Questions List

123Posted onMarch 5, 2021 8:13 am

bye all! congrats, elisabetta abruzzese Posted onFebruary 28, 2021 11:16 am

what about the difference in JAK2 happening in dividing cells vs bcr-abl in quiescent cellsPosted onFebruary 28, 2021 11:12 am

Posted onFebruary 28, 2021 11:11 am

Size of clone does mot necessarily determine pathogenecity e. g. portal vein thrombosis. Would you also see Posted onFebruary 28, 2021 11:01 am

****************Posted onFebruary 28, 2021 10:34 am

Do we need to report if IS is less than 0.0032?Posted onFebruary 28, 2021 10:26 am

Which TkI is recommended in p190 for cml? Zeeshan Pakistan Posted onFebruary 28, 2021 10:21 am

Posted onFebruary 28, 2021 10:21 am

In some patients during TFR the level of BCR-ABL continue to decrease and the pts obtain even stable PCR negativity. What is the role of immune system in TFR? Thanks!Posted onFebruary 28, 2021 10:21 am

in case of relapse we restart the same TKI ?Posted onFebruary 28, 2021 10:00 am

If CML patient resistance to all types of TKI. what is the best choices?Posted onFebruary 28, 2021 9:42 am

Why do we think that patients treated with momelotinib appear to have less thrombocytopenia than those treated with ruxolitinib? Is neuropathy still a relevant adverse event with this drug? Posted onFebruary 28, 2021 9:27 am

while you (N Cross) only touched on the IS. What is your experience with respect to how well it accomplishes it intended purpose (interlaboratory standardization of results)? Results from CAP surveys over the years might imply that there remains much interlaboratory variation even using the same commercial kits/platforms.Posted onFebruary 28, 2021 9:06 am

4Posted onFebruary 28, 2021 7:24 am

****** Day ***********Posted onFebruary 28, 2021 7:24 am

Why to stop ruxolitinib before transplant as long as it has benefit in GVHD?Posted onFebruary 27, 2021 5:47 pm

Do you perform splenic radiotherapy?Posted onFebruary 27, 2021 5:46 pm

***************** BMS**************Posted onFebruary 27, 2021 5:06 pm

@N.Kroeger:How do you deal with jak2 positivity following allogeneic hsct in myelofibrosis? When to start preemptive therapies in clinical routine? Do you use other preemptive strategies then DLI? Posted onFebruary 27, 2021 4:56 pm

2Posted onFebruary 27, 2021 4:29 pm

There is a recent paper by DeFilipp et al stating that there is no benefit from TKI maintenance therapy after allogeneic SCT. Can you comment on this? Thank youPosted onFebruary 27, 2021 4:24 pm

In blast phase MPN, how do you decide HMA/VEN vs HMA/JAKi? Posted onFebruary 27, 2021 4:23 pm

If in CML blast crisis a CR is reached with a TKI, do you need chemotherapy pre transplant? Posted onFebruary 27, 2021 4:23 pm

was the e1a3 transcript at blast crisis due to new alternative splicing (e1a3 expression on a background of an e13a3 genomic break) or genomic clonal evolution?Posted onFebruary 27, 2021 4:10 pm

Do you consider p53-mutation in MPN-BP predictive for venetoclax-efficacy favoring this vs TX?Posted onFebruary 27, 2021 4:02 pm

In the countries that doesn't perform allogenic bone marrow transplant wich is the best treatment plan in last crisis?Posted onFebruary 27, 2021 4:01 pm

If you choose to use Azacitidine and Rux in blast phase MF - not suitable for intensive therapy. How long do you continue for? What is your strategy for stopping if you do stop?Posted onFebruary 27, 2021 3:54 pm

Posted onFebruary 27, 2021 3:53 pm

Do you advice TKI treatment after alloSCT for CML blast crisis? Posted onFebruary 27, 2021 3:37 pm

