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Medeiros, L. J.

Publications and source records attributed to Medeiros, L. J..

3 recordsLinked to original sources

Prognostic and Therapeutic Implications of BRAF Mutations in Acute Myeloid Leukemia

Mutations in the RAS/MAPK signaling pathway are recurrent in acute myeloid leukemia (AML), primarily involving NRAS and KRAS. In contrast, mutations in the gene encoding an effector protein, BRAF, occur at relatively lower frequencies in AML and are associated with poor outcomes. To date, no comprehensive analysis has assessed the clinical and molecular characteristics of BRAF-mutated AML. In this study, we report the identification of canonical and non-canonical BRAF mutations in [~]1% of 5,779 consecutive clinically and molecularly fully-annotated AML patients treated at two major United States Cancer Centers (50/5779 AML patients: 21 newly diagnosed AML; 9 relapsed/refractory; 20 newly diagnosed secondary AML). We performed single-cell multiomic analysis on a subset of AML samples. BRAF mutations were enriched in myelodysplasia-related AML (AML-MR), and most mutations were located outside the V600 hotspot. Single-cell multiomic profiling delineated BRAF mutation class-specific patterns of co-mutations, clonality, and immunophenotypes. Notably, BRAF mutations and other signaling co-mutation(s) could be found in the same cell, a finding that significantly diverges from prior studies of RAS-mutant AML. In this cohort, BRAF-mutant AML patients had poor overall survival with currently available treatments, including venetoclax-based regimens. Drug sensitivity data suggest possible avenues for targeted treatment of BRAF-mutated AML. Statement of SignificanceCanonical and non-canonical BRAF mutations are enriched in AML-MR and associate with poor survival outcomes. Single-cell multiomic profiling revealed unique co-mutation patterns and immunophenotypes that highlight RAS pathway addiction and nominate BRAF-mutated disease as a distinct subtype within RAS pathway-aberrated leukemias. Drug sensitivity screens suggest broad CDK or HSP90 inhibition in addition to BRAF/RAS-directed inhibition may be effective targeted therapies in this prognostically poor AML subtype.

cancer biology↗

Only SF3B1 Mutation involving K700E (And Not Other Codons), Independently Predicts Overall Survival in Myelodysplastic Syndromes

