Chemotherapy

anticancer drugs is a very important topic for pg entrance....so all important points and mcqs with images have been given here....do make use of it

1. -DR.AKIF A.B

2. Anti cancer drugs acts on
1)Bone marrow : causes Bone marrow suppression
2)GIT : causes Nausea and vomiting
3)Hairs: Alopecia
4)Causes increase in Serum Uric Acid : Due to lysisof tumor cells
This Side effects are common to all anticancer drugs.

3. -G0 phase is most chemoresistantphase

5. -M.O.A: It attaches to N7 of Guanine of DNA dimerand destroys DNA
-Side effects :
1)Bone marrow : causes Bone marrow suppression
2)GIT : causes Nausea and vomiting
3)Hairs: Alopecia
4)Causes increase in Serum Uric Acid : Due to lysisof tumor cells
5)Secondary Leukemias: MC : AML
6)Infertility

6. 1)Mechlorethamine
2)Melphalan
3)Busulfan
4)Cyclophosphomide
5)Ifosfamide
6)Chlorambucil
7)Procarbaine= causes DisulfiramLike Reaction
8)Dacarbazine
9)Nitrosureas: Carmustine/ Lomustine/Semustine

7. 1)MECHLORETHAMINE
-Single most effective drug in treating Hodgkin Lymphoma

8. -Treatment of choice : ABVD Regimen
A–Adriamycin(Doxorubocin)
B–Bleomycin
V-Vinblastine
D-Dacarbazine

9. MELPHALAN
-Single most effective drug in treating Multiple Myeloma
Mnemonic : M for Melphalanand M for Multiple Myeloma

10. BUSULFAN
-Causes Lung Fibrosis
-Drugs causing Pulmonary fibrosis
A –Acyclovir / Amiodarone/ Azathioprine
B –Busulfan/ Bleomycin
C –Carmustine/ Chlorambucil/ Cyclophosphomide

11. CYCLOPHOSPHOMIDE
AND
IFOSFAMIDE
On metabolism
produces
Acrolein
Hemorrhagic
Cystitis
MESNAis given along
with these Drugs
To Prevent

12. NITROSUREAS
Carmustine = Causes Persistent Neutropenia
Lomustine
Semustine
-Can cross Blood Brain Barrier. Hence used in Brain Tumors

13. -Treatment of Choice : CHOP +/-R
C -Cyclophosphomide
H -Hydroxyrubocin
O -Oncovin
P -Prednisolone
R -Rituximab

14. FOLFOX or FOLFIRI regimen
FOL -FolinicAcid
F -5-FU
OX -Oxyplatinum
FOL -FolinicAcid
F -5-FU
IRI -Irinotecan

15. Cisplatin -Most emitogenicAnticancer drug
-Most important side effect :
Nephrotoxicity
-Other S/E : Ototoxicity
-Marrowsparing drug
Carboplatin Maximum Bone marrow suppression
(Most hematotoxic)
Oxaliplatin Used for Colorectal cancers

16. 1)Nephrotoxicityis seen with: (DNB Dec 2010)
AAzathioprine
BLeflunomide
CMycophenolatemofetil
DTacrolimus

17. Ans. D) Tacrolimus
I.It is a MacrolideAntibiotic
II.Tacrolimus(FK 506) inhibits IL-2 transcription like cyclosporine does.
II. The drug is more potent than cyclosporine and requires therapeutic drug
monitoring.
III. Patients treated with the calcineurininhibitors cyclosporine and tacrolimus
are at high risk of developing renal injury.
Side Effects
1)Nephrotoxicity
2)Neurotoxic
3)Precipitates DM
4)Hepatotoxicbut not Ototoxic
Inhibits IL-2 transcription
IL-2 activates T cell
Thus Tacrolimusdecreases T-cell
activity

18. -Prodrugof Anti Cancer drug 6-Mercaptopurine
-Drug of choice for Steroid Resistant Ulcerative Colitis
Side effects :
1)Bone marrow suppression ; Most Important
2)Hepatotoxicity
3)Nephrotoxicity: Rare

19. Leflunomideis an immunomodulatorand is used in severe
rheumatoid arthritis.
SIDE EFFECTS
1) severe liver injury
2) interstitial lung diseases,
3) myelosupressionand anemia.