****************Posted onFebruary 27, 2021 3:01 pm

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damien le paz excellent clear clinically significant informative talk thnak you Posted onFebruary 27, 2021 2:57 pm

damien le paz excellent clear clinically significant informative talk thnak you Posted onFebruary 27, 2021 2:57 pm

What about association Azacytidine and Ruxolitinib in PMF?Posted onFebruary 27, 2021 2:46 pm

What about Merkel skin carcinoma and Ruxo?Posted onFebruary 27, 2021 2:34 pm

Posted onFebruary 27, 2021 2:12 pm

Couple of years back there was a small case series and prior lab data indicating that low dose methotrexate (anti-inflammatory dosing) may have therapeutic benefit in myelofibrosis. What is the potential of this approach taking off?Posted onFebruary 27, 2021 2:04 pm

Why do we think that patients treated with momelotinib appear to have less thrombocytopenia than those treated with ruxolitinib? Is neuropathy still a relevant adverse event with this drug? Posted onFebruary 27, 2021 1:50 pm

In the case of aggressive non melanoma skin cancer is it mandatory to stop ruxolinitib?Posted onFebruary 27, 2021 1:43 pm

Why do we think that patients treated with momelotinib appear to have less thrombocytopenia than those treated with ruxolitinib? Is neuropathy still a relevant adverse event with this drug? Posted onFebruary 27, 2021 1:38 pm

ruxolitinibePosted onFebruary 27, 2021 1:32 pm

For Dr. Adam Mead. Thank ou for your talk. Any consideration about meanoma or non melanoma skin cancers and these medciations?Posted onFebruary 27, 2021 1:30 pm

When would the panelists use fedratinib rather than ruxolitinib as a front line therapy for MF?Posted onFebruary 27, 2021 1:06 pm

***********************Posted onFebruary 27, 2021 1:01 pm

When would the panelists use fedratinib rather than ruxolitinib as a front line therapy for MF?Posted onFebruary 27, 2021 1:01 pm

10 mg RuxolitinibPosted onFebruary 27, 2021 12:59 pm

What is the role of ruxolotinib in patients of ET with thrombotic events?Posted onFebruary 27, 2021 12:43 pm

In a patient with overt MF , splenomegaly , symptomatic and <50.000 platelets, if you only have Ruxo, would you start low dose Ruxo,5mg? use IFNPosted onFebruary 27, 2021 12:42 pm

What would you consider an early treatment start with Ruxo in MF ? What is your approach to finding early this patients?Posted onFebruary 27, 2021 12:36 pm

What is the recommended testing interval on patients with Asciminib? does it remain at q3mos?Posted onFebruary 27, 2021 12:33 pm

Plz tell me the best treatment as first line in CML young ptsPosted onFebruary 27, 2021 12:32 pm

What options of TKI in patient with chronic phase CML on imatinib and a recent diagnosis of GISTPosted onFebruary 27, 2021 12:32 pm

Elderly woman, CALR+MPN with thrombocytosis > 1000 and moderate anaemia (alleviated with r-EPO) intolerant to Hydrea/Busulfan (worsening anaemia and GIT symptoms; what would be your best approach since RUX does not improve anaemia. Posted onFebruary 27, 2021 12:31 pm

*Posted onFebruary 27, 2021 12:28 pm

************* Novartis ************Posted onFebruary 27, 2021 11:46 am

what about a 30yo patient treated with DASA 1st line, achieving CCyR and MR2, switched after 2 years to PONA and fluctuating between MR2-MR3 very reluctant in being transplanted, with a sibling compatible? would you insist to transplant or maybe adding IFN or trying another inhibitor? No mutations. Posted onFebruary 27, 2021 11:14 am

Posted onFebruary 27, 2021 11:14 am

Hyploidentical SCT - is it an option for patients in the first CP CML? Myeloablative or non-myeloablative SCT in chronic phase?Posted onFebruary 27, 2021 11:13 am

If the patient went into molecular remission with either Ponatinib/Bosutinib and had HSCT, would could consider these drugs again if there is persistence or rise in BCR-ABL post HSCTPosted onFebruary 27, 2021 11:13 am

