Devita, Hellman, and Rosenberg's Cancer

LWBK1006-32 LWW-Govindan-Review November 24, 2011 11:28

452 DeVita, Hellman, and Rosenberg’s CANCER: Principles and Practice of Oncology Review

Question 32.11. A 71-year-old woman presents with a mature lymphocytosis, diffuse lym-

phadenopathy, splenomegaly, thrombocytopenia, and an autoimmune

hemolytic anemia. Workup is consistent with CLL. Treatment is initi-

ated with four cycles of fludarabine and cyclophosphamide with a partial

response (PR). The patient elects to undergo a treatment break for the

next 6 months. She is then noted to have return of her lymphocytosis,

lymphadenopathy, and thrombocytopenia. Fludarabine and cyclophos-

phamide are reinitiated, but she demonstrates continued disease progres-

sion. What is the MOST appropriate next line of therapy?

A. Chlorambucil

B. Single-agent rituximab

C. Combination fludarabine, cyclophosphamide, with addition of ritux-

imab

D. Alemtuzumab

Question 32.12. Which of the following cytogenetic abnormalities is associated with poor

prognosis in patients with CML?

A. Iso-17q

B. Trisomy 8

C. Trisomy 19

D. Duplication of Philadelphia chromosome

Question 32.13. The Philadelphia chromosome and BCR-ABL fusion gene are observed

in all of the following hematologic malignancies, EXCEPT:

A. Acute myeloid leukemia (AML)

B. Acute lymphocytic leukemia (ALL)

C. Chronic myeloid leukemia (CML)

D. Chronic lymphocytic leukemia (CLL)

Question 32.14. Which of the following treatments are curative in patients with CML?

A. Imatinib

B. Dasatinib

C. Nilotinib

D. None of the above

Question 32.15. Which of the following statements is CORRECT regarding BCR-ABL in

CML?

A. The breakpoint in ABL is highly variable, and is almost always

upstream of exon 2.

B. The BCR-ABL fusion protein resides in the cytoplasm.

C. BCR breakpoints occur either between exon 13 and 14 or between

exon 14 and 15.

D. All of the above.