20. -Mycophenolateis a prodrug
-It is an inosinemonophosphatedehydrogenaseinhibitor.
-Common Side Effect :
1) gastrointestinal upset
2) bone marrow depression.

21. -Immunomodulator
-Side Effects : SPORT Channel
S -Sedation
Po -Phocomelia/Peripheral Neuropathy
R -Rash
T -Thrombosis
Channel-Constipation
Phocomelia
Limb bud formation defect

22. 2. Cerebellarataxia is caused by (DNB June 2012)
AArabinofuranosylcytidine
BBleomycin
CCisplatin
DBusulfan

23. Ans. AArabinofuranosylcytidine
Cytarabine(Arabinofuranosylcytidine) is used intrathecallyfor meningeal
leukemia.
This can cause cerebellartoxicity –ataxia & slurred speech as well as cerebral
toxicity –seizures, dementia, coma etc.
The other side effects are potent myelosuppression, GIT & mucosal side effects,
dermatitis, reversible rise in LFT & pulmonary side effects.

24. Anti Folate
Anti PyramidinesAnti Purines
-Methotrexate
-Pemetrexed
-Pralatrexate
-6-mercaptopurine
6-thioguanine
Cladribine
Fludrabine
-5-FU
-Capecitabine
-Gemcitabine
-Cytarabine
(Arabinofuranosyl
cytidine)

25. -Methotrexateinhibits DihydrofolateReductase

26. C -Choriocarcinoma
A -Autoimmune diseases
N -Non Hodgkin Lymphoma
C -Crohn’sDisease
E -Ectopic Pregnancy
R -Rheumatoid Arthritis

27. 1)Bone marrow : causes Bone marrow suppression
2)GIT : causes Nausea and vomiting
3)Hairs: Alopecia
4)Causes increase in Serum Uric Acid : Due to lysisof
tumor cells
5)MegaloblasticAnemia
6)Hepatotoxicity

28. -Methotrexateresistance is due to overproduction of Dihydrofolate
Reductase(DHFRase)
-Methotrexateis a weak acid and hence its excretion is increased by
Alkalinisation

29. Weak-Warfarin
A -Aspirin/ Antiepileptics
C -Chlorthiazide
I -Ibuprofen
D -Dopa(Levodopa)

30. Drug Feature
6-mercaptopurine -Metaboliosedby XanthineOxidase
-S/E : Hepatotoxicity
6-thioguanine S/E : Hepatotoxicity
Cladribine DOC in Hairy cell Leukemia
Fludrabine DOC in CLL
-Purines: Adenine and Guanine

31. 5-FU S/E:Hand and foot Syndrome
Capecitabine -Prodrugand is metabolisedto 5-FU
-S/E:Hand and foot Syndrome
Gemcitabine DOCin Pancreatic Cancers
Cytarabine S/E: Cerebellarataxia
-Pyramidines: Cytosine, Thymine and Uracil.

32. Cute -Chloroquine
P -Penicillamine
A -Azathioprine
G -Gold Salts
L -Leflunomide
I -Immunosuppresantdrugs
Malika -Methotrexate(DOC)
Sherawat-Sulfasalazine
TNF-@ Inhibitors
1)Adalizumab
2)Etanarcept
3)Infliximab
IL-1 Receptor Antagonist
Anakinra
IL-6 Inhibitor
Tocilizumab
Disease Modifying Anti Rheumatoid Drugs

33. 3. Which of the following is highly emetogenic:
ACisplatin
BHigh dose methotrexate
CHigh dose cyclophosphamide
DCarboplatin

34. Ans. A) Cisplatinas well as option
C. High dose Cyclophosphamide
Nausea & vomiting is a prominent feature of many of cytotoxicdrugs.
This is due to CTZ stimulation as well as generating the emetogenicstimuli from
upper GIT as well as other areas.
A.High emetogenic–cisplatin, mustine,cyclophosphamide, actinomycinD,
dacarbazine, lomustine.

35. -Located in Area Postrema
-Remember its location: Can come in exam.

