SOHO/MLI R/R CLL Continuous Learning Collaborative – Assessment

SOHO/MLI R/R CLL Continuous Learning Collaborative - Assessment

Thinking of the live intensive, please answer the following questions.

Please enable JavaScript in your browser to complete this form.

- Step 1 of 9

Name *

First

Last

Email *

1. Which of the following changes have you made in your practice after participating in this program (select all that apply)?

Ordered more tests for TP53, del17, and IgHV mutational status to assess risk
Updated practice protocols to align with the latest guidelines
Increase the use of non-covalent BTK inhibitors
Increase referral to CAR T-cell therapies
Optimized sequencing of BTK inhibitors and venetoclax-based regimens based on patient-specific factors and risk
Improved monitoring of BTK inhibitor- and venetoclax-related AEs
Reached more often to colleagues for complex patient cases
Increased time for patient education on molecular/genetic testing and treatment choices
Initiated shared decision-making discussions with my patients
Other

Other (please specify): *

Please describe other changes you have made in your practice after participating in this program.

2. A 70-year-old man with CLL (unmutated IgHV, no del(17p), no TP53 mutation) was started on ibrutinib. After 10 months, he developed grade 3 atrial fibrillation requiring drug discontinuation. He now shows mild progression of lymphadenopathy but remains asymptomatic. Which next line of therapy is most appropriate?

Venetoclax plus obinutuzumab
Bendamustine and rituximab
Acalabrutinib
Idelalisib plus rituximab

3. A 74-year-old woman with CLL (unmutated IGHV, TP53 mutation, no del17p) achieved a partial response to venetoclax + rituximab as initial therapy. At relapse, she was started on ibrutinib but discontinued after 4 months due to intolerance (diarrhea and arthralgias). Her disease is now progressing again. Which of the following is the most appropriate next-line therapy?

Restart venetoclax
Pirtobrutinib
Acalabrutinib
Idelalisib plus rituximab

4. A 59-year-old man with CLL (mutated IGHV, no TP53 mutation, no del17p) was treated with obinutuzumab + chlorambucil and achieved a partial remission. Two years later, he presents with biochemical progression, rising lymphocyte counts, and moderate fatigue (PS 1). Which of the following is the most appropriate second-line therapy?

Repeat obinutuzumab and chlorambucil
Idelalisib plus rituximab
Venetoclax plus obinutuzumab
Ibrutinib

5. A 68-year-old man with relapsed CLL has been on acalabrutinib for 3 months. He develops a grade 1 rash (localized, nonpruritic, no systemic symptoms) on his face and trunk. His counts remain stable, and there is no CLL progression. What is the most appropriate management?

Permanently discontinue acalabrutinib and switch to venetoclax-based therapy
Continue acalabrutinib and start topical corticosteroids for rash management
Temporarily hold acalabrutinib and initiate systemic corticosteroids
Switch to an alternative BTK inhibitor due to intolerance

6. A 75-year-old woman with R/R CLL is being treated with zanubrutinib. She develops new-onset atrial fibrillation, medically managed for heart rate. The cardiologist in charge recommends continuing rate control and anticoagulation medication. How would you manage this patient?

Permanently discontinue zanubrutinib and initiate venetoclax-based therapy
Continue zanubrutinib with appropriate cardiac management
Immediately switch to acalabrutinib
Hold zanubrutinib indefinitely and observe

7. A 65-year-old man with relapsed CLL and bulky lymphadenopathy starts venetoclax with appropriate clinical tumor lysis syndrome (TLS) prophylaxis and inpatient monitoring. Despite these precautions, he develops TLS during ramp-up, with severe arrhythmia. How would you manage this patient?

Restart venetoclax at a lower dose after recovery
Delay venetoclax for 2 weeks, then resume ramp-up
Discontinue venetoclax permanently and switch to a BTK inhibitor
Continue venetoclax with more aggressive hydration

8. A 70-year-old woman with relapsed CLL is treated with pirtobrutinib and achieved a partial response. After 10 weeks on therapy, routine labs reveal grade 3 neutropenia (ANC at 700/µL), but the patient has no fever and does not show signs of infection. This is the first occurrence of neutropenia. She is otherwise tolerating the therapy well. What is the most appropriate management strategy?

Permanently discontinue pirtobrutinib and switch to venetoclax
Hold pirtobrutinib and resume at a lower dose when ANC gets back within normal range
Continue pirtobrutinib and initiate prophylactic antibiotics
Continue pirtobrutinib and add supportive measure with G-CSF

9. A 70-year-old woman with R/R CLL is being treated with pirtobrutinib. She presents to clinic with new spontaneous bruising on her arms and reports minor gum bleeding when brushing her teeth. Her platelet count is within normal range. What is the most likely etiology underlying her bleeding symptoms?

