By re-transplanting the AML cells that relapse after different treatments, we will further determine how the various
subclonal architectures generated impacts disease progression and responses to re-treatment.
Detection
of subclonal L1 transductions in colorectal cancer by long - distance inverse - PCR and Nanopore sequencing
Targeted Deep Sequencing Reveals Clinically
Relevant Subclonal IgHV Rearrangements in Chronic Lymphocytic Leukemia
The recent emergence of next generation sequencing (NGS) technologies has revolutionized our understanding of the extent and nature of
subclonal diversification.
Overall, including all genomic variations present in most if not all tumor cells (clonal) as well as those present only in subsets of the cancer cells (
subclonal) from tumor tissue, the researchers detected a total of 864 genetic changes in tissue samples across the three tumor types, and 627 (73 %) of those were also found in the blood.
The observations, published in Leukemia & Lymphoma, could have clinical relevance in
that subclonal composition of AML could impact diagnosis and treatment for the disease.
Used in combination with Invivoscribe's proprietary MyInformatics ® Software these assays identify and can track primary driver mutations as well as
the subclonal architecture and emergence of new driver mutations in patients with hematologic disease.
Invivoscribe's clinical laboratories also offer comprehensive MyAML ®, MyHeme ®, MyMRD ®, and custom gene panels, that when used in combination with Invivoscribe's proprietary MyInformatics ® Software can identify and track primary driver mutations as well as
the subclonal architecture and emergence of new driver mutations in patients with hematologic disease.
Invivoscribe also offers comprehensive MyAML ®, MyHeme ®, MyMRD ®, and custom gene panels, that when used in combination with Invivoscribe's proprietary MyInformatics ® Software can identify and track primary driver mutations as well as
the subclonal architecture and emergence of new driver mutations in patients with hematologic disease.
Panels run at the time of diagnosis identify both clinically - actionable driver mutations associated with the primary tumor, as well as
the subclonal architecture that may be present.