Dr. Rofida Nofal is a physician scientist with special interest in benign hematology, immune-hematology and stem cell transplant. She is a postdoc scholar at the Czechowicz lab in the Stanford University’s Department of Pediatrics, Hematology, Oncology, Stem Cell Transplantation and Regenerative Medicine Division.
Dr. Nofal’s primary clinical interests are immune-hematological disorders, primary immune-deficiency/immune dysregulations disorders as well as non-malignant transplant and non-genotoxic conditioning. Her current research interests are in bone marrow failure syndromes focusing on Fanconi Anemia (FA); understanding the disease biology, the immune profile of patients with FA as well as determinants of disease severity, progression, and response to therapy.
Her current main research project at the Czechowicz lab addresses clonal hematopoiesis in patients with Fanconi Anemia, trying to understand leukemogenesis and identify good biomarkers for early detection of clonal evolution to inform treatment decisions in an effort to improve outcome of stem cell therapy in Fanconi Anemia. Other research projects she is involved in, include gene therapy and alternative donor therapy for Fanconi Anemia; addressing how therapy affects disease phenotype, leukemogenesis and stem cell biology and function.
Dr. Nofal completed a pediatric residency in the Children’s Hospital Zagazig university in Egypt, after which she worked as an assistant lecturer in the department of Pediatrics. During that time, she pursued specialty training in the Primary Immune Deficiency (PID) in Cairo University Children’s Hospital, where she developed her interests in immune-hematology, immune-deficiency and dysregulations. Dr. Nofal then moved to the US and completed a pediatric residency in St. John Hospital in MI where she continued to pursue her specialty interests during her rotations in the Comprehensive Immune-Hematology program in Mott Children’s Hospital in Ann Arbor, the Diagnostic Immunology Lab in Cincinnati Children’s Hospital, and the BMT center in Children’s Hospital LA. Dr. Nofal then joined the pediatric hematology oncology program at UCSF Benioff Children’s Hospital with focus on immune-hematology, BMF syndromes, non-malignant and in-utero transplant.
Clinical Fellowship, UCSF Benioff Children’s Hospital Oakland, CA, Pediatric Hematology Oncology (2019)
Clinical Residency, Ascension St. John Children’s Hospital Detroit, MI, Pediatrics (2017)
Clinical Residency, Zagazig University Children’s Hospital Zagazig, Egypt, Pediatrics (2011)
MS, University of Zagazig School of Medicine Zagazig, Egypt, Pediatrics and Neonatology (2011)
MD, University of Zagazig School of Medicine Zagazig, Egypt, Medicine and Surgery (2007)
Agnieszka Czechowicz, Postdoctoral Faculty Sponsor
Reduced-Intensity/Reduced-Toxicity Conditioning Approaches Are Tolerated in XIAP Deficiency but Patients Fare Poorly with Acute GVHD
JOURNAL OF CLINICAL IMMUNOLOGY
2022; 42 (1): 36-45
X-linked inhibitor of apoptosis (XIAP) deficiency is an inherited primary immunodeficiency characterized by chronic inflammasome overactivity and associated with hemophagocytic lymphohistiocytosis (HLH) and inflammatory bowel disease (IBD). Allogeneic hematopoietic cell transplantation (HCT) with fully myeloablative conditioning may be curative but has been associated with poor outcomes. Reports of reduced-intensity conditioning (RIC) and reduced-toxicity conditioning (RTC) regimens suggest these approaches are well tolerated, but outcomes are not well established. Retrospective data were collected from an international cohort of 40 patients with XIAP deficiency who underwent HCT with RIC or RTC. Thirty-three (83%) patients had a history of HLH, and thirteen (33%) patients had IBD. Median age at HCT was 6.5 years. Grafts were from HLA-matched (n = 30, 75%) and HLA-mismatched (n = 10, 25%) donors. There were no cases of primary graft failure. Two (5%) patients experienced secondary graft failure, and three (8%) patients ultimately received a second HCT. Nine (23%) patients developed grade II-IV acute GVHD, and 3 (8%) developed extensive chronic GVHD. The estimated 2-year overall and event-free survival rates were 74% (CI 55-86%) and 64% (CI 46-77%), respectively. Recipient and donor HLA mismatch and grade II-IV acute GVHD were negatively associated with survival on multivariate analysis with hazard ratios of 5.8 (CI 1.5-23.3, p = 0.01) and 8.2 (CI 2.1-32.7, p < 0.01), respectively. These data suggest that XIAP patients tolerate RIC and RTC with survival rates similar to HCT of other genetic HLH disorders. Every effort should be made to prevent acute GVHD in XIAP-deficient patients who undergo allogeneic HCT.
