Purpose: Participation in acute leukemia clinical trials is inequitable across multiple sociodemographic categories. Tools that provide researchers with performance feedback on the representativeness of the patients they enroll are limited. We aimed to develop an electronic health record (EHR)-based dashboard to provide such feedback and to describe any enrollment inequities uncovered.
Methods: We created a visual dashboard linking leukemia clinical trial registration and EHR data at the Dana-Farber Cancer Institute. Accuracy of a patient inclusion and assignment algorithm was tested with a target area under the receiver-operator curve (AUROC) of >0.90 against manual review. Demographic metric identification, visualization construction, and dashboard refinement were performed through stakeholder cognitive testing. Analysis of a recent 5-year cohort generated by the final algorithm assessed bivariate associations between enrollment and demographic metrics. Multivariable logistic regression included significant bivariate results.
Results: The final algorithm assignment AUROC was 0.98. Metrics were identified and visualizations successfully constructed. Fourteen individuals participated in testing and identified areas for revision: category mergers, denominator filters, and data delivery preferences. In the initial cohort of 1,315 patients, 1,020 (77.6%) had enrolled in any study protocol: 553 (42.1%) in a treatment trial and 936 (71.2%) in a biobanking study. In a multivariable model, older age (odds ratio [OR], 0.83 [95% CI, 0.73 to 0.94]) and Non-Hispanic Black race-ethnicity (OR, 0.38 [95% CI, 0.18 to 0.82]) were associated with lower enrollment, and English primary language with higher enrollment (OR, 2.50 [95% CI, 1.30 to 4.79]).
Conclusion: We developed a research participation equity performance feedback dashboard for clinical researchers, and we identified actionable inequities. Next steps include feasibility and efficacy testing as well as implementation.
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http://dx.doi.org/10.1200/OP.24.00319 | DOI Listing |
Cureus
December 2024
Radiology, Tata Main Hospital, Jamshedpur, IND.
We report a 37-year-old male patient who had nonbilious vomiting, no passage of flatus, and recurring abdominal pain. This patient had de novo intestinal myeloid sarcoma (MS), a rare and chameleonic presentation of acute leukemia of myeloid origin. The initial diagnostic evaluation suggested Koch's abdomen, and surgical excision of the bowel was performed with a clinical suspicion of Koch's or lymphoma.
View Article and Find Full Text PDFOncol Lett
March 2025
Department of Hematology, Shengli Oilfield Central Hospital, Dongying, Shandong 257000, P.R. China.
The FAT atypical cadherin 1 (FAT1) gene is the ortholog of the fat gene and encodes the protocadherin FAT1. FAT1 belongs to the cadherin superfamily, a group of full-length membrane proteins that contain cadherin-like repeats. In various types of human cancer, FAT1 is one of the most commonly mutated genes, and is considered to be an emerging cancer biomarker and a potential target for novel therapies.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Clinical Pathology, South Egypt Cancer Institute, Assiut University, Assiut, Egypt.
Background And Aim: Acute myeloid leukemia (AML) is a remarkably complex malignancy; with considerable genetic, epigenetic, and phenotypic heterogenicity. Circ-RNAs are a novel class of non-coding RNA. They may influence leukemia development and offer exciting possibilities for targeted AML diagnosis and therapy.
View Article and Find Full Text PDFInt J Lab Hematol
January 2025
Department of Hematology and Coagulation, Princess Iman Center for Research and Laboratory Sciences, Amman, Jordan.
Introduction: Disseminated intravascular coagulation (DIC) is associated with acute leukemia. DIC prevalence and clinical consequences are complex and varies across acute leukemia subtypes. The International Society of Thrombosis and Hemostasis (ISTH) scoring system is used for the detection of overt DIC.
View Article and Find Full Text PDFCurr Hematol Malig Rep
January 2025
Division of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Purpose Of Review: More than a decade following the discovery of Calreticulin (CALR) mutations as drivers of myeloproliferative neoplasms (MPN), advances in the understanding of CALR-mutant MPN continue to emerge. Here, we summarize recent advances in mehanistic understanding and in targeted therapies for CALR-mutant MPN.
Recent Findings: Structural insights revealed that the mutant CALR-MPL complex is a tetramer and the mutant CALR C-terminus is exposed on the cell surface.
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