Questions List

I have a question.... Posted onOctober 6, 2020 2:21 pm

Thank you so much!!!! Posted onOctober 4, 2020 6:50 pm

CONGRATULATION TO EVERY BODY Posted onOctober 4, 2020 6:22 pm

Susanne dr. JAnuzzi: Can you give an example of an AOE that was recallsified as no AOE?Posted onOctober 4, 2020 5:50 pm

Javier the DLT question was from me- mike mauroPosted onOctober 4, 2020 5:31 pm

In the era of targeted therapy and often lack of ´DLT’ - ideas on design to tailor studies away from such approaches?Posted onOctober 4, 2020 5:24 pm

Mhairi Copland Are there particular trail designs that are better suited to answering therapy questions in rare leukemias, e.g advanced phase CML?Posted onOctober 4, 2020 5:19 pm

*********final session **************Posted onOctober 4, 2020 5:00 pm

These data were very useful regarding the delay in therapy and prognosis. Have the patients have longer term follow up for those in the 6 to 12 month group. CatPosted onOctober 4, 2020 4:40 pm

Mohamed Elbogdady: Nice to finally see you Dr Radich even if it is onlinePosted onOctober 4, 2020 4:39 pm

Do you have generic imatinib in your country? Posted onOctober 4, 2020 4:39 pm

***************Prize***************Posted onOctober 4, 2020 4:25 pm

Nobuko Hijiya, Ped Oncology, Columbia Univ We have not seen any cardiovascular events in published pediatric studies of dasatinib, nilotinib or ponatinib so far. Posted onOctober 4, 2020 4:14 pm

Nobuko Hijiya, Pediatric Oncology, Columbia University, USA For young adults and adolescents, I have no problem with switching to 2G. They have very few co-morbidities. But we do not know long-term effects after several decades. Posted onOctober 4, 2020 4:13 pm

Maaike Luesink - pediatric oncologist - Prinses Máxima Center - The Netherlands What is your opinion on switching to 2G-TKI in younger patients like adolescent and young adults who probably have a lower risk of cardiovascular adverse events?Posted onOctober 4, 2020 4:06 pm

Dear Beppe- for us the CML patients community TFR can not be a cure and we should not use this term. Cure might implicate that there is no need for contonious monitoring and this is too dangerous to tell a patient on TFR since it is agreed that ongoing monitoring is a must due to late relapses. GioraPosted onOctober 4, 2020 3:49 pm

Charlie Great Mask for both this debate and for our countryPosted onOctober 4, 2020 3:13 pm

2Posted onOctober 4, 2020 3:13 pm

I missed the first part of the talk. Assuming there are somatic mutations in addition to CALR and JAK2 mutations, do you see relative differences across the MF pts? (Mike Deininger)Posted onOctober 4, 2020 3:06 pm

Vignir Helgason: It's very likely that the changes in proliferation and differentiation of the megakaryocytes require some metabolic remodelling - did you see any great changes in expression of genes involved in central metabolic pathways? Posted onOctober 4, 2020 3:03 pm

Thanks Beth. Posted onOctober 4, 2020 2:58 pm

If samples are collected longitudinally, do you think that by using single cell analysis, we can find targets that can help in the conversion of a bystander normal cell to a neoplastic cell, along with the progression of the disease. Thanks, Soumen Chakraborty, IndiaPosted onOctober 4, 2020 2:55 pm

****************** special lecture ****************Posted onOctober 4, 2020 2:34 pm

By generating individual prognosis, how do you incorporate upcoming research drugs in whatever disease field? Dr Johnson HyacinthePosted onOctober 4, 2020 1:56 pm

****************** Day 4 ************************Posted onOctober 4, 2020 10:04 am

Posted onOctober 3, 2020 5:15 pm

What about HbF levels and their O2 disassociation curvesPosted onOctober 3, 2020 5:15 pm

O2 consumption goes up in hyperthyroid populations....would that not offset and benefit of an increased spleen size ?Posted onOctober 3, 2020 5:11 pm

*************************************************Posted onOctober 3, 2020 5:05 pm

Surely the reason to look for associations predictive of stopping is not to help predict patients (where the best test is just to stop and see) but to try and understand what is the biological reason for success so that we can try and manipulate (by immunotherapy, HDACs, BCL2/ inhibition etc) more patients to be able to stopPosted onOctober 3, 2020 4:49 pm

1 Does the slope of doubling time match halving time's? I suppose you had a look at that. 2 To which extent could fluctuation during TFR (hinting also the role of immune system) blur the accuracy of the doubling time?Posted onOctober 3, 2020 4:46 pm

Posted onOctober 3, 2020 4:41 pm

Dr. Kim and Dr. Gale: Your presentations back-to-back seemed to be in contradiction of how much we can value the models and analyses of duration of DMR. Dr. Kim's did a very thorough and interesting analysis, but Dr. Gale had just told me to question such analyses. What should I do?Posted onOctober 3, 2020 4:32 pm

