Honors & Awards


  • Exchange Programme Paediatric Radiology Fellowship Grant, European Society of Radiology (2017)
  • Invest in Youth, European Society of Radiology (2019)

Stanford Advisors


All Publications


  • Brain MRI changes in children and young adults with B-cell acute lymphoblastic leukemia following chimeric antigen receptor T-cell therapy. European radiology Kim, H. G., Yeom, K. W., Vasyliv, I., Shokri Varniab, Z., Erickson, C., Baggott, C., Schultz, L. M., Daldrup-Link, H. E. 2025

    Abstract

    To evaluate brain MRI findings in children and young adults after chimeric antigen receptor (CAR) T-cell therapy for B-cell acute lymphoid leukemia (B-ALL) and associate results with clinical and neurological symptoms.We reviewed pre- and post-CAR-T cell therapy brain MRIs of B-ALL patients aged 25 years or younger who underwent therapy between April 2015 and October 2023 at a single institution. MRI abnormalities were categorized as no change, exacerbation of preexisting lesion, or newly developed lesion. Clinical CAR-mediated toxicities, including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) grades, were recorded. Patients were grouped into those with and without 'exacerbated/new lesion,' and clinical and neurological symptoms were compared using Fisher's exact test.Sixteen patients with pre- and post-CAR brain MRIs (median age 16 years [interquartile range, 11-21]; 9 males, 7 females) were included in the analysis. Post-CAR brain abnormalities were observed in 81% (13/16) of patients, including white matter (WM) signal changes (12/16), leptomeningeal enhancement (1/16), and cerebellar embolic infarction (1/16). Of the post-CAR WM lesions, 50% (6/12) were exacerbated, 33% (4/12) were newly developed, and 17% (2/12) remained unchanged compared to pre-CAR brain MRI. No difference in CRS (p = 0.079) or ICANS grades (p > 0.99) was observed between patients with and without 'exacerbated/new lesions'.Children and young adults with B-ALL can develop brain MRI abnormalities after CAR T-cell therapy, predominantly WM signal changes. These brain abnormalities did not show an association with higher CRS or ICANS grade.Question Brain MRI findings after chimeric antigen receptor (CAR) T-cell therapy for B-cell acute lymphoid leukemia (B-ALL) and their association with clinical and neurological symptoms are not well understood. Findings Brain MRI abnormalities, mostly white matter changes, were seen in 81% of patients but were not associated with CAR-mediated toxicities. Clinical relevance Brain MRI abnormalities, commonly observed post-CAR T-cell therapy, do not correlate with the severity of CAR-related toxicities, aiding in the clinical management and monitoring of these patients.

    View details for DOI 10.1007/s00330-025-11515-2

    View details for PubMedID 40111490

    View details for PubMedCentralID 4058440

  • Overall survival and central nervous system activity of crizotinib in ROS1-rearranged lung cancer-final results of the EUCROSS trial. ESMO open Michels, S., Massutí, B., Vasyliv, I., Stratmann, J., Frank, J., Adams, A., Felip, E., Grohé, C., Rodriguez-Abreu, D., Bischoff, H., Carcereny I Costa, E., Corral, J., Pereira, E., Fassunke, J., Fischer, R. N., Insa, A., Koleczko, S., Nogova, L., Reck, M., Reutter, T., Riedel, R., Schaufler, D., Scheffler, M., Weisthoff, M., Provencio, M., Merkelbach-Bruse, S., Hellmich, M., Sebastian, M., Büttner, R., Persigehl, T., Rosell, R., Wolf, J. 2024; 9 (2): 102237

    Abstract

    In 2019, we reported the first efficacy and safety analysis of EUCROSS, a phase II trial investigating crizotinib in ROS1 fusion-positive lung cancer. At that time, overall survival (OS) was immature and the effect of crizotinib on intracranial disease control remained unclear. Here, we present the final analysis of OS, systemic and intracranial activity, and the impact of co-occurring aberrations.EUCROSS was a prospective, single-arm, phase II trial. The primary endpoint was best overall response rate (ORR) using RECIST 1.1. Secondary and exploratory endpoints were progression-free survival (PFS), OS, and efficacy in pre-defined subgroups.Median OS of the intention-to-treat population (N = 34) was 54.8 months [95% confidence interval (CI) 20.3 months-not reached (NR); median follow-up 81.4 months] and median all-cause PFS of the response-evaluable population (N = 30) was 19.4 months (95% CI 10.1-32.2 months). Time on treatment was significantly correlated with OS (R = 0.82; P < 0.0001). Patients with co-occurring TP53 aberrations (28%) had a significantly shorter OS [hazard ratio (HR) 11; 95% CI 2.0-56.0; P = 0.006] and all-cause PFS (HR 4.2; 95% CI 1.2-15; P = 0.025). Patients with central nervous system (CNS) involvement at baseline (N = 6; 20%) had a numerically shorter median OS and all-cause PFS. Median intracranial PFS was 32.2 months (95% CI 23.7 months-NR) and the rate of isolated CNS progression was 24%.Our final analysis proves the efficacy of crizotinib in ROS1-positive lung cancer, but also highlights the devastating impact of TP53 mutations on survival and treatment efficacy. Additionally, our data show that CNS disease control is durable and the risk of CNS progression while on crizotinib treatment is low.

    View details for DOI 10.1016/j.esmoop.2024.102237

    View details for PubMedID 38350336

    View details for PubMedCentralID PMC10937203