36. Drugs which are effective in
chemotherapy induced vomiting :
A.5-HT
3receptor antagonists –granisetron, palanocetron, ondansetron
etc.
B. NK1 antagonists (Substance Pantagonist): Aprepitant
C. Dexamethasone
CHEMOTHERAPY INDUCED VOMITING DOC
Early Onset Ondansetron
Late Onset Aprepitant

37. 4. Which is not a alkylatingagent
ACyclophosphamide
BChlorambucil
C5-FU
DMelphalan

38. Ans. C5-FU
5-FU( 5 FluroUracil) is a antimetabolite–classified as anti-pyrimidine
compound.
Rest all are alkylatingagents –act by formation of active carboniumion which
damages DNA.
The alkylatingagents are further classified as
Nitrogen mustards –mechlorethanamine, cyclophosphamide’s, ifosfamide,
melphalan&chlorambucil
Ethyleneimine& methylmelamines–altretamine& thiotepa
Methyl hydrazine derivatives –procarbazine.
Alkyl sulfonates–busulfan
Nitrosoureas–carmustine, lomustine.
Triazenes–Dacarbazine, temozolomide
Platinum co-ordination complexes –cisplatin, carboplatinand oxiliplatin.

39. 5. Ifosfamideis a (DNB Dec 2012)
AAlkylatingagents
BAntimetabolite
CFolateantagonists
DPlant Alkaloids

40. Ans. A alkylatingagent
Ifosfamideis a synthetic isomer of cyclophosphamide.
Importantly, it is not a metabolite of cyclophosphamide.
It causes greater neurotoxicity and cystitis than cyclophosphamide

41. CYCLOPHOSPHOMIDE
AND
IFOSFAMIDE
On metabolism
produces
Acrolein
Hemorrhagic
Cystitis
MESNAis given along
with these Drugs
To Prevent

42. 6. All of the following are side effects of thalidomide except (AIIMS Nov 2009)
AHypothyroidism
BDiarrhea
CTeratogenicity
DDeep Vein Thrombosis

43. Ans. BDiarrhea
Thalidomide causes constipation and not diarrhea
The most common adverse effects are sedation and constipation
the most serious one is treatment-emergent peripheral sensory
neuropathy.

44. -Immunomodulator
-Side Effects : SPORT Channel
S -Sedation
Po -Phocomelia/Peripheral Neuropathy
R -Rash
T -Thrombosis
Channel-Constipation
Phocomelia
-TeratogenicS/E
-Limb bud formation defect

45. 7.
Which of the following is cell cycle specific
AIfosfamide
BBleomycin
CVinblastine
DCyclophosphamide

46. Ans. CVinblastine
Vinblastineis a M phase specific vincaalkaloid.
It blocks the mitotic spindles and produces metaphase arrest.
Since it produces an interference with chromosomal segregation it is useful in
tumors that are rapidly dividing.
The drug is used in blood and reproductive cancers.
Side effects
nausea, vomiting, myelosupressionand bone marrow depression.

47. DRUGS INHIBITING
FORMATION OF SPINDLE
FEATURES
VINCRISTINE -Doesn’t cause bone marrow
suppression(marrow sparing
drug)
-S/E: SIADH and Peripheral
Neuropathy
VINBLASTINE S/E; Bone marrow suppression
-M Phase Specific

48. DRUGS INHIBITING BREAK
OF SPINDLE
FEATURES
PACLITAXEL -StabilisesMicrotubule
-S/E :
1)Allergy
2)Peripheral Neuropathy

49. TOPOISOMERASE –IInhibitor TOPOISOMERASE –IIInhibitor
Irinotecan Etoposisde
Anthracyclines
Doxorubocin
Daunorubocin
Used in Colorectal Cancer
(FOLFORI Regimen)
-Etoposidecauses Secondary
Leukemias
-Anthracyclinescauses Cardiotoxicity

50. ANTHRACYCLINES
Doxorubocin
Daunorubocin
-Anthracyclinescauses Cardiotoxicity

51. 1)ALKYLATING AGENTS
2)ETOPOSIDE
-MC Secondary Leukemia due to Anti cancer drugs is : AML
ALKYLATIN
G AGENTS
ETOPOSIDE
Secondary
Leukemias
Develops long
4-5yrs
1-2yrs
MyelodysplasiaOccurs Doesn’t occur