One point is very important in Euroski the predictive model was performed only to predict TFR at 6 Months. . FX Mahon to robert Gale. Posted onOctober 3, 2020 4:17 pm

To Giora: Thank you for doing these studies that educate us doctors about patients' views. They are very valuable, but do you think there is still some patient selection, of patients who are proactive in reaching out to patient organizations and that overall the understanding of TFR is much less when we consider the many patients who have not heard from their doctor and do not reach out to patient organizations? Posted onOctober 3, 2020 3:58 pm

Test questionPosted onOctober 3, 2020 3:27 pm

Rather like hitting ELN milestones which predicts excellent outcome to a TKI, isn't the best predictor of being able to stop, the fact that patients are still off treatment 6 months later? Do we really need all these extra tests?Posted onOctober 3, 2020 3:26 pm

FX Mahon = congratulation Agnes for this Very good présentation I think we need to make différence between late Molecular relapse and early relapse Alter TFR , what is your idea ? Posted onOctober 3, 2020 3:26 pm

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If e.g. more NK cells are beneficial for a successful TKI stop: Would you see any tolerable novel intervention treatment alternative to increase this cell population in individual pts, and thus perhaps improve the chance for a longer TFR? Leif Stenke Stockholm Posted onOctober 3, 2020 3:24 pm

I see that you did not mention the prognostic score presented last year by the Hammersmith group. They also found age to be a predictive factor. Have any other groups found this?Posted onOctober 3, 2020 3:23 pm

Could the decline of WBC from the start of the disease be a surrogate marker for halving time. Dr Johnson-AnsahPosted onOctober 3, 2020 2:56 pm

Naoto Takahashi (Japan) Question to Dr. Katia Pagnnano: I understand Pioglitazon with IM was feasible and safe. My question is 60% TFR rate at 30 month was fit to your expectation of the endpoint in this trial or not ? Posted onOctober 3, 2020 2:55 pm

couPosted onOctober 3, 2020 2:53 pm

Thank you for the presentations. Is there a cheaper, reliable alternative to bcr-abl test. The price of doing it limits proper patient monitoring in some countries and makes drug free remission almost impossible. What do you do to encourage drug adherence in your patients. Thank you. Oguns OlatokunboPosted onOctober 3, 2020 2:50 pm

Posted onOctober 3, 2020 2:48 pm

Nice presentation. Q: Several pts developed blast crisis after 6-10 yrs of treatment with ima: Did any these pts progress while in MMR or better? If during non-MMR, why suboptimal responses? BR Leif Stenke StockholmPosted onOctober 3, 2020 2:33 pm

A question for Naranie Shanmuganathan From Ram Thakur, Sweden: Regarding 9-days vs. 21-days halving time of BCR-ABl1 levels, what could be the possible biological mechanisms of differences between the two groups? Possibility 1: Are the CML cells more resistant to tyrosine kinase induced cell death in 9-day versus 21-day halving groups? Possibility 2: The CML cells in the two groups of patients are equally sensitive but are replenished faster (potentially from a pool of CML stem cells) ensuring the decline is slower in 21-day group versus 9-day group? Posted onOctober 3, 2020 2:32 pm

It was not clear to me whether the 2GTKI were given first line. Because you have such a good population based registry, you probably have a very good idea of the change in first-line therapy over time. What proportion have a 2GTKI first line?Posted onOctober 3, 2020 2:21 pm

@dr. Shanmuganathan: did you notice if the halving time upon TKI treatment correlated with the rapidity of losing response in TFR (i.e. patients who initially reduced rapidly BCR-ABL but relapsed in TFR did also lose response in the first months of TFR, or not?) thanks Massimiliano Bonifacio, Verona, ItalyPosted onOctober 3, 2020 2:14 pm

What do you think went wrong for the 30% of patients who had very fast halving times but did not reach eligibility for a trial of discontinuation? Were they all on imatinib? Did they develop secondary mutations? Was compliance a factor?Posted onOctober 3, 2020 2:10 pm

I meant imagining not imaging. ThanksPosted onOctober 3, 2020 1:52 pm

Thank you for the presentation. Would it be useful to check the serum calcium and phosphate levels in CML patients on Imagining with muscle cramps? Oguns OlatokunboPosted onOctober 3, 2020 1:51 pm

How do you choose the treatment for a patient who tried TFR and relapsed? Do you give the same treatment or change and when? GioraPosted onOctober 3, 2020 1:48 pm

what about dealing with occurence of F359C mutation resistant on asciminib in patients failing in CABL trial? Combination strategy to recover sensibilityPosted onOctober 3, 2020 12:48 pm

For both: Would it make sense to have a uniform starting dose of 200mg BID, given universal activity? Are we risking to select T315I with time and lose the opportunity to deal with T315I (Mike Deininger)Posted onOctober 3, 2020 12:43 pm