Thrombocytopenia due to marrow infiltration of CLL
Acquired hemophilia
BTK inhibitor–associated platelet dysfunction
BTK-inhibitor-induced thrombocytopenia

10. A 65-year-old man with R/R CLL is on day 7 after receiving liso-cel. He has no fever, but suddenly becomes confused and unable to write his name or follow simple commands. His vitals are stable, and head CT appears normal. What do you think is the underlying cause of his symptoms?

ICANS
Delirium associated with sepsis
Stroke
Brain metastases

the in Other

11. An 82-year-old man with R/R CLL has been receiving venetoclax plus obinutuzumab for 5 months. He presents with a 2-week history of worsening fatigue, weight loss, and persistent night sweats. He has no signs of infection. Laboratory values remain stable compared to prior exams. Imaging reveals new intra-abdominal lymphadenopathy and enlargement of both the liver and spleen. What is the most likely explanation for his current presentation?

Venetoclax-related tumor lysis syndrome
Rituximab-associated infusion reaction
Progressive CLL disease
Regimen--induced liver injury

12. Which of the following changes have you made in your practice related to adverse event management for BTK inhibitors? (select all that apply)

Implemented routine cardiovascular risk assessment before initiating BTK inhibitor therapy
Increased monitoring for signs/symptoms of atrial fibrillation in patients treated with BTK inhibitors
Collaborated more closely with cardiologists for patients with pre-existing cardiovascular conditions
Initiated earlier management or referral for hypertension
Educated patients about bleeding risks
Increased monitoring and infection prophylaxis (e.g., antiviral, antifungal, or antibacterial prophylaxis)
Adapted treatment plans for patients with recurrent infections while on BTK inhibitor therapy
Increase the use of growth factors for patients with neutropenia
Incorporated dose holds, reductions, or switches to alternative therapies due to adverse events
Increased patient education for AE self-reporting
Other

Other *

Please describe what other changes you have made in your practice related to adverse event management for BTK inhibitors.

13. Consider your 65-year-old patient waiting for molecular/genetic testing results. Which of the following results carries the poorest prognostic value?

Mutated TP53/del17p/mutated IgHV
Del17p/mutated IgHV and S481 mutations
Mutated TP53/del17p/unmutated IgHV
Mutated TP53 /unmutated IgHV and S481 mutations
Unsure

14. What is your current understanding of the role of pirtobrutinib based on the latest US/NCCN guideline recommendations?

It can be used instead of a covalent BTK inhibitor at any therapy line
It can only be used as third-line therapy after a covalent BTK inhibitor- and a venetoclax-based regimen
It can be used as early as second-line after a covalent BTK inhibitor-based regimen
It can be used after chemoimmunotherapy

15. How many of your patients avoided switches due to better AE management (e.g., Afib/HTN with pirtobrutinib)?

0
1-3
4-6
6-10
>10

16. Based on the NCCN guidelines, what biomarker molecular/mutational status would you assess for a patient with R/R CLL as part of prognostic evaluation?

IgHV mutational status
TP53 overexpression
BTK mutational status
SF3B1 mutational status

17. How many patient consultations have you conducted where you confidently used NCCN guidelines to facilitate shared decision-making in treatment decisions in the last 2 weeks?

0
1-3
4-6
7-10
>10

18. Have you discussed with your patients this week how genetic or molecular test results affect treatment choices?

19. How many patients with CLL/SLL have shown improved outcomes (e.g, fewer bleeds, better QoL) due to changes in sequencing approaches since this activity?

0
1-3
4-6
7-10
>10
N/A

20. How many patients starting venetoclax-based regimens have you proactively assessed and mitigated TLS risk for since this activity?

0
1-3
4-6
7-10
>10
N/A

21. How many patients avoided switches due to better AE management (e.g., Afib/HTN) with pirtobrutinib in the last 3 months?

0
1-3
4-6
7-10
>10

22. In the ELEVATE-TN trial, one arm combined the BTK inhibitor acalabrutinib with the anti-CD20 monoclonal antibody obinutuzumab. What was the added toxicity with obinutuzumab?

Atrial fibrillation
Thrombocytopenia
Hypertension
Infections

23. How many patients with R/R CLL received updated sequencing with pirtobrutinib since the activity?

0
1-5
6-10
>10
N/A

24. Liso-cel was granted accelerated approval in patients with R/R CLL, based on the phase 1/2 TRANSCEND CLL 004 trial. Which of the following patients would liso-cel be the most appropriate for?

Patient who relapsed on ≥ 4 lines of prior therapy irrespective of risk category
Patient who relapsed on ≥ 2 (high risk) or ≥ 3 (standard risk) lines of prior therapy
Patient who relapsed on ≥ 1 (high-risk) or ≥ 2 (standard risk) lines of prior therapy
Patient who relapsed following allogeneic hematopoietic stem cell transplantation

25. Based on this activity, are you likely to modify your approach to using non-covalent BTK inhibitors (e.g., pirtobrutinib)?