52. 1)Vincristine
2)Cisplatin
3)Bleomycin
4)L-Asparaginase

53. 8) Bleomycintoxicity affects which type of cells.
AType 1 pneumocyte
BType 2 pneumocyte
CEndothelial cell.
DAlveolar macrophages

54. Ans. A Type 1 pneumocytes
Bleomycin
causes destruction of type 1 pneumocytethereby causing hyperplasia of
type-II pneumocytes.
-Bleomycinis an Anticancer Antibiotic
-Bone marrow sparing drug

55. -Used in Acute Lymphocytic Leukemia
-Side Effects:
1) Allergy
2) Pancreatitis
3) HypercoagulableSyndrome

56. 9) ‘Hand Foot’ syndrome can be caused by?
A5FU
BVincristine
CCapecitabine
DMitomycin-C

57. Ans. A5FU as well as C. Capecitabine
5-FU can cause hand foot mouth disease. It is given I.V.
Generally, this disease affects infants and children.
Adults with immunodeficiency can also be affected.
Capecitabineis a oral 5FU analog, that obviate the need for I.V.

58. 5-FU S/E:Hand and foot Syndrome
Capecitabine -Prodrugand is metabolisedto 5-FU
-S/E:Hand and foot Syndrome
Gemcitabine DOCin Pancreatic Cancers
Cytarabine S/E: Cerebellarataxia
-Pyramidines: Cytosine, Thymine and Uracil.

59. 10) Topical MITOMYCIN-C is used in: (DNB Dec 2009)
ASturgewebersyndrome
BUrinary bladder cancer
CEndoscopic angiofibroma
DSkull base osteomyelitis

60. Ans. BUrinary bladder cancer
I. Mitomycinis an anti-tumor antibiotic with alkylatingagent like property. It is
used in superficial cancer of urinary bladder.
II. The drug has radiomimetic effects, and also sensitizes hypoxic tumor cells to
the effects of hypoxia. Hemolytic uraemicsyndrome is a known
complication of mitomycin.
III. The drug also produces bone marrow depression.
The drug of choice for superficial cancer of urinary bladder is BCG
given intravesically.

61. 11) Which of the following statement is false regarding vincristine? (AIIMS May 2012)
AIt is an alkaloid
BIts use is associated with neurotoxicity
CIt does not cause alopecia
DIt is useful drug for induction of remission in acute lymphoblastic leukemia

62. Ans. CIt does not cause alopecia
(Mnemonics :
Vincristine: CNS side effect;
Vinblastine: Blood/Bone marrow side effect)
a. Vincristineis a vincaalkaloid.
Vincristineis very useful for inducing remission in childhood acute leukemia.
b. It is also used for treatment of chronic lymphocytic leukemia and chronic
myelocyticleukemia.
Prominent adverse effects are peripheral neuropathy and alopecia.

63. DRUGS INHIBITING
FORMATION OF SPINDLE
FEATURES
VINCRISTINE -Doesn’t cause bone marrow
suppression(marrow sparing
drug)
-S/E: SIADH and Peripheral
Neuropathy
VINBLASTINE S/E; Bone marrow suppression
-M Phase Specific

64. 12. Allopurinolshould be avoided, or reduced doses should be used if given
with which of the chemotherapeutic agent ?
ABleomycin
BCisplatin
CCyclophosphamide
DMercaptopurine

65. Ans. DMercaptopurine
I. Mercaptopurineand other thiopurineare purineantimetabolitesthat are
metabolically inactivated by xanthineoxidase.
-Allopurinolinhibits XanthineOxidase
As a result Xanthineoxidaseis not available to degrade Mercaptopurine
Leads to Toxicity of Mercaptopurinei.eSevere hepatotoxicity
Thus decreased dose of Mercaptopurineshould be given if co-administered with
Allopurinol.

66. 13. AMIFOSTINE is protective to toall except:
ASalivary gland
BSkin
CCNS
DGIT

67. Ans. C) CNS
-Amifostineis a cytoprotectivedrug .
-It doesn’t cross Blood Brain Barrier. Hence is not protective to CNS.
-Amifostineis protective to salivary glands (reduces xerostomia) and GIT
(prevents esophagitis).
-Its xerostomiapreventing action can also be considered to be protective to
skin.