What is the optimal DLI cell dose?Posted onFebruary 27, 2021 11:12 am

What about hypomethylation drugs after SCT&Posted onFebruary 27, 2021 11:12 am

what is you opinion on three way translocation (9;22;22)? Posted onFebruary 27, 2021 11:10 am

After SCT do you use maintenance therapy and what kind of therapy?Posted onFebruary 27, 2021 11:09 am

Should TKI be used post SCT and for how long?Posted onFebruary 27, 2021 11:08 am

What is the treatment of CML patient who relapsed after SCT?Posted onFebruary 27, 2021 11:04 am

The onset of TET2 and SETBP1 mutations is an iindication to transplant in chronic phase CML with persistent MMR1 after second tki and ponatinib? Posted onFebruary 27, 2021 11:02 am

What is the role of mutations outside BCR-ABL (ASXL1 ...) in the management of CML? Thanks! Posted onFebruary 27, 2021 11:02 am

In which situations should allograft be considered second line ie after failure of a single 2GTKI? Eg ACAs etc, contraindications to ponatinib but transplant feasible Posted onFebruary 27, 2021 11:00 am

What are current TRM rates for allo-SCT for CML?Posted onFebruary 27, 2021 10:59 am

What is the role in decision making of additional mutations (ASXL1)Posted onFebruary 27, 2021 10:53 am

**** Debate 2 ***Posted onFebruary 27, 2021 10:39 am

noPosted onFebruary 27, 2021 10:29 am

yesPosted onFebruary 27, 2021 10:29 am

Question for Professor M. Griesshammer: Does interferon start at the beginning of pregnancy or in the 2nd trimester? (Emilia Niculescu-Mizil, Romania)Posted onFebruary 27, 2021 10:12 am

What about if the husband was on TKI not the female partner are there any precaustions to follow?Posted onFebruary 27, 2021 10:08 am

Is there any difference in obstetrical outcomes in MPN patients based on driver mutation?Posted onFebruary 27, 2021 10:08 am

Thank you for all these very interesting presentations ! My question is about A male Cml patient, 52 years old. Chronic phase CML diagnosed in 2008. He was treated by Imatinib 400 mg. CHR at 3 months, CCYR at 12 months. The molecular response can not be assessed because he has a Bcr-abl transcript variant. He is in CCyR. The risk of relapse can not be assessed accurately. He wants to have a second kid. Should Imatinib be kept or stopped 3 months before the baby conception ? Thank you so much.Posted onFebruary 27, 2021 10:01 am

What are the safety data on peg Interferon and newer Interferon in pregnancy?Posted onFebruary 27, 2021 9:59 am

What dose / treatment scheme of interferon-alpha can be recommended during high-risk pregnancy in woman with MPN? And for pegylated interferon? Does the effectiveness depend on hematological response?Posted onFebruary 27, 2021 9:59 am

What dose of LMWH do you use? E.g. standard thromboprophylactic dose or an intermediate dose?Posted onFebruary 27, 2021 9:59 am

@ Martin Griesshammer: is this pegylated interferon?Posted onFebruary 27, 2021 9:58 am

Are you happy to use PEGylated interferon rather than standard interferon?Posted onFebruary 27, 2021 9:58 am

which pregnancy test do you recommend? what is the earliest time point to test for pregnancy under TKI? Posted onFebruary 27, 2021 9:28 am

When do you start CML therapy when patients are pregnant? When PCR >1%? When PCR >10%? When haematological relapse? When WCC >50? When would you use TKI in pregnancy? E.g. only second trimester? Only if INF does not bring about haematological remission?Posted onFebruary 27, 2021 9:28 am

Do you sperm bank men prior to starting TKI? Some data suggest sperm count/morphology is impacted by TKI.Posted onFebruary 27, 2021 9:25 am

Which is safe TKI in pregnancyPosted onFebruary 27, 2021 9:20 am

Iron deficiency can be deleterious in pregnancy. How do the panel manage this issue in PRV patients who may already be iron deficient or might require venesection during pregnancy?Posted onFebruary 27, 2021 9:16 am

