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Cessation of nilotinib in patients with CML who have kept deep molecular responses for 2yrs

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Submitted by sandy craine on Thu, 03/10/2019 - 12:50pm

Patients who maintained MR4.5 at 24 months of consolidation therapy proceeded to discontinuation of nilotinib. The study enrolled 149 patients; 112 patients proceeded to consolidation therapy with nilotinib; 90 patients maintained MR4.5 with consolidation therapy, and 87 proceeded to discontinuation of nilotinib. The treatment-free remission (TFR) (MR4.5) rate at both 1 and 3 years after discontinuation of nilotinib was the same, at 60.9% (90% CI 51.6–69.7).

19 September 2019

Combining Asciminib with Ponatinib Suppresses Emergence Highly Resistant BCR-ABL1 Mutants

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Submitted by sandy craine on Thu, 03/10/2019 - 12:42pm

We demonstrate that combining asciminib with ATP site TKIs enhances target inhibition and suppression of resistant outgrowth in Ph+ clinical isolates and cell lines. Inclusion of asciminib restores ponatinib's effectiveness against currently untreatable compound mutants at clinically achievable concentrations. Our findings support combining asciminib with ponatinib as a treatment strategy for this molecularly defined group of patients.

Long‐term follow‐up of lower dose dasatinib (50 mg daily) as frontline therapy in newly diagnosed chronic CML

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Submitted by sandy craine on Thu, 03/10/2019 - 12:06pm

Dasatinib, a potent Bcr‐Abl tyrosine kinase inhibitor, is approved for the treatment of chronic‐phase chronic myeloid leukemia (CML‐CP) in the frontline and salvage settings. Notable side effects include pleural effusions and myelosuppression. Dasatinib at 50 mg daily has previously been reported to be active and better tolerated than the approved 100‐mg daily dose. The aim of this study was to update the long‐term follow‐up results of dasatinib at 50 mg daily as frontline therapy for CML‐CP. ClinicalTrials.gov (NCT02689440)

CML: the concepts of resistance and persistence and the relationship with BCR-ABL1

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Submitted by sandy craine on Thu, 03/10/2019 - 11:55am

Chronic myeloid leukaemia is driven by a hybrid gene, BCR-ABL1, that codes for a leukemogenic tyrosine kinase (TK) protein of 210 KDa (p210BCR-ABL1). Resistance to TK inhibitor (TKI) therapy occurs in relatively few patients, no more than 10%, while persistence of minimal residual disease during TKI therapy occurs in the great majority of patients.  Leukemia vol 33, pgs 2358–2364 (2019

https://www.nature.com/articles/s41375-019-0562-1

Cortes Highlights Second-Generation TKIs for Frontline Therapy in CML

David Fitz's picture
Submitted by David Fitz on Fri, 09/08/2019 - 10:59am

Jorge Cortes sees the future of CML care in earlier treatments. “I think that a lot of the focus now is to see if we should do some interventions early on to try to optimize the number of patients who get to the deepest molecular responses and that would, at some point, be eligible for treatment discontinuation,” he said in an interview with Targeted Oncology.

Read the full article. 

Video Recordings: UK Chronic Myeloid Leukaemia Patient Day 2019

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Submitted by David Fitz on Mon, 15/07/2019 - 4:46pm

Chronic Myeloid Leukaemia Patient Day

Saturday, 21st September 2019, Leeds

Agenda

9.30 – 10.00  Registration

CML and its Treatment

10.00 – 10.05  Introduction and Welcome 

10.05 – 10.20  Chronic myeloid leukaemia – what is it? Dr Kate Rothwell

CML Horizons 2019 Presentations and Video streams are available now!

David Fitz's picture
Submitted by David Fitz on Sat, 06/07/2019 - 11:14am

Videos and PDF copies of presentations from the CML Advocates conference, 2019, are now available and can be found by following the link below:

https://www.cmladvocates.net/cmlhorizons/cml-horizons-2019/conference-information

Below is an overview of the available materials, but you will find that and more by following the link above.

Presentations, Video streams and Photo Gallery are available now!

 

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