Yes, I plan to incorporate non-covalent BTK inhibitors more frequently in appropriate patients
Yes, I will re-evaluate my current approach and consider adjustments based on what I learnt
No, my current approach aligns with the information presented in this activity
Not likely, this activity did not change my approach to using non-covalent BTK inhibitors

26. What common non-C481 BTK mutations have been detected for patients with CLL treated with acalabrutinib, zanubrutinib and pirtobrutinib?

T474I and L528W mutations
E513G / E513Q mutations
A428D and V416L
L528W and A428D

27. After participating in this activity, are you considering using BTK inhibitors as bridging therapy for allo-HCT especially for high-risk patients?

Yes, I will consider BTK inhibitors as bridging therapy for high-risk patients
No, my clinical approach prior to allo-HCP will not change
I need more evidence or guidance before considering BTK inhibitors in that setting
I have already been using BTK inhibitors in this setting and I will continue
I plan to discuss this approach with my multidisciplinary team on a case-by-case basis

28. A 76-year-old female patient with CLL was initially diagnosed 2.5 years ago and harbored high-risk features (TP53 mutation and unmutated IGHV status). She was treated for frontline therapy with venetoclax + obinutuzumab and relapsed within 5 months of completing therapy. She was then treated with acalabrutinib but progressed after 6 months. Her PS is 2, and she has an inflammatory disorder (ulcerative colitis). She also presents with lingering cytopenia. Which of the following is the most appropriate next line of treatment?

Idelalisib plus rituximab
Non-covalent BTK inhibitor (e.g., pirtobrutinib)
Bendamustine plus rituximab
Liso-cel
Repeat venetoclax with anti-CD20 antibody

29. After participating in this activity, what remaining concerns, if any, do you have about prescribing a non-covalent BTK inhibitor? (Select all that apply)

Limited long-term data/follow-up
Access or reimbursement issues
Safety/tolerability concerns or unfamiliar with AE management
Lack of familiarity with this class of agent
Potential for cross-resistance to covalent BTK inhibitors
It is not included in institutional formulary
No concerns
Other

Other *

Please describe what other remaining concerns you have about prescribing a non-covalent BTK inhibitor.

30. Which of the following is potentially the biggest barrier to shared decision-making (SDM) when discussing treatment sequencing in relapsed/refractory CLL?

Availability of few approved therapies for R/R CLL
Limited patient understanding of the importance of asking questions and expressing concerns and preferences during SDM encounters
Universal agreement among hematology/oncology clinicians on optimal sequencing strategies

31. After participating in this activity, how will you NOW typically approach the selection of venetoclax regimens vs BTK inhibitors in relapsed/refractory CLL?

I will lean toward venetoclax-based regimens for their time-limited and deep responses
I continue to prefer BTK inhibitors for ongoing disease control
I individualize therapy based on patient-specific factors and comorbidities
I still lack confidence regarding that matter

32. How many patient consultations have you conducted where you confidently used NCCN guidelines to facilitate shared decision-making in treatment decisions in the last 2 weeks?

0
1-3
4-6
7-10
>10

33. A 73-year-old man with relapsed/refractory CLL, who showed signs of cognitive decline for few weeks, is overwhelmed by all the treatment options after progressing on both a venetoclax-based regimen and a covalent BTK inhibitor. He meets with his care team, in the presence of his daughter. Which of the following best represents an effective approach to shared decision-making in this clinical scenario?

Recommend the treatment option most appropriate based on current guidelines and explain that it offers the highest likelihood of disease control
Provide a reduced list of treatment options, discuss treatment options with the daughter and ask her to select on behalf of the patient
Discuss the patient’s values, preferences, and daily limitations with him and his daughter, then present treatment options tailored to those priorities
Defer treatment selection, until the patient and his daughter first discuss together when they are at home, and call the care team to communicate their decision

34. How many patients have been impacted by changes you made based on this activity?

<2
2-5
6-10
11-20
21-40
≥ 40

35. Have you discussed with your patients this week how genetic or molecular test results affect treatment choices?

36. How many patients with CLL/SLL have shown improved outcomes (e.g, fewer bleeds, better QoL) due to changes in sequencing approaches since this activity?

0
1-3
4-6
7-10
>10
N/A

37. How many patients starting venetoclax-based regimens have you proactively assessed and mitigated TLS risk for since this activity?

0
1-3
4-6
7-10
>10
N/A

38. For a patient with high-burden R/R CLL starting pirtobrutinib, what is a key AE prophylaxis strategy per NCCN guidelines?

Premedicate with antihistamines to prevent infusion reactions
Monitor for bleeding and withhold before any surgical procedures
Start concurrent corticosteroids to prevent cytokine release syndrome
Use prophylactic growth factors to prevent neutropenia

39. How many patients avoided switches due to better AE management (e.g., Afib/HTN) with pirtobrutinib in the last 3 months?

0
1-3
4-6
7-10
>10