For Delphine: The inclusion criteria regarding CV history are different in OPTIC vs, PACE. Can you speculate how much of the toxicity is really avoidable in the 'real world'? (Mike Deininger)Posted onOctober 3, 2020 12:40 pm

1- It seems that asciminib is a promising agent to manage patients with advanced line cml. What is known about dosage/dose optimization. 2- regarding second line patients is the lack of response or the intolerance in your experience that drives more the choice to change therapy to a third line? (Laura)Posted onOctober 3, 2020 12:31 pm

*****************Posted onOctober 3, 2020 12:12 pm

when evaluating intolerance to TKI how do you relate to the gap between the perception of Drs and patients in relations to the severity of teh side efect? GioraPosted onOctober 3, 2020 11:43 am

Toni Montserrat: As a patient, I would like to be able to try the TFR (under control, obviously), even there is a relapse... I'll have had some months with less "toxicity" on my body. For sure my liver and other organisms will be happy with that¡¡¡ When deciding go to TFR you're accepting the possibility (50%) to relapse...with pleasure¡¡¡ ;-)Posted onOctober 3, 2020 9:47 am

Thank you so much Jane for an amazing talk. You are a living testimonie for teh change in CML treatment and thanks to you and your friends we the patients are here alive today. GioraPosted onOctober 3, 2020 9:36 am

Congratulations to Jane from FX Mahon I am proud to you No Specific question just thank you for your very nice talk.Posted onOctober 3, 2020 9:27 am

Question to Sara: very nice data. Have you verified whether the transfer of membrane receptors you observed between CAF and endothelial cells is bidirectional? Or is it the one way transfer?Posted onOctober 3, 2020 7:56 am

https://global.gotomeeting.com/join/742194453Posted onOctober 3, 2020 7:09 am

*********** Day 3 ******************Posted onOctober 3, 2020 6:15 am

*********** Special lecture 3 **********Posted onOctober 2, 2020 4:44 pm

Thank you. Posted onOctober 2, 2020 4:07 pm

For Justin, Have you identified any neo-antigens in your mouse studies of using PD-1 blocker in myeloid leukemia. Posted onOctober 2, 2020 4:06 pm

Which is more feasible, immunotherapy or targeted inhibitors, for the treatment of AML. Soumen Chakraborty, IndiaPosted onOctober 2, 2020 3:24 pm

**********Special Symposium on Onco ********************Posted onOctober 2, 2020 3:09 pm

Very nice talk. Do you know why upregulated TNF signaling is not reduced after TKI treatment (since it is BCR-ABL related)? Thanks- Ravi Bhatia Posted onOctober 2, 2020 2:00 pm

Question for Makela (D. Vetrie): Given that levels of normal CIP2A mRNA is prognostic, could the relationships between NOCIVA and prognosis be a transcriptional bystander effect driven by expression of the CIP2A locus?Posted onOctober 2, 2020 1:11 pm

There seems to be a disconnect between dose associated molecular response and PFS/OS which shows no dose effect. Given that PFS/OS is the clinically relevant endpoint, why not just start using 15 mg and increase dose if no response ?Posted onOctober 2, 2020 11:58 am

Congratulation on the presentations - in a primary resistant patient to 3 tki, not eligible for transplant, treated with ponatinib with complete hematologic response, but no cytogenetic or molecular response after more than one year of treatment, do you see a benefit in maintaining ponatinib (the only toxicity so far is controlled hypertension) Posted onOctober 2, 2020 11:58 am

Tim Hughes - in which patients do you NOT dose reduce regardless of response?Posted onOctober 2, 2020 11:57 am

Questions for Prof Cortes***************Posted onOctober 2, 2020 11:39 am

Some patients stay in the suboptimal window for years, do these patients need to be switched to 2G TKIPosted onOctober 2, 2020 11:30 am

You mentioned no data after 2G fail, however bosutinib showed really good results on 3l and 4L. What is your opinion? Posted onOctober 2, 2020 11:29 am

What about mutation analysis at the diagnosis time to safe time and avoid switching TKIPosted onOctober 2, 2020 11:29 am

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Posted onOctober 2, 2020 11:28 am

Dr Tibelli mentioned DMR achieved on Ponatinib for resistant 2 GEN TKI as an option for future TFR. Is this today recomended? i thought resistance to a TKI prevents a future TKI.Posted onOctober 2, 2020 11:28 am

Does treatment line affect the response rates to ponatinibPosted onOctober 2, 2020 11:25 am

• Is there any recommendations or guidelines on how to determine the CV risk of patient?Posted onOctober 2, 2020 11:24 am

How would you monitor CV risk for CML patients receiving TKI treatment?Posted onOctober 2, 2020 11:24 am

Test question from Midori Posted onOctober 2, 2020 11:10 am

*********Incyte**********Posted onOctober 2, 2020 10:58 am