**** Day 3 ****Posted onFebruary 27, 2021 9:13 am

Posted onFebruary 27, 2021 9:07 am

Posted onFebruary 26, 2021 6:51 pm

Based on the fact that the interruption of Ruxolitinib can induce the ruxolitinib cytokine storm , perhaps the interruption of the treatment in the ICU MF patiients could be the reason of worsening the decurse of the disease ?Posted onFebruary 26, 2021 5:19 pm

In this case is recommended discontinuation of ruxolitinib during cytokine storm reactions? What is more lethal in pat. with covid -19 and MPN cytokine storm or therapy discontinuation?Posted onFebruary 26, 2021 4:42 pm

to Dr Barbui: could there via a bias with mortality and ruxolitinib discontinuation due to the possibility that this discontinuation is more common in severe cases, like ICU cases, intubation and so on, in wich manteining ruxo is more complicatedPosted onFebruary 26, 2021 4:39 pm

Dr Rea: the mortality in severe cases at the CANDID study is high. Could you comment on thatPosted onFebruary 26, 2021 4:30 pm

Many patients with CML are asking, if they are in the voulnerable group, some on TKI's, others on stop, others have been through BMT for many years. or they can wait with vaccine as the rest of the population? This is a question from a patient organization in Denmark.Posted onFebruary 26, 2021 4:30 pm

*****************Posted onFebruary 26, 2021 4:28 pm

63 Yrs old lady with plt 800 , borderline diabetes and triple negative. do u give cytoreduction Posted onFebruary 26, 2021 4:14 pm

Do you see differences in safety and efficacy between the different kinds of IFNs, meaning Peg-IFN vs. Ropeg in your clinical practice?Posted onFebruary 26, 2021 4:09 pm

Posted onFebruary 26, 2021 4:09 pm

Regarding Ruxolitinb: Should we consider second neoplasias to avoid it in young-middle age patients? Posted onFebruary 26, 2021 4:09 pm

Do you feel a history of depression is a contraindication to interferon, even if very well controlled? Posted onFebruary 26, 2021 4:06 pm

Posted onFebruary 26, 2021 4:02 pm

Taking a cue from CML-TFR trials. What about time limited upfront IFN to effect some form of immune response, then followed by RUX.Posted onFebruary 26, 2021 4:02 pm

Taking a cue from CML-TFR trials. What about time limited upfront IFN to effect some form of immune response, then followed by RUX.Posted onFebruary 26, 2021 4:02 pm

in low risk ET with thrombocytosis higher than 1000G how do we manage please? Posted onFebruary 26, 2021 4:02 pm

To the two speakers: Since clinical trials having thrombosis as primary end-point are poorly feasible, which is the intermediate/surrogate end point you can consider? Keeping HCT less than 45% alone, with normal leukocytes...Posted onFebruary 26, 2021 4:01 pm

What is the effect of interferon on spleenomegaly?Posted onFebruary 26, 2021 4:00 pm

Posted onFebruary 26, 2021 4:00 pm

do you believe in the safety of peg IFN during pregnancy?Posted onFebruary 26, 2021 3:59 pm

maybe a bit off topic but... if one was to perform JAK2 MRD - . what is the concordance of JAK2 V617F molecular burden between PB and BM specimens. It this different in PV, ET, MF patients. What would be the optimal specimen type. Would you compare only like specimens.Posted onFebruary 26, 2021 3:59 pm

No (but Yes, for the majority ;-))Posted onFebruary 26, 2021 3:58 pm

NOPosted onFebruary 26, 2021 3:58 pm

I have patient with Jak2 positive PV (background: DM, Dyslipidemia), presented with portal vein thrombosis, splenomegaly, early grade 1oesophageal varices. She was started on anticoagulation but no cytoreduction as blood counts was ok. Now, she is having fluctuating mild leucocytosis, thrombocytosis but iron deficiency anemia. She developed liver cirrhosis and Gastroenterology team don't recommend Interferon. How to manage?Posted onFebruary 26, 2021 3:52 pm

