Edward F. Attiyeh
University of Pennsylvania · Rehabilitation Medicine
Active 1993–2026
About
Edward F. Attiyeh, M.D., is an Adjunct Assistant Professor of Pediatrics (Oncology) in the Department of Pediatrics at the University of Pennsylvania's Perelman School of Medicine. He holds an A.B. in Molecular Biology from Princeton University, obtained in 1995, and an M.D. from Albert Einstein College of Medicine, completed in 1999. His professional focus is on pediatric oncology, with particular expertise in neuroblastoma and related research areas. His contributions include investigating the genomic and molecular mechanisms underlying neuroblastoma, identifying prognostic markers, and exploring tumor suppressor activities. Dr. Attiyeh is involved in research that advances understanding of tumor genomics and treatment outcomes in pediatric cancers.
Research topics
- Biology
- Cancer research
- Genetics
- Medicine
- Internal medicine
Selected publications
Cancer Chemotherapy and Pharmacology · 2026-01-06 · 3 citations
articleOpen accessCorrespondingAbstract Purpose Prostate-specific membrane antigen (PSMA) has been identified as a therapeutic target for metastatic castration-resistant prostate cancer (mCRPC). The recent success of radioligands targeting PSMA spurred development of new PSMA-targeting agents including immunotherapy. JNJ-80038114 is a bispecific antibody that binds PSMA on tumor cells and CD3 on T cells to induce anti-tumor activity. Methods This was a phase 1, open-label, multicenter study of JNJ-80038114 in participants with mCRPC and ≥ 1 prior systemic therapy. JNJ-80038114 was administered subcutaneously every 3 weeks (Q3W), starting at 0.1 mg. The primary endpoint was safety. Secondary endpoints included pharmacokinetics (PK), immunogenicity, and prostate-specific antigen (PSA). Results At final analysis, 39 participants received 0.1–180 mg JNJ-80038114 across 11 dose-escalation cohorts for a median of 9.3 weeks (range, 0.1–31.1). The most common treatment-related adverse events (TRAEs; ≥20%) included cytokine release syndrome (CRS, 51.3%, all Grade 1–2), injection-site reactions (46.2%), and fatigue (30.8%). Related Grade ≥ 3 TRAEs occurred in 51.3% of participants; dose-limiting toxicities occurred in 3 (7.7%). Four participants (10.3%) developed clinically significant neuropathies. In 37 PK-evaluable participants, mean exposure (C max , AUC) increased with increasing doses. Anti-drug antibodies (ADA) were reported in 56.8% (21/37) participants. One participant had confirmed PSA decrease ≥ 50%. Three participants had radiological responses in the context of rapidly rising PSA. Following a review of data, the study was terminated. Conclusions This first-in-human study of JNJ-80038114 was discontinued early due to its lack of preliminary clinical activity, neurologic toxicities, high rates of CRS, and the development of ADAs impacting PK. Clinicaltrial.Gov information NCT05441501, Registered July 1, 2022.
