an inhibitory protein IκB.
• Hypoxia, cytotoxic drugs, DNA breaks and other stressful
stimuli activate proteasome which cleaves and degrades IκB
to release NF-κB which then translocates to the nucleus and
transcripts certain genes to produce molecules that oppose
apoptosis and promote cell proliferation.
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75. • Some neoplasms overexpress NFκΒ which
plays an important role in their survival.
• By inhibiting proteasome,bortezomib prevents
the breakup and degradation of IκB, so that
NFκB is not released to transcript survival
molecules.
• It also causes build up of‘Bax’, an apoptosis
promoting protein, and affects other regulators
of cell cycle.
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76. Unarmed monoclonal antibodies
• Monoclonal antibodies are a fast-growing class of
targeted anticancer agents.
• The fragment antigen binding (Fab) portion of an
antibody binds to a specific antigen on a particular type
of cancer cell, leading to disruption of an essential
cancer cell process.
• Some antibodies target growth factors or their
receptors, whereas others release a cytotoxic isotope or
enhance host immunity.
• Because of their protein structure, these agents must be
given intravenously, and they are prone to cause
immune system toxicities.
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77. • The names of monoclonal antibodies end in
mab or monab.
• The letters before mab indicate the source of
the antibody: o for mouse, u for human, and xi
for chimeric.
• An internal letter or syllable identifies the
therapeutic use of the antibody, for example, tu
for tumor, vi for virus, and c or ci for
circulation.
• For example, rituximab is a chimeric human
murine antibody used in treating tumors.
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78. • Malignant cells express certain unique antigens on
their surface to which MAbs could be directed.
• These unmodified (also called unarmed or naked)
MAbs kill the target cells by several mechanisms
including direct signalling of apoptosis, or
antibody-dependent cellular cytotoxicity (ADCC),
or complement-dependent cytotoxicity (CDC).
• They could also be used as missiles to carry
biological bombs (toxins) and are called
immunotoxins, or a radioactive isotope as
radiopharmaceuticals. These are called
‘armed’MAbs.
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80. GLUCOCORTICOIDS
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81. • They have marked lympholytic action—are
primarily used in acute childhood leukaemia
and lymphomas.
• They induce remission rapidly but relapses
inevitably occur after variable intervals and
gradually the responsiveness is lost.
• Glucocorticoids have a secondary role in some
hormone responsive breast cancers.
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82. Selective estrogen receptor
modulators
MECHANISM
• Bind to estrogen receptor
• Decreases the DNA synthesis
• And effect of estrogen
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84. Selective estrogen receptor down
regulators
Mechanism
• Inhibits ER dimerization & prevents
interaction of ER with DNA
• ER is down regulated resulting in more
complete supression of ER responsive gene
function
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86. Aromatase inhibitors
Mechanism
• Aromatase ,hormane that produces estrogen,is
found in high level in endometrial tissues.
• Inhibit aromatase which catalyses conversion
of androstenedione (androgenic precursor) to
estrone ( estrogenic hormone
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87. Thank you
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