
Normal serum protein electrophoresis and mutated IGHV genes detect very slowly evolving chronic lymphocytic leukemia patients
Author(s) -
Chauzeix Jasmine,
Laforêt MariePierre,
Deveza Mélanie,
Crowther Liam,
Marcellaud Elodie,
Derouault Paco,
Lia AnneSophie,
Boyer François,
Bargues Nicolas,
Olombel Guillaume,
Jaccard Arnaud,
Feuillard Jean,
Gachard Nathalie,
Rizzo David
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1510
Subject(s) - ighv@ , lymphocytosis , chronic lymphocytic leukemia , medicine , biology , gastroenterology , stage (stratigraphy) , leukemia , immunology , oncology , paleontology
More than 35 years after the Binet classification, there is still a need for simple prognostic markers in chronic lymphocytic leukemia ( CLL ). Here, we studied the treatment‐free survival ( TFS ) impact of normal serum protein electrophoresis ( SPE ) at diagnosis. One hundred twelve patients with CLL were analyzed. The main prognostic factors (Binet stage; lymphocytosis; IGHV mutation status; TP 53 , SF 3B1 , NOTCH 1, and BIRC 3 mutations; and cytogenetic abnormalities) were studied. The frequencies of IGHV mutation status, cytogenetic abnormalities, and TP 53 , SF 3B1 , NOTCH 1, and BIRC 3 mutations were not significantly different between normal and abnormal SPE . Normal SPE was associated with Binet stage A, nonprogressive disease for 6 months, lymphocytosis below 30 G/L, and the absence of the IGHV 3‐21 gene rearrangement which is associated with poor prognosis. The TFS of patients with normal SPE was significantly longer than that of patients with abnormal SPE (log‐rank test: P = 0.0015, with 51% untreated patients at 5.6 years and a perfect plateau afterward vs. a median TFS at 2.64 years for abnormal SPE with no plateau). Multivariate analysis using two different Cox models and bootstrapping showed that normal SPE was an independent good prognostic marker for either Binet stage, lymphocytosis, or IGHV mutation status. TFS was further increased when both normal SPE and mutated IGHV were present (log‐rank test: P = 0.008, median not reached, plateau at 5.6 years and 66% untreated patients). A comparison with other prognostic markers suggested that normal SPE could reflect slowly advancing CLL disease. Altogether, our results show that a combination of normal SPE and mutated IGHV genes defines a subgroup of patients with CLL who evolve very slowly and who might never need treatment.