Journal of Clinical Oncology · 2024-06-01 · 1 citations
article10003 Background: A subset of children with INRGSS Stage MS neuroblastoma (NBL) may be observed without treatment, while others have rapidly evolving symptoms that can be life-threatening. ANBL1232 adapted a previously developed semi-quantitative objective scoring system (OSS) to assign a numeric value to symptoms and laboratory abnormalities. The goal was to standardize monitoring, therapy initiation, and treatment duration in this cohort. Methods: Patients with newly diagnosed Stage MS NBL were eligible for this prospective trial. An OSS score (OSSS) was assigned at enrollment; the total number was based on scoring in 5 systems: gastrointestinal (GI), respiratory, circulatory, renal, and hepatic. Within the 5 systems, individual clinical and laboratory parameters were scored as not present = 0, mild/moderate = 1 [Grade 2 CTCAEv4.0 adverse event (AE)] or severe = 2 (Grade ≥3 AE). The OSSS was the sum of highest score within each organ system (maximum score: 2 per system, 10 total). Asymptomatic MS patients with an OSSS < 2 who were either < 3 months (mo) of age without hepatomegaly or 3-18 mo of age with favorable biology tumors were eligible for observation without initial treatment. Observed patients underwent monthly physical examinations and laboratory assessments for the first 6 mo following diagnosis. Tumor imaging was performed every 3 mo for 1 year, then every 6-12 mo through 36 mo. An OSSS ≥2 or a protocol-defined increase in primary tumor size prompted initiation of therapy. Results: From July 2014 to February 2021, 89 eligible and evaluable patients with newly diagnosed stage MS NBL enrolled. Among these, 18 (20.2%; 5 male and 13 female) were eligible for observation. Observed patients were older at diagnosis (median age: 2.87 vs. 1.81 mo, p = 0.23) and more likely to have primary tumors without image-defined risk factors (62.5% vs. 30.0%, p = 0.0166) than those assigned to therapy up front. Nearly all observed patients (17/18) had abdominal/adrenal primaries. The initial OSSS was 0 in all observed patients. Median reported observation time was 36 mo (range: 1-36 mo); 13 patients completed all required monthly assessments for the first 6 mo. No patients in the observation cohort required initiation of therapy for an increase in OSSS. One patient with OSSS = 1 at mo 3 had complete GI symptom resolution by mo 5. Conclusions: An OSSS of 0 at diagnosis can aid in identifying a favorable group of patients with stage MS NBL who can be safely observed. No patients in the observation cohort developed evidence of organ dysfunction or OSSS > 1 despite frequent physical examination and comprehensive laboratory testing, suggesting that follow up may be safely liberalized in this population over time. Clinical and laboratory criteria implemented at diagnosis could be used to identify patients requiring prompt treatment. Clinical trial information: NCT02176967 .
Annals of Oncology · 2024-09-01 · 5 citations
articleJournal of Clinical Oncology · 2024-06-01 · 12 citations
article5010 Background: hK2 (encoded by the KLK2gene) is a novel target expressed on the cell surface of prostate cancer cells with restricted expression elsewhere. JNJ-6420 is a first-in-class anti-hK2 antibody–based targeted radiotherapy delivering 225 Ac, a high-energy short-range alpha-particle emitter, to prostate cancer cells. Here we report the first-in-human study evaluating JNJ-6420 in heavily pretreated biomarker-unselected participants (pts) with mCRPC who received ≥1 prior androgen receptor pathway inhibitor. Methods: Intravenous JNJ-6420 was escalated from 50 μCi to 400 μCi every 8-12 weeks in the outpatient setting with no residential radioprotective restrictions. Prior radioisotopic therapy was an exclusion criterion. Primary objectives were safety and defining a recommended phase 2 dose (RP2D). Secondary objectives included preliminary assessment of clinical activity. Results: As of January 5, 2024, 67 pts received ≥1 JNJ-6420 dose. Exposure and clinical activity for the 57 pts in the ≥150 μCi JNJ-6420 cohorts are summarized (see Table); 35/57 (61.4%) experienced grade ≥3 TEAEs, and 21 (36.8%) had a serious TEAE. TEAEs of note included thrombocytopenia (63.2%) and interstitial lung disease (ILD, 9%). All instances of ILD occurred at cumulative doses ≥500 μCi and prior to implementation of pulmonary function surveillance. Grade ≥3 TEAEs (≥10%) included anemia (26.3%), thrombocytopenia (17.5%), lymphopenia (10.5%), and leukopenia (10.5%). 