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January 8, 2021 by Charlie Silver 3 min read

Incredible Discoveries Made by Our Customers in 2020

As we enter this new year, many of us are happy to leave 2020 behind. But while the last year was fraught with challenges, it also reminded us of the vital importance of science. At Mission Bio, we remain steadfast in our mission to help researchers unravel the complexity of cancer, and we applaud the cancer research that was accomplished in 2020 using our innovative single-cell multi-omics platform, Tapestri. 

This past year, researchers gained a deeper understanding of various hematological malignancies using the Tapestri Platform. Several studies elucidated how tumors evolve and develop resistance to treatments. Additionally, single-cell multi-omics analysis revealed new genotype-phenotype correlations in acute myeloid leukemia (Miles et al., Morita et al., Demaree et al.), and Tapestri has also facilitated high-throughput single-cell analysis of genome editing for the first time (ten Hacken et al.).

We compiled a list of publications from 2020 that utilized Tapestri technology to help better our understanding of cancers so that we can one day eradicate them. We hope you take the time to look over this impressive list and celebrate your scientific peers as we do. As we welcome 2021, we are eager to see the role that Tapestri plays in supporting even more great work from the cancer research community and remain committed to helping our customers drive progress forward toward a greater understanding of cancer and the development of new therapeutics. 

Tapestri Multi-omics

Miles L et al., Nature
Single-cell mutation analysis of clonal evolution in myeloid malignancies
Clonal architecture and evolution across patients with AML, myeloproliferative neoplasms (MPN), and clonal hematopoiesis (CH). Description of genotype-phenotype associations in AML.

Morita K et al., Nature Communications
Clonal evolution of acute myeloid leukemia revealed by high-throughput single-cell genomics
Characterization of clonal architecture and evolution in a large cohort of AML patients (n=123), with associations made between specific mutations and cell-surface markers. 

Dillon LW et al., MedRxiv
Personalized single-cell proteogenomics to distinguish acute myeloid leukemia from nonmalignant clonal hematopoiesis
Distinguished malignant variants of AML from age-related clonal hematopoiesis by resolving immunophenotypic identity of clonal architecture.

Demaree B et al., BioRxiv
Joint profiling of proteins and DNA in single cells reveals extensive proteogenomic decoupling in leukemia
Demonstrated decoupling of genotype-phenotype relationships over the course of disease progression and treatment.

Profiling Heme Malignancies

Xiao W et al., Blood Advances
A JAK2/IDH1-mutant MPN clone unmasked by ivosidenib in an AML patient without antecedent MPN
Clonal architecture of a relapsed AML patient, in which treatment with an IDH1 inhibitor promoted outgrowth of a minor myeloproliferative neoplasm (MPN) clone.

Kennedy AL et al., BioRxiv
Distinct genetic pathways define pre-leukemic and compensatory clonal hematopoiesis in Shwachman-Diamond syndrome
Zygosity and CN-LOH are reliably measured with high sensitivity (0.1%) and predict progression to leukemia in patients with Shwachman-Diamond Syndrome.

Taylor J. et al., Blood
Single-cell genomics reveals the genetic and molecular bases for escape from mutational epistasis in myeloid neoplasms
Studied a rare phenomenon in biology where 2 splicing mutations co-occur in the patient sample.

Maia C et al., Blood
Biological and clinical significance of dysplastic hematopoiesis in patients with newly-diagnosed multiple myeloma
Identified biomarkers from multiple myeloma samples that develop into myelodysplastic syndrome (MDS) using multidimensional flow cytometry and single-cell DNA sequencing.

Thompson ER et al., Haematologica
Clonal independence of JAK2 and CALR or MPL mutations in co-mutated myeloproliferative neoplasms demonstrated by single cell DNA sequencing
First publication in T-cell acute lymphoblastic leukemia (T-ALL) that highlights SNVs/ indels and minimal residual disease (MRD) detection.

Alberti-Servera L et al., Blood
Single-cell DNA amplicon sequencing reveals clonal heterogeneity and evolution in T-cell acute lymphoblastic leukemia
A longitudinal study of T-cell acute lymphoblastic leukemia (T-ALL) patients comparing clonal architecture at diagnosis and after treatment. Illustrated detection of SNVs and CNVs in the same cells using the Tapestri workflow.

Patel BA et al., Haematologica
Detectable mutations precede late myeloid neoplasmia in aplastic anemia
Identified evolution of mutations in a rare case where a severe aplastic anemia (SAA) patient who received immunosuppressive therapy developed MDS/AML with normal cytogenetics.

Understanding Resistance, Relapse, and Minimal Residual Disease (MRD)

Wang F et al., BioRxiv
Leukemia stemness and co-occurring mutations drive resistance to IDH inhibitors in acute myeloid leukemia
This study investigates the clonal architecture of AML patients who relapse after receiving IDH inhibitor treatment.

Choe S et al., Blood Advances
Molecular mechanisms mediating relapse following ivosidenib monotherapy in IDH1-mutant relapsed or refractory AML
Biopharma study that showed molecular resistance mechanisms in 174 patients following ivosidenib monotherapy for relapsed/refractory AML.

DiNardo CD et al., Blood
Molecular patterns of response and treatment failure after frontline venetoclax combinations in older patients with AML
Molecular basis for treatment resistance or durable remission in older patients with AML given venetoclax combination therapy.

Ediriwickrema A et al., Blood Advances
Single-cell mutational profiling enhances the clinical evaluation of AML MRD
MRD detection identified clones at remission that expanded into the dominant clone at relapse in patients with AML.

Measuring Genome Editing

ten Hacken E et al., Genome Biology
High throughput single-cell detection of multiplex CRISPR-edited gene modifications
First study to use Tapestri to analyze single and multiplexed CRISPR edits in individual cells.

About the Author

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