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Ramakrishnan, S. M.

Publications and source records attributed to Ramakrishnan, S. M..

2 recordsLinked to original sources

Long read sequencing reveals novel isoforms and spliceosome-mutant-enriched transcripts in AML and MDS

The alternative splicing landscape of the leukemia transcriptome remains poorly characterized, since short-read sequencing cannot resolve complete transcript structures. Using the Oxford Nanopore cDNA platform, we generated nearly 2 billion long reads (median 25.8 million per sample) from 71 human samples, including 48 acute myeloid leukemia or myelodysplastic syndrome samples, 25 of which had splicing-factor gene mutations (in SRSF2, U2AF1, or SF3B1). An additional 23 samples were from sorted hematopoietic cell populations from healthy individuals. Using this dataset, we created a transcript assembly containing 174,162 novel isoforms that are not described in the reference transcriptome. Deep-scale proteomic validation confirmed that many of these transcripts are translated into protein. We also identified isoforms enriched in spliceosome-mutant samples and found proteomic evidence of frequent nonsense-mediated decay regulation of novel transcripts. This dataset is a valuable community resource, enabling detection of new transcripts in short-read data sets. An interactive portal to explore splicing patterns in these data is available at https://leylab.org/isoforms/. Key PointsLong-read sequencing enables the detection of many novel transcripts in AML, including many from splice-factor-mutant patient samples This expanded transcriptome is a valuable community resource and can be used to improve analyses of short-read RNAseq data

cancer biology↗

Immunosuppression and Outcomes in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) patients rarely have long first remissions (> 5 years) after standard-of-care chemotherapy, unless classified as favorable risk at presentation. Identification of the mechanisms responsible for long vs. more typical, short remissions may help to define prognostic determinants for chemotherapy responses. Using exome sequencing, RNA-sequencing and functional immunologic studies, we characterized 28 Normal Karyotype (NK)-AML patients with >5 year first remissions after chemotherapy (Long First Remissions, LFR) and compared them to a well-matched group of 31 NK-AML patients who relapsed within 2 years (Standard First Remissions, SFR). Our combined analyses indicated that genetic risk profiling at presentation (as defined by ELN 2017 Criteria) was not sufficient to explain the outcomes of many SFR cases. Single cell RNA-sequencing studies of 15 AML samples showed that SFR AML cells differentially expressed many genes associated with immune suppression. The bone marrow of SFR cases had significantly fewer CD4+ Th1 cells; these T-cells expressed an exhaustion signature and were resistant to activation by T-cell receptor stimulation in the presence of autologous AML cells. T-cell activation could be restored by removing the AML cells, or blocking the inhibitory MHC Class II receptor, LAG3. Most LFR cases did not display these features, suggesting that their AML cells were not as immunosuppressive. These findings were confirmed and extended in an independent set of 50 AML cases representing all ELN 2017 risk groups. AML cell-mediated suppression of CD4+ T-cell activation at presentation is strongly associated with unfavorable outcomes in AML patients treated with standard chemotherapy.

cancer biology↗