BackgroundSF3B1 mutations (SF3B1mut) in myelodysplastic syndromes (MDS) frequently involve codon K700E and have a favorable prognosis. The prognostic effect of non-K700E SF3B1mut is uncertain. MethodsWe analyzed the clinical-pathologic features and outcomes of a single-institutional series of 94 SF3B1mut and 415 SF3B1wt newly diagnosed untreated MDS patients and explored the differences between K700E and non-K700E subgroups. FindingsNinety-four (19%) patients had SF3B1mut: median age, 74 years. Fifty-five (60%) patients carried K700E. Recurrent non-K700E mutations (39, 40%) included R625, H662 and K666. Compared to SF3B1mut K700E, non-K700E patients had a lower median ANC (1{middle dot}8 vs. 2{middle dot}4, p=0{middle dot}005) and were frequently "high" R-IPSS (revised International Prognostic Scoring System) [7(19%) vs. 2(4%), p=0{middle dot}031]. Non-K700E MDS frequently associated with RUNX1 (26% vs. 7%, p=0{middle dot}012) and exclusively with BCOR, IDH2, and SRSF2 mutations. There was no significant difference in karyotype or SF3B1 variant allele frequency. Most ([~]80%) were treated with hypomethylating agents. SF3B1mut had superior overall survival (OS) than SF3B1wt in all MDS categories [not-reached vs. 25{middle dot}2 months, p=0{middle dot}0003], low-grade MDS, and MDS with ring sideroblasts (MDS-RS). Compared to SF3B1wt, SF3B1mut K700E had superior outcomes in all MDS categories (25 months vs. not-reached, p=0{middle dot}0001), low-grade MDS, and MDS-RS, but no significant difference was seen with non-K700E. By multivariate analysis, absence of SF3B1mut K700E (not non-K700E) independently associated with prognosis. InterpretationSF3B1mut MDS show distinct clinical and mutational profiles, with K700E showing a significantly better OS compared to non-K700E mutations and SF3B1wt. Our study highlights the importance of SF3B1 mutation type in MDS risk assessment. Data Sharing StatementThe datasets generated during and/or analyzed during the current study are not publicly available due to patient privacy concerns but are available from the corresponding author on reasonable request. Research in ContextO_ST_ABSEvidence before this studyC_ST_ABSWe designed this study based on the collective evidence from a systematic search of the literature for outcomes of patients MDS with SF3B1 mutations (SF3B1mut) from January 2013 to June 2020. Both the International Working Group for the Prognosis of MDS (IWG-PM) proposal and 2016 revisions to the World Health Organization (WHO) Classification of Myelodysplastic Syndromes recognize SF3B1mut MDS with <5% blasts (or ring sideroblasts >5% for WHO) as a distinct sub-category, in the absence of other unfavorable features. This was largely based on favorable prognostic outcomes, a distinct gene expression profile, and association with ring sideroblasts. However, the natural history of SF3B1mut MDS is heterogeneous. A high proportion of SF3B1 mutations occur within codon K700, leading to large-scale mRNA downregulation due to branch point recognition error, while the rest occur outside of this codon. The downstream functional effects of SF3B1 mutations outside of the K700 codon are unclear. The clinical course of SF3B1mut MDS patients likely depends on the type of SF3B1 mutation and other features such as variant allele frequency, concomitant gene mutations, and karyotype. Until now, the effects of the different types of SF3B1 mutations were largely unknown. Added value of this studyIn this study, we report distinctive clinicopathologic characteristics and outcomes of MDS patients with SF3B1 mutations segregated based on mutation type: K700E vs. non-K700E. We show that [~]40% of SF3B1 mutated MDS patients have non-K700E mutations. Non-K700E SF3B1mut MDS have distinct clinico-pathologic features, such as lower ANC and frequent association with mutations in RUNX1, BCOR, IDH2, and SRSF2. There was no significant difference in karyotype or SF3B1 variant allele frequency. Importantly, K700E SF3B1mut MDS had superior overall survival compared to SF3B1wt, in all MDS, low-grade MDS, and MDS with ring sideroblasts, but no significant difference was seen with non-K700E. By multivariate analysis, absence of SF3B1mut K700E, but not non-K700E, independently associated with prognosis. Implications of all the available evidenceTo the best of our knowledge, this is the first study to report these findings from a single-institutional series of MDS primarily treated with hypomethylating agents. Our study highlights the importance of determining the SF3B1 mutation type in MDS risk assessment. These findings are important in light of the recent FDA approval of luspatercept based on the results of the MEDALIST trial that suggested sustained hematological responses in SF3B1mut MDS patients.

cancer biology↗

Simplified Molecular Classification of Lung Adenocarcinomas Based on EGFR, KRAS, and TP53 Mutations

IntroductionGene expression profiling has consistently identified three molecular subtypes of lung adenocarcinoma that have prognostic implications. To facilitate stratification of patients with this disease into similar molecular subtypes, we developed and validated a simple, mutually exclusive classification.\n\nMethodsMutational status of EGFR, KRAS, and TP53 was used to define six mutually exclusive molecular subtypes. A development cohort of 283 cytology specimens of lung adenocarcinoma was used to evaluate the associations between the proposed classification and clinicopathologic variables including demographic characteristics, smoking history, fluorescence in situ hybridization and molecular results. For validation and prognostic assessment, 63 of the 283 cytology specimens with available survival data were combined with a separate cohort of 428 surgical pathology specimens of lung adenocarcinoma.\n\nResultsThe proposed classification yielded significant associations between these molecular subtypes and clinical and prognostic features. We found better overall survival in patients who underwent surgery and had tumors enriched for EGFR mutations. Worse overall survival was associated with older age, stage IV disease, and tumors with comutations in KRAS and TP53. Interestingly, neither chemotherapy nor radiation therapy showed benefit to overall survival.\n\nConclusionsThe mutational status of EGFR, KRAS, and TP53 can be used to easily classify lung adenocarcinoma patients into six subtypes that show a relationship with prognosis, especially in patients who underwent surgery, and these subtypes are similar to classifications based on more complex genomic methods reported previously.

cancer biology↗