Chromosomes and Revlimid
 

Hi All,
In this article they show that patients with several different chromosome aberrations - not only del5q - can respond well when they are treated with Revlimid. Some patients were treated with Revlimid in combination with Vidaza. As you can see the patient groups are very small:
"The most frequent cytogenetic abnormality among the patients who received Revlimid was gain of chromosome 8 material (6/42), followed by the loss of chromosome 20 material (5/42). Patients with gain of chromosome 8 had high overall response rate to Revlimid (5 out of 6, 83%) and overall response rate in patients with chromosome 20 abnormalities was 3 out of 5."
http://www.jhoonline.org/content/pdf/1756-8722-5-4.pdf
Kind regards
Birgitta-A

Complex chromosomal abnormalities + options
 

Thank you to the person who posted his karyotype previously. Mine is 45,XX, der(5;17)(p10;q10), +8, psudic(14;22)(p11.2;11.2),-20, +22[cp10]. I've just completed my 4th round of Vidaza. Last time my WBCs seemed to have responded:) From what I understand between round 4 and 6 is when one knows if there is a response. I was rather down this week when Hemonc and I talked about Revlimid as I had read that 3% in complex chromosomal abnormalities respond vs. 67% in 5q- only. So... given you've said +8 and -20 respond that's 2 more abnormalities I have. Perhaps there are options. Does anyone have a source for understanding what different chromosomes control?

Vidaza + Revlimid
 

Hi winkryda,
Perhaps your doctor will combine Vidaza (azacitidine) and Revlimid (lenalidomide)? This combination shows the best response rate I have seen - 72%.

Phase 2 study of the lenalidomide and azacitidine combination in patients with higher-risk myelodysplastic syndromes
Mikkael A. Sekeres1, Ramon V. Tiu2, Rami Komrokji et al
Leukemia Program, Department of Hematologic Oncology and Blood Disorders, Cleveland Clinic Taussig Cancer Institute, Cleveland, OH, United States;
Blood Aug 2012

Lenalidomide and azacitidine each have activity in myelodysplastic syndromes (MDS) patients, where both microenvironment and cell regulatory mechanisms contribute to disease pathogenesis.

The objective of this multicenter, Phase 2 expansion trial was to determine the efficacy and safety of combination therapy with azacitidine (75mg/m2/d x 5 days) and lenalidomide (10mg/d x 21 days (28-day cycle)) in patients with higher-risk MDS.

Among 36 patients enrolled (18 Phase 1, 18 Phase 2), median age was 68 years (range 47-78) and follow-up was 12 months (range 3-55). IPSS categories included Intermediate-1 (n=5 patients with excess blasts), Intermediate-2 (20), and High (11).

Common grade 3/4 non-hematologic adverse events included febrile neutropenia (22% of patients), other infection (11%), pulmonary (11%), cardiac (11%), constitutional (11%), and dermatologic (11%).

The overall response rate (per modified MDS International Working Group criteria) was 72%: 16 patients (44%) achieved a complete response (CR), 10 (28%) had hematologic improvement.

Median CR duration was 17+ months (range, 3-39+); median overall survival was 37+ months (range, 7-55+) for CR patients, 13.6 months for the entire cohort (range, 3-55).

TET2/ DNMT3A/ IDH1/2 mutational status was associated with response in a limited number of patients.

The lenalidomide/azacitidine combination is well-tolerated and highly active in treating higher-risk MDS.

As far as I understand only the del5q aberration has been studied so they have some idea of what the aberration control.

This week we ought to be able to read the abstract from the hematology conference i Stockholm with 10 000 hematologists. Perhaps this study will be updated.
Kind regards
Birgitta-A