68. 14. Which of the following causes persistent leucopenia? (AIIMS Nov 2011)
ACisplatin
BVinblastin
CDoxorubicin
DCarmustine

69. D Carmustine
NITROSUREAS
Carmustine = Causes Persistent Neutropenia
Lomustine
Semustine
-Can cross Blood Brain Barrier. Hence used in Brain Tumors

70. 15.Temozolomideis a(DNB June 2011)
ACarbonic anhydraseinhibitor
BAlkylatingagent
CAnti metabolite
DTyrosine kinaseinhibitor

71. Ans. BAlkylatingagents
-Temozolomideis a Newer alkyaltingagent
-It can cross BBB , hence used for brain cancer (anaplasticastrocytoma
and glioblastomamultiforme)
-commonly used oral and intravenous
S/E: Nausea, vomiting, headache, constipation , myelosuppression

72. 16. SIADH is caused by the following drugs except?
AVincristine
BVinblastine
CActinomycinD
DCyclophosphamide

73. Ans. CActinomycinD
Drugs Causing SIADH
1. Intravenous cyclophosphamide
2. Carbamazepine
3. Vincristineor vinblastine
4. Phenothiazines
5. Haloperidol
6. Tricyclicantidepressants or serotonin-reuptake inhibitors
7. Monoamine oxidaseinhibitors
8. Bromocriptine
9. Clofibrate
10. Narcotics, opiate derivatives

74. 17.Alkalinisationof urine ameliorates the toxicity of which of the
following drugs? (AIIMS May 2009)
AArabinoside-cytosine
BIfosfamide
CCisplatin
DMethotrexate

75. -Methotrexateresistance is due to overproduction of Dihydrofolate
Reductase(DHFRase)
-Methotrexateis a weak acid and hence its excretion is increased by
Alkalinisation

76. Weak-Warfarin
A -Aspirin/ Antiepileptics
C -Chlorthiazide
I -Ibuprofen
D -Dopa(Levodopa)

77. 18) Which anticancer drug causes hypercoagulablesyndrome?
A5-FU
BL-asparaginase
CMelphalan
DCarmustine

78. -Used in Acute Lymphocytic Leukemia
-Side Effects:
1) Allergy
2) Pancreatitis
3) HypercoagulableSyndrome

79. 19. Methotrexateresistance is due to:
ADepletion of Folate
BOverproduction of DHFRase
COverproduction of Thymidylatekinase
DDecreased DHFRase

80. Ans. BOverproduction of DHFRase
Mechanisms of methotrexateresistance
I. Impaired transport of methotrexateinto cells
II. Production of altered forms of DHFR that have decreased affinity for the
inhibitor
III. Increased concentrations of intracellular DHFR through gene amplification or
altered gene regulation
IV. Decreased ability to synthesize methotrexatepolyglutamates
V. Increased expression of a drug efflux transporter, of the MRP (multidrug
resistance protein) class.

81. 21. High dose methotrexateis given in:
AOsteosarcoma
BColon Cancer
CRetinoblastoma
DEwing's sarcoma

82. Ans. AOsteosarcoma
Drugs effective in osteosarcomaare: .
doxorubicin,
ifosfamide,
cisplatin, and
high-dose methotrexatewith leucovorin.
Osteosarcomais radioresistant; radiation therapy has no role in the routine
management.

83. -Tyrosine KinaseInhibitor
-DOC : 1) CML
2) GIST
-Effective orally (All Tyrosine kinaseInhibitors)
-Metabolisedby CYP3A4
-S/E : Skin Rash (All Tyrosine kinaseInhibitors)

84. CML INDia Imatinib(DOC)
Nilotinib
Dasatinib
Lung cancer After ECG we look for
Lungs
After –Afatinib
E-Erlotinib
C-Ceritinib
G-Geftinib
RCC WePASS urine due to
kidney
P -Pazotinib
A-Axitinib
S-Sorafenib
S-Sunitinib
HCC We feel Sorryfor Liver
cancer
Sorry-Sorafenib
GIST Imatinib(DOC)
Malignant Melanoma DVT D-Dabrefinib
V-Vemurafenib
T-Trameltenib
Medullarycarcinoma thyroidVandematram Vandetanib

85. 22) Which of the following drug acts by inhibiting tyrosine kinaseactivated by EGF
receptor as well as HER2
AImatinib
BGeftinib
CErlotinib
DLapatinib