View details for DOI 10.1007/s10875-021-01103-6
View details for Web of Science ID 000701344000001
View details for PubMedID 34586554
View details for PubMedCentralID PMC8478634
- Reduced Intensity/Reduced Toxicity Conditioning Approaches Are Tolerated in XIAP Deficiency But Patients Fare Poorly With Acute GVHD. Transplantation and Cellular Therapy 2021; 27 (3): S13-S14
- SPLENIC INFARCTION INDUCED BY EPSTEIN-BARR VIRUS INFECTION IN A PATIENT WITH SICKLE CELL TRAIT JOURNAL OF PAEDIATRICS AND CHILD HEALTH 2019; 55 (2): 249-251
- Cardiac Considerations for Treating Cancer in Infants and Children In Cancer and The Heart 2019
Neuroblastoma in North East Egypt: A 5-Year Multicenter Study
WILEY. 2018: S251-S252
View details for Web of Science ID 000445195002097
Title: If You Do Not Think of It, You Will Not Look for It, GATA2 Mutation Diagnosis Triggered by Immunohematological Profile
SPRINGER/PLENUM PUBLISHERS. 2018: 412
View details for Web of Science ID 000431311600183
INTRAVENOUS IMMUNOGLOBULIN-RELATED HEMOLYSIS IN KAWASAKI DISEASE: CASE REPORT AND REVIEW OF LITERATURE
SPRINGER/PLENUM PUBLISHERS. 2017: 256
View details for Web of Science ID 000396924700152
- Case Report of An Adolescent Male with Unexplained Pancytopenia: GATA2-associated Bone Marrow Failure and Genetic Testin Global Pediatric Health 2017; 4: 1-4
Splenic Infarction Induced By Epstein-Barr Virus Infection in a Patient with Sickle Cell Trait
AMER SOC HEMATOLOGY. 2015
View details for Web of Science ID 000368021802225
Clinico-epidemiology of neuroblastoma in north east Egypt: A 5-year multicenter study
2015; 10 (2): 1054-1062
Neuroblastoma, an embryonal malignancy of the sympathetic nervous system, is the most frequent extracranial solid tumor The clinico-epidemiological features of neuroblastoma in infants and children were investigated between January 2005 and January 2010 at the Pediatric Oncology units of Mansoura, Zagazig, and Tanta University Children's Hospitals (Egypt). Of 142 cases of neuroblastoma, 10 were omitted from the study due to defective data. The median age of the patients was 30 months, with 75.8% aged ≥1 year and 24.2% aged <1 year at time of diagnosis. The male-to-female ratio was 1.06. Suprarenal glands were the most common primary tumor site (72.7%). The majority of the patients (76.7%) had stage IV disease. Favorable pathology was observed in 43.8% of patients, while 56.2% exhibited unfavorable pathology. The estimated survival rate of patients was 30.7±10.0%, and mean survival time was 24.2±5.2 months. The rate of mortality was 28.6% for patients aged <1 year, and 81.8% for those aged ≥1 year (P=0.005). For patients with favorable pathology, the rate of mortality was significantly lower (28.6%) compared with that of patients with unfavorable pathology (77.8%; P=0.049). Although the association between outcome and each of the primary tumor sites, children's oncology group risk and gender was statistically insignificant, a large effect size was identified between outcome and primary tumor site, as well as children's oncology group risk and a medium effect size was identified between outcome and gender. Additionally, an age of ≥1 year was associated with unfavorable pathology (P=0.024), stage IV disease (P=0.026) and a suprarenal primary tumor site (P=0.001).
View details for DOI 10.3892/ol.2015.3335
View details for Web of Science ID 000358676200091
View details for PubMedID 26622625
View details for PubMedCentralID PMC4509073
- Two-year Old Egyptian Child with Chediak-Higashi Syndrome Journal of Clinical Immunology 2012; 32: 352–409