See clonal architecture, cell by cell
Bulk RNA often masks the biology that matters in AML and MDS. Different cell populations such as HSCs, progenitors, blasts, and leukemic stem cells are averaged into one signal, making it difficult to understand what is actually driving disease and resistance.
TapestriⓇ connects mutation status including FLT3-ITD, IDH1/2, and NPM1 with transcriptional state in the same cell. This allows you to see how genotype relates to blast identity, differentiation state, and therapy response.
This targeted RNA panel includes more than 50 state classifier genes across key AML cell states. It enables:
- Single-cell LSC scoring
- Quantification of blast populations relevant to MRD
- Identification of resistant subpopulations that expand at relapse
Download the full gene set list to explore the panel design and coverage.
Frequently Asked Questions
1. What is the gene capacity of the Mission Bio Heme Malignancy RNA Panel? The panel targets 268 genes specifically curated to cover leukemic cell states, differentiation block mechanisms, and clonal architecture. The genes are organized into 7 functional categories to provide a high-resolution characterization of the myeloid and lymphoid disease continuum at single-cell resolution.
2. Which hematologic indications are covered by this RNA panel? The panel is designed for a broad range of indications, including:
- Acute Myeloid Leukemia (AML)
- Myelodysplastic Syndromes (MDS)
- Myeloproliferative Neoplasms (MPN)
- Acute Lymphoblastic Leukemia (ALL) and Chronic Lymphocytic Leukemia (CLL)
- MDS/AML overlap syndromes
3. How does Tapestri technology differ from bulk RNA sequencing for hematology? Bulk RNA sequencing averages data across all cells, which can obscure the rare populations driving relapse, such as Leukemic Stem Cells (LSCs). Tapestri uniquely enables the simultaneous co-detection of DNA genotype and RNA transcriptomic state from the same individual cell, allowing researchers to link specific somatic mutations (e.g., FLT3-ITD, IDH1/2) directly to blast identity and therapy resistance programs.
4. Can this panel resolve AML blast hierarchies? Yes. The panel includes over 50 genes dedicated to cell state and differentiation hierarchies, specifically based on the van Galen 6-state AML model. This allows for the quantification of HSC-like, progenitor-like, GMP-like, and monocyte-like AML cell states at single-cell resolution.
5. Does the panel address Targeted Therapy resistance? The panel includes dedicated categories for Apoptosis and Therapy Resistance (32 genes), featuring markers like the BCL-2 family (e.g., BCL2, MCL1, BAX) to determine venetoclax sensitivity. It also covers multidrug efflux markers and nucleoside metabolism genes to track resistance to therapies like cytarabine and hypomethylating agents.
6. How are Leukemic Stem Cells (LSCs) identified with this panel? The panel contains a robust set of LSC identity markers, including CD34, CD38, HOXA9, MEIS1, and CXCR4. By combining these transcriptomic markers with somatic genotype data, researchers can identify and score the quiescent LSC compartment that often serves as a Measurable Residual Disease (MRD) reservoir.
7. What curation sources were used for the Heme Malignancy RNA Panel? The panel was curated from over 6 distinct sources, including:
- Commercial Panels: FoundationOne Heme, Illumina TruSight Myeloid, and Tempus xT.
- Public Databases: TCGA LAML, COSMIC myeloid census, and the Human Cell Atlas.
- Literature: ELN 2022 risk classifications and peer-reviewed single-cell AML atlases.
8. Does the panel include epigenetic and splicing regulators? Yes. A dedicated category for Epigenetic, Splicing, and DNA Repair (28 genes) includes critical myeloid regulators such as DNMT3A, TET2, ASXL1, SF3B1, and SRSF2. This enables the correlation of spliceosome or epigenetic mutations with specific transcriptional phenotypes.