86. DLapatinib

87. 23) Paclitaxelacts by (DNB June 2011)
ATopoisomeraseinhibitor
BInhibition of Microtubule formation
CMitotic cell inhibitor
DExaggerates polymerization and causes the stabilization of the microtubules

88. Ans. DExaggerates polymerization and causes the stabilization of the
microtubules
II. It enhances polymerization of tubulin: a mechanism opposite to that of vinca
alkaloids.
III. The microtubules are stabilized and their depolymerizationis prevented.
IV. This stability results in inhibition of normal dynamic reorganization of the
microtubule network that is essential for vital interphaseand mitotic functions.
V. Abnormal arrays or ‘bundles’ of microtubules are produced throughout the
cell cycle.

89. 24. ATRA is useful in the treatment of which of the following type of AML?
(AIIMS Nov 2012)
AMonocyticleukemia
BMyelomonocyticleukemia
CPromyelocyticleukemia
DErythroleukemic leukemia

90. Ans. CAcute Promyelocyticleukemia {APL}
Treatment of promyelocyticleukemia is by tretinoin.
It is an oral drug that induces the differentiation of leukemia cells bearing the t
(15,17)
It is not effective in other forms of AML.

91. 25. Leucovorinis used as Rescue therapy for patients who are on one of the
following drug therapies
AAsparagine
BMethotrexate
C6-mercaptopurine
DCyclophosphamide

92. Ans. BMethotrexate
a.Methotrexatetoxicity: Folinicacid (Leucovorin, citrovorumfactor),is an
active coenzyme form which does not need to be reduced by DHFRasebefore
it can act.
b. Methotrexateis a DHFRaseinhibitor; its toxicity is not counteracted by folic
acid, but antagonized by folinicacid.
c. Folinicacid is expensive and not needed for the correction of simple folate
deficiency for which folic acid is good enough.

93. 26. Which phase of the cell cycle is resistant to most chemotherapeutic agents:
AG
0
BG
1
CG
2
DM

94. Ans. AG
0
a. The G
0phase is the resting or dormant stage of the cell cycle.
b. No cell division takes place. This phase is, overall, the most resistant to
chemotherapeutic agents because most of the (phase-specific) anti cancer
drugs produce their lethal effects quickest and best on cells that are actively
proliferating, whether synthesizing or preparing to synthesize DNA, or to
undergo mitosis.
Good examples of drugs that are reasonably effective against cells in G
0(or
any other phase) are the alkylatingagents (e.g., cyclophosphamide) and
several of the antitumor antibiotics (e.g., dactinomycin, doxorubicin).

95. 27.A cancer patient develops severe, irreversible cardiomyopathybecause the
maximum lifetime dose of an anticancer drug was exceeded. Which of the following
is most likely responsible for this patient’s symptoms? (AIPG 2011)
AAsparaginase
BBleomycin
CCisplatin
DDoxorubicin

96. Ans. DDoxorubicin
I.Doxorubicin, an antitumor antibiotic, is cardiotoxic, and the risk for and
severity of cardiomyopathyis dose-related.
II.[There is a maximum recommended lifetime (cumulative) dose for this
drug, and if it exceed the risk of cardiac damage rises significantly]

97. 28. Which of the following are the most common and worrisome adverse
responses associated with cyclosporine therapy? (AIPG 2010)
ACardiotoxicityand hepatotoxicity
BHepatotoxicityand nephrotoxicity
CHypotension and pulmonary fibrosis
DNephrotoxicityand infection risk

98. Ans. DNephrotoxicityand infection risk
a.Nephrotoxicity; occurs in about 8 of 10 patients receiving cyclosporine. It is
typically dose-dependent and, particularly in renal transplant patients, could
be due to either the drug (too much) or to rejection. Infection occurs about as
often as renal dysfunction.
b. Cyclosporine can cause hepatotoxicity, but the incidence is far lower than that
of renal responses or infection. Blood pressure changes can occur, but with
cyclosporine the change usually involves increased pressure, and it is common.
c. Cardiac or pulmonary toxicities and thromboembolismdue to the drug itself
are extremely uncommon. The drug blocks transcription of IL-2 and thus reduces
activity of CD-4 lymphocytes. This increases risk of infections.