Would you indicate Ruxolitinib first line to a PV patient , asymptomatic but diabethic, with Grade 1 reticullin fibrosis or you would prefer IFN? or HU first line?Posted onFebruary 26, 2021 3:31 pm

***************88Posted onFebruary 26, 2021 3:23 pm

I have Jak2 positive PV with portal vein thrombosis, Background of DM, Dyslipidemia... leucocytosis and thrombosytosis but can not give interferon due to liver cirrhosis. How to manage ?Posted onFebruary 26, 2021 3:13 pm

I have MPN patient Jak2 postive, with huge splenomegaly 27 cm and massive splanchnic thrombosis upon diagnosis, with portosystemic shunt and gastric varices (GI team refused to give anticoagulation for fear of variceal bleeding and gastric varices can not be ligated).. Blood Counts are not high, almost within range...no CV risk... how to treat?Posted onFebruary 26, 2021 3:11 pm

how do you manage Hct>45% in ET patients? in the same way as patients with PV or not?Posted onFebruary 26, 2021 2:57 pm

Emanuel, MPN should not be considered as a normal population. Thus, the concept of primary prevention cannot be applied in these diseases.Posted onFebruary 26, 2021 2:54 pm

I am apediatric haematologist: in ET we have tried to avoid cytoreduction in very young pts even with high plt counts and behave according to symptoms. If some hemorrhages apper, then cytorection . We think trials with IFN should be performed in these rare cases. Posted onFebruary 26, 2021 2:54 pm

Posted onFebruary 26, 2021 2:53 pm

In BC/Canada if the case could be reasonably be made for NGS in PV/ET, re-imbursement is not a issue as the test would be publicly funded. This is different than the funding environment in the US.Posted onFebruary 26, 2021 2:53 pm

Cocerning treatment according to the number of platelts in ET, may I suggest to follow-the guidelines rather than personal experience ? For instance, NCCN or ELN.Posted onFebruary 26, 2021 2:49 pm

this was for Nasseem - she repeatedly said that they do not NGS on PV patients but also talked about the value of NGS data in prognosis. maybe ngs in a perfect funding environment. Posted onFebruary 26, 2021 2:49 pm

Dr Gangat, very nice presentation. I believe that the number of phlebotomy per year in a patient at low-risk may depend on the frequency you see your patient during the follow-up. How often you see a low-risk patient during the follow-up?Posted onFebruary 26, 2021 2:46 pm

Patient was assymptomatic. And triple negativePosted onFebruary 26, 2021 2:43 pm

is there a role for simple plasmapherisis...Posted onFebruary 26, 2021 2:42 pm

There has been interest in pulmonary hypertension in MPN last couple of years. Would you screen for pulmonary artery hypertension in patients with MPN and how would that influence your management of these patientsPosted onFebruary 26, 2021 2:39 pm

In triple negative MF- should cytoreduction be introduced earlier?Posted onFebruary 26, 2021 2:38 pm

Dr. Messas, thoughts on your Vascular risk experience in CML and how to apply to PV? MF?Posted onFebruary 26, 2021 2:37 pm

Which antihypertensive drug do you suggest in PV?Posted onFebruary 26, 2021 2:34 pm

If the PLT count is more than 1 milion is recomended the use of aspirin?Posted onFebruary 26, 2021 2:29 pm

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*Posted onFebruary 26, 2021 2:26 pm

Posted onFebruary 26, 2021 2:12 pm

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Posted onFebruary 26, 2021 2:12 pm

T:o dr Gangat: When the number year of phlebotomies is so high to indicate cytoreducyion?Posted onFebruary 26, 2021 2:06 pm

Why aspirin twice a day ? The halftime of the effect is much longer.Posted onFebruary 26, 2021 1:55 pm

Do you recommend NGS screening for all newly diagnosed patients with JAK +ve disease for use in prognostication? Posted onFebruary 26, 2021 1:54 pm

