(A) P,R
(B) Q,S
(C) P,Q
(D) R,S
(A) Omalizumab
(B) OndanPageron
(C) Vincristine
(D) Prednisone
R-CHOP is a multi drug regimen that includes rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone. Hydroxydaunorubicin is also called as doxorubicin and oncovin as vincristine.
(A) P
(B) Q
(C) R
(D) P,S
Dacarbazine in vivo converted into methyltriazenoimidazole carboxamide that acts as alkylating agent and produces methylation of O6 of guanine in DNA.
(A) The resistance towards 6-MP is due to alteration of HGPRT
(B) Allopurinol increases the action of 6-MP
(C) Azathioprine is prodrug of 6-MP
(D) 6-MP is given with leucovorin
6-MP can be metabolized by xanthine oxidase enzyme to thiouric acid which is inhibited by allopurinol. Hence allopurinol may increase the levels of methotrexate leading to its toxicity. 6-MP requires bioactivation into 6-thioinosinic acid by the enzyme hypoxanthine-guanine phosphoribosyl transferase
(A) Leucovorin is given along with 5-FU to decrease megaloblastic anemia
(B) Capecitabine is a prodrug of 5-FU converted by tumor specific thymidine phosphorylase
(C) The dose of 5-FU should be reduced in dihydropyridine dehydrogenase deficient patients
(D) Cytarabine inhibits DNA polymerase
Dihydropyridine dehydrogenase is responsible for metabolism of 5-fluorouracil. Patients who are deficient in DPD will have elevated levels of 5-FU in blood leading to its toxicity. Hence the dose of 5-FU should be individualized based on the DPD levels in the patient. Capecitabine is a prodrug of 5-FU. Methotrexate produces megaloblastic anemia and requires leucovorin supplement.