9/57 (15.8%) pts discontinued treatment due to TRAEs; 4 TRAEs resulted in death. At doses ≥150 μCi, the PSA50 rate was 45.6%. To date, across all dose cohorts, 31 pts (46%) remained on treatment for ≥24 weeks. Prolonged clinical, biochemical, and radiographic responses were noted in pts receiving doses of 150 μCi and higher. Durable responses included pts on treatment for 112 weeks (96 weeks since last dose), 88 weeks (13 weeks since last dose), and 46 weeks (after a single dose). Conclusions: In this first-in-human study, key TEAEs of JNJ-6420 were thrombocytopenia and ILD, both associated with repeated dosing. At ≥150 μCi, 1-2 doses of JNJ-6420 elicited profound and durable biochemical and radiographic responses. Evaluation of the RP2D is ongoing. These data highlight hK2 as a novel target for targeted alpha-particle therapy. Clinical trial information: NCT04644770 . [Table: see text]
2023-03-31
supplementary-materialsOpen access<p>Supplementary Table 1 - PDF file 78K, Genomic aberrations in the Cyclin D/CDK4/CDK6/RB pathway occur frequently in neuroblastoma cell lines</p>
Data from Dual CDK4/CDK6 Inhibition Induces Cell-Cycle Arrest and Senescence in Neuroblastoma
2023-03-31
preprintOpen access<div>Abstract<p><b>Purpose:</b> Neuroblastoma is a pediatric cancer that continues to exact significant morbidity and mortality. Recently, a number of cell-cycle proteins, particularly those within the Cyclin D/CDK4/CDK6/RB network, have been shown to exert oncogenic roles in neuroblastoma, suggesting that their therapeutic exploitation might improve patient outcomes.</p><p><b>Experimental Procedures:</b> We evaluated the effect of dual CDK4/CDK6 inhibition on neuroblastoma viability using LEE011 (Novartis Oncology), a highly specific CDK4/6 inhibitor.</p><p><b>Results:</b> Treatment with LEE011 significantly reduced proliferation in 12 of 17 human neuroblastoma-derived cell lines by inducing cytostasis at nanomolar concentrations (mean IC<sub>50</sub> = 307 ± 68 nmol/L in sensitive lines). LEE011 caused cell-cycle arrest and cellular senescence that was attributed to dose-dependent decreases in phosphorylated RB and FOXM1, respectively. In addition, responsiveness of neuroblastoma xenografts to LEE011 translated to the <i>in vivo</i> setting in that there was a direct correlation of <i>in vitro</i> IC<sub>50</sub> values with degree of subcutaneous xenograft growth delay. Although our data indicate that neuroblastomas sensitive to LEE011 were more likely to contain genomic amplification of <i>MYCN</i> (<i>P</i> = 0.01), the identification of additional clinically accessible biomarkers is of high importance.</p><p><b>Conclusions:</b> Taken together, our data show that LEE011 is active in a large subset of neuroblastoma cell line and xenograft models, and supports the clinical development of this CDK4/6 inhibitor as a therapy for patients with this disease. <i>Clin Cancer Res; 19(22); 6173–82. ©2013 AACR</i>.</p></div>
2023-03-31
preprintOpen access<p>Supplementary Figure 4 - PDF file 88K, Protein level expression of FOXM1 in neuroblastoma</p>
2023-03-31
preprintOpen access<p>Supplementary Figure 6 - PDF file 75K, Statistical analysis of in vivo growth suppression. (A) Growth rates of BE2C, 1643, and EBC1 xenografts treated with 200 mg/kg LEE011 or vehicle, as determined by linear mixed effects analysis. (B) Summary table of statistics</p>
2023-03-31
supplementary-materialsOpen access<p>Supplementary Table 1 - PDF file 78K, Genomic aberrations in the Cyclin D/CDK4/CDK6/RB pathway occur frequently in neuroblastoma cell lines</p>
2023-03-31
preprintOpen access<p>Supplementary Figure 2 - PDF file 55K, Neuroblastoma tissue microarray. A tissue microarray demonstrates expression of RB in neuroblastoma that is higher in high-risk and MYCN amplified samples compared to low-risk or non-amplified samples (p = 0.03)</p>
Recent grants
NIH · $697k · 2013
Frequent coauthors
- 255 shared
John M. Maris
- 134 shared
Yaël P. Mossé
University of Pennsylvania
- 123 shared
Sharon J. Diskin
Children's Hospital of Philadelphia
- 108 shared
Kristina A. Cole
University of Pennsylvania
- 82 shared
Andrew Wood
Edinburgh Royal Infirmary
- 82 shared
Bruce Pawel
- 77 shared
Cuiping Hou
Children's Hospital of Philadelphia
- 72 shared
Håkon Håkonarson
University of Pennsylvania
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