****************Posted onFebruary 26, 2021 1:50 pm

Hould we treat with cytoreductive drugs a patients with ET Jak neg without CV risk factors?Posted onFebruary 26, 2021 1:41 pm

So in a case ofa 24-year-old patient with ET with JAK2V617F mutated and platelet 2.000.000 at presentation would you consider citorreduction? Posted onFebruary 26, 2021 1:37 pm

thrombocytosis; splenomegalyPosted onFebruary 26, 2021 1:19 pm

leukocytosis and thrombocytosisPosted onFebruary 26, 2021 1:16 pm

2Posted onFebruary 26, 2021 1:15 pm

Should we monitor JAK2 during MF management?Posted onFebruary 26, 2021 12:46 pm

What would you consider as early intervention in MF related toPV and ET? Would you start treatment with JAK2i, even if there are no symptoms nor splenomegaly? Posted onFebruary 26, 2021 12:45 pm

Hello, the voice is lowPosted onFebruary 26, 2021 12:27 pm

***** Day 2 *******Posted onFebruary 26, 2021 12:09 pm

Were there any changes in the RT-qPCR test methodology in the time period shown on the graph of responses?Posted onFebruary 25, 2021 6:21 pm

Do you think the combination of both drugs momelotinib and ruxolitinib together can increase more spleen response and maitain Hb level ?Posted onFebruary 25, 2021 5:47 pm

ponatinib as a bridge to transplant. two mutations portends a bad outcome...Posted onFebruary 25, 2021 4:39 pm

BPosted onFebruary 25, 2021 4:39 pm

BPosted onFebruary 25, 2021 4:39 pm

BPosted onFebruary 25, 2021 4:38 pm

dPosted onFebruary 25, 2021 4:37 pm

DPosted onFebruary 25, 2021 4:34 pm

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CPosted onFebruary 25, 2021 4:34 pm

dPosted onFebruary 25, 2021 4:34 pm

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A Posted onFebruary 25, 2021 4:33 pm

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I would check adherence and check again in 4-6Posted onFebruary 25, 2021 4:32 pm

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APosted onFebruary 25, 2021 4:30 pm

aPosted onFebruary 25, 2021 4:30 pm

dPosted onFebruary 25, 2021 4:27 pm

When Imatinib fails, should we look for new cytogenetic abnormalities (CCA) in the patient, in addition to TKD mutations?Posted onFebruary 25, 2021 4:13 pm

I think biggest issue for offering TFR is not data or disease, it is monthly PCR testing for first 12 months which significantly affects QOL. This certainly cause many patients decline TFR. What is the evidence for monthly PCR? Can this be done 3 monthly as sudden blast crisis is exceptionally rare! Posted onFebruary 25, 2021 3:31 pm

It would appear that this patient has a continued reduction in molecular burden. Stopping treatment now would likely halt this. If the patient had reached a plateau the stopping treatment would be ok - no?Posted onFebruary 25, 2021 3:30 pm

It would appear that this patient has a continued reduction in molecular burden. Stopping treatment now would likely halt this. If the patient had reached a plateau the stopping treatment would be ok - no?Posted onFebruary 25, 2021 3:30 pm

I think the answer related to the second case depends on our goal and the patient's .Posted onFebruary 25, 2021 3:28 pm

Do you have experience with TFR and generics? Which generics? Posted onFebruary 25, 2021 3:07 pm

************* Session 2 ***************Posted onFebruary 25, 2021 3:05 pm

Can we use Ruxolitinib as first line therapy in high risk polycythemia Vera patients with history of thrombosis??Posted onFebruary 25, 2021 2:58 pm

Thanks for this wonderful session, Please how do we manage a patient classified as low risk TE with thrombocytosis higher than 1000G, Posted onFebruary 25, 2021 2:56 pm

How important is it to keep the platelet count within normal limits in low risk ET patients who do not have any other symptoms? Cytoreduction with hydrea is not recommended in low risk ETPosted onFebruary 25, 2021 2:54 pm

