Molecular response of follicular lymphoma to cyclophosphamide, doxorubicin, vincristine, prednisone C(H)OP or COP-based therapy as measured by polymerase chain reaction evidence of translocation (14;18)(q32;q21).
OBJECTIVE
Existing data suggest that conventional C(H)OP (cyclophosphamide, doxorubicin, vincristine, prednisone) regimen may not be intensive enough to achieve molecular response, as measured by polymerase chain reaction (PCR) evidence of translocation (14;18)(q32:q21) for follicular lymphoma. This study was undertaken to study the molecular response rate of follicular lymphoma to C(H)OP-based therapy and to analyze prognostic factors for molecular response.


METHODS
Twenty patients with pretreatment PCR evidence of t(14;18)(q32; q21) and at least one posttreatment PCR analysis after the initiation of the treatment with C(H)OP with or without radiation therapy constituted the basis for this analysis. The random effects logistic model was used to analyze the data. The following factors were investigated for their relationship to molecular response: gender, age, beta2-microglobulin, use of radiation therapy, Ann Arbor stage, and international Prognostic Index for malignant lymphoma.


RESULTS
Median follow-up was 56 months (range, 23-153 months). A total of 135 PCR results were available, 33 from bone marrow and 102 from peripheral blood. Overall, there was a clear and steady decreasing trend toward loss of PCR positivity with increasing time aftertreatment. By univariate analysis, stage > or = 3, stage = 4, International Prognostic Index > or = 2, and no radiation therapy were adverse factors for molecular response. On multivariate analysis, Ann Arbor stage IV and no radiation therapy were independent risk factors for PCR positivity, both for the peripheral blood data analyzed alone and for all data combined.


CONCLUSIONS
It is possible to achieve molecular response with C(H)OP with or without radiation therapy in patients with follicular lymphoma. Response rate depends on the Ann Arbor stage and radiation therapy.
Department of Radiation Oncology, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, Texas 77030, USA. chulha@mdanderson.org
Chul S
CS
Ha
Ming-Sheng
MS
Lee
Peter
P
McLaughlin
Susan L
SL
Tucker
Richard B
RB
Wilder
James D
JD
Cox
Fernando
F
Cabanillas
D000328:Adult; D000368:Aged; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D002883:Chromosomes, Human, Pair 14 / Q000737:chemistry / Q000235:genetics; D002887:Chromosomes, Human, Pair 18 / Q000737:chemistry / Q000235:genetics; D003520:Cyclophosphamide / Q000627:therapeutic use*; D004317:Doxorubicin / Q000627:therapeutic use*; D005069:Evaluation Studies as Topic; D005260:Female; D005500:Follow-Up Studies; D019254:Genes, bcl-2 / Q000235:genetics*; D006801:Humans; D016015:Logistic Models; D008224:Lymphoma, Follicular / Q000188:drug therapy* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011241:Prednisone / Q000627:therapeutic use*; D011379:Prognosis; D018714:Radiotherapy, Adjuvant; D014178:Translocation, Genetic / Q000235:genetics*; D016896:Treatment Outcome; D014750:Vincristine / Q000627:therapeutic use*; D001613:beta 2-Microglobulin / Q000097:blood
D001613:beta 2-Microglobulin; D014750:Vincristine; D004317:Doxorubicin; D003520:Cyclophosphamide; D011241:Prednisone