The TLR9 agonist (GNKG168) induces a unique immune activation pattern in vivo in children with minimal residual disease positive acute leukemia: Results of the TACL T2009-008 phase I study.
Of 90 patients with IG/TR MRD at TP1, nine were negative and none relapsed, while 11 with MRD<5×10<sup>-4</sup> and 70 with MRD≥5×10<sup>-4</sup> had a comparable 5-year cumulative incidence of relapse of 36.4 (15.4) and 35.2 (5.9), respectively.
More importantly, BCL2L12 expression was associated with disease remission, while the reduced BCL2L12 expression was able to predict patients' poor response to BFM therapy, in terms of M2-M3 response and MRD≥0.1% on day 15.
These observations suggest that ddPCR can sensitively detect the MYD88L265P mutation in cell-free DNA and could be used as non-invasive diagnostics, but may not be applicable for monitoring minimal residual diseases in PCNSL.
Further studies to validate SALL1 as a potential biomarker for minimal residual disease (MRD) and to determine SALL1's role in prognostication are ongoing.
A MRD significantly increased energy expenditure (e.g. fatty acid oxidation, glycolysis, and tricarboxylic acid cycle metabolism), regulated protein homeostasis, improved gut microbiota functions, prevented thyroid dysfunction, increased plasma thyroxine and triiodothyronine levels, decreased plasma thyroid stimulating hormone levels, increased type 2 deiodinase (DIO2) activity, and up-regulated mRNA and protein expression levels of DIO2 and thyroid hormone receptor α1 in the skeletal muscle.
Thus, dual PP2A and BCR-ABL inhibition may be a valuable therapeutic strategy to synergistically target drug-insensitive LSCs that maintain minimal residual disease in patients.
This CRLF2-driven network could be more effectively disrupted by SRC/ABL inhibition than single-agent JAK or PI3K inhibition, and this could be demonstrated even in primary minimal residual disease (MRD) cells.
We conclude that our novel metric - ERM-D8 - based on time-series GEP after 8 days of remission-induction therapy can independently predict relapse even after adjusting for NCI risk, genetics, Day 8 peripheral blood response and MRD.
A MRD significantly increased energy expenditure (e.g. fatty acid oxidation, glycolysis, and tricarboxylic acid cycle metabolism), regulated protein homeostasis, improved gut microbiota functions, prevented thyroid dysfunction, increased plasma thyroxine and triiodothyronine levels, decreased plasma thyroid stimulating hormone levels, increased type 2 deiodinase (DIO2) activity, and up-regulated mRNA and protein expression levels of DIO2 and thyroid hormone receptor α1 in the skeletal muscle.
This CRLF2-driven network could be more effectively disrupted by SRC/ABL inhibition than single-agent JAK or PI3K inhibition, and this could be demonstrated even in primary minimal residual disease (MRD) cells.
This CRLF2-driven network could be more effectively disrupted by SRC/ABL inhibition than single-agent JAK or PI3K inhibition, and this could be demonstrated even in primary minimal residual disease (MRD) cells.
Our findings indicate that including both CD58 and CD81 markers in addition to CD19, CD34, CD20, CD38, and CD10 are helpful in MRD detection by flow cytometry.
The median minimal residual disease (MRD) was lower in CRLF2pos than CRLF2-negative (CRLF2neg) patients on day 15 (MRD15) after induction therapy [0.01% (0.001-0.42%) vs. 0.45% (0.05-3.50%); p=0.001].
An electrosurgical snare was performed to resect the neoplasm and several APC were administered at the sites of the resection to provide hemostasis and further coagulate for the residual neoplasm.
This CRLF2-driven network could be more effectively disrupted by SRC/ABL inhibition than single-agent JAK or PI3K inhibition, and this could be demonstrated even in primary minimal residual disease (MRD) cells.
It will then provide a current summary of the applications of HTS-IR technology in the diagnosis and monitoring of minimal residual disease (MRD), focusing on immune reconstitution after the treatment of allogeneic hematopoietic stem cell transplantation (allo-HSCT) in B/T-cell malignancies, and the precise detection of tumor-infiltrating lymphocytes (TILs) in non-B/T-cell malignancies.
Collectively, TFDP3 confers chemoresistance in MRD within childhood T-ALL, indicating that TFDP3 is a potential gene therapy target for residual cancer.
<sup>18</sup>F-FDG PET/CT can be coupled with sensitive bone marrow-based techniques to detect minimal residual disease (MRD) inside and outside the bone marrow, helping to identify those patients who are defined as having imaging MRD negativity.