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Background:Early detection and intervention seem to improve development in autistic children, and teachers form an important part of their early social environment.Objectives:The objective of this study was to assess baseline knowledge and misconceptions regarding autism among school teachers and evaluate factors influencing their knowledge.Materials and Methods:This is a cross-sectional survey enrolling primary school teachers using a self-administered questionnaire.Results:Seventy-three teachers (mean age of 34 years, 66% females) responded. Gaps in awareness and knowledge were found. About 52 (71.2%) teachers identified themselves as having some knowledge about autism, with 23 (44.2%) among this group understanding autism as a neurological/mental disorder. The majority (73.1%) believe that special education is a helpful intervention. The only significant factor that influenced knowledge among teachers was attendance of behavioral classes (P = 0.01).Conclusion:Results suggest that teachers have an inadequate understanding of autism due to several misconceptions. This calls for increased education of teachers with regard to autism and other childhood disorders.

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Patients with multiple myeloma (MM) who are treated with lenalidomide rarely develop a secondary B-cell acute lymphoblastic leukemia (B-ALL). The clonal and biological relationship between these sequential malignancies is not yet clear. We identified 17 patients with MM treated with lenalidomide, who subsequently developed B-ALL. Samples were evaluated with sequencing, cytogenetics/FISH, immunohistochemical staining (IHC), and IgH clonality assessment. Samples were assessed for shared mutations and recurrently mutated genes. Through whole exome sequencing and cytogenetics/FISH analysis of 7 paired samples (MM versus matched B-ALL), no mutational overlap between samples was observed. Unique dominant IgH clonotypes between the tumors were observed in 5 paired MM / B-ALL samples. Across all 17 B-ALL samples, 14 (83%) had a TP53 variant detected. Three MM samples with sufficient sequencing depth (>500X) revealed rare cells (average of 0.6% VAF, or 1.2% of cells) with the same TP53 variant identified in the subsequent B-ALL sample. A lack of mutational overlap between MM and B-ALL samples shows that B-ALL developed as a second malignancy arising from a founding population of cells that probably represented unrelated clonal hematopoiesis caused by a TP53 mutation. The recurrent variants in TP53 in the B-ALL samples suggest a common path for malignant transformation that may be similar to that of TP53-mutant, treatment-related acute myeloid leukemia. The presence of rare cells containing TP53 variants in bone marrow at the initiation of lenalidomide treatment suggests that cellular populations containing TP53 variants expand in the presence of lenalidomide to increase the likelihood of B-ALL development.