What is the experience of the speakers with anagrelide in the second line treatment of ET. Do you still use it ? Do you fear inferior outcome on the long term as suggested by long term registry data from Mayo Clinic ?Posted onFebruary 25, 2021 2:44 pm

Once on cytoreduction do you often replete iron to help with symptoms of iron deficiency? Posted onFebruary 25, 2021 2:41 pm

Does ruxolitinib suspention an obligation in case of non melamomona skin cancer? Does the predisposition persist? Posted onFebruary 25, 2021 2:37 pm

is there any role for JAK2 MRD in patients treated with IFN? might it be predictive of medium term control of symptoms.Posted onFebruary 25, 2021 2:34 pm

For the single institution interferon analyses that demonstrated improved OS, did that analysis take into consideration CVD risk factors, disease duration and number of previous lines of therapy? It seems like it is typically the lowest thrombotic risk patients that are chosen for that therapyPosted onFebruary 25, 2021 2:33 pm

Heinz, any experience yet on dosing and switching patients from peg infa2a (roche) to Ro-PEG?Posted onFebruary 25, 2021 2:30 pm

Pending the availability of molecules like PTG-300, in patients with symptomatic iron deficiency because of phlebotomy (low risk PV, young patients) - do you consider cytoreduction for that indication, and if so, do you use hydroxyurea or would you favor ruxolitinib ?Posted onFebruary 25, 2021 2:28 pm

Question to Dr Stein Young man, 37 years old presents with a Portal and mesenteric vein thrombosis. Appears to be acute on chronic. Smoker, no other sig hx. Jak2 positive. Platelets at time of presenting 414. Now plat and white cell count within normal range. Anaemic due to ongoing varcies. Would you cyto reduce? How do you decide your parameters. Thanks Posted onFebruary 25, 2021 2:19 pm

in cases of HU resistance where Ruxo is not available, what is the next best line of drug to use, in resource poor country. Thank you Posted onFebruary 25, 2021 2:16 pm

BPosted onFebruary 25, 2021 2:13 pm

c Posted onFebruary 25, 2021 2:13 pm

DPosted onFebruary 25, 2021 2:13 pm

What is the evidence that not achieving an hematologic remission in ET by using HU is a risk factor for subsequent thrombosis?Posted onFebruary 25, 2021 2:12 pm

Brady, great talk, have you used ruxolitinb plus a second agent (Anagrelide? HU/ INF) as combination therapy in tough ET cases?Posted onFebruary 25, 2021 1:58 pm

Is progression to MF correlated to JAK2 allele burden?Posted onFebruary 25, 2021 1:48 pm

What was the proportion of patients with AML transformation on Besremi vs. other treatment modalities?Posted onFebruary 25, 2021 1:45 pm

It is recommended a combination of Interferon with another medicament (Hydroxiurea or Ruxolitinib ) in case 3 patient?Posted onFebruary 25, 2021 1:44 pm

Does liver enzyme elevation include gamma-glutamyl transferase or just GOT/GPT? Posted onFebruary 25, 2021 1:44 pm

Regarding the risk of varicella zoster reactivation in ruxolitinib treated patients: would you consider primary or at least secondary prevention with valaciclovir? What about the new shingrix vaccine ?Posted onFebruary 25, 2021 1:33 pm

What about association of non-JAK2 mutations with HU resistance or intolerance? Did you perform any NGS analysis to investigate that?Posted onFebruary 25, 2021 1:30 pm

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10 mgPosted onFebruary 25, 2021 1:12 pm

2Posted onFebruary 25, 2021 1:11 pm

4Posted onFebruary 25, 2021 1:07 pm

2Posted onFebruary 25, 2021 1:07 pm

Welcome and thanks to our amazing first session of speakers on MPN Cytoreduction!Posted onFebruary 25, 2021 1:03 pm

Day 1Posted onFebruary 25, 2021 6:06 am

...Posted onFebruary 24, 2021 8:27 pm

testPosted onFebruary 9, 2021 3:53 pm