Chr del(13)(q14)

Genomic complexity, del(16)(p13)/CREBBP and gain at 6q27 involving MLLT4 maintained their significance in multivariate analysis for survival outcome. Our study thus demonstrated that whole genome analysis of imbalances provides new insights to refine risk stratification in T-ALL.

Deletion of chromosome 13q14 was frequent. The PBL cases in Taiwan showed recurrent mutations involving JAK-STAT, RAS-MAPK, epigenetic regulation, and NOTCH signaling pathways, findings similar to that from the West.

ConclusionsLeukoPrint is an automated, convenient and cost-effective approach to depict CNA profile in genomic DNA or cfDNA. This method is superior to conventional approaches when used for CNA testing, and the practice of this method could improve prognostic stratification of MM patients.

In a low risk population defined by <10% BMPC, patients treated with HD melphalan did not show a statistical PFS difference when compared to patients treated without ASCT.

Cytogenomic profile was concordant with the literature data, however the role of IGH rearrangement, 14q deletion and 5q35.2 gain need to be explored. We anticipate that further characterization of RT lesions will probably facilitate better understanding of the RT clonal evolution.

P and B-MCL have the highest degree of aneuploidy and exhibit an immune cold tumor microenvironment. Further studies are ongoing to refine the molecular differences among B and P-MCL compared to C-MCL.

Our study demonstrated that the whole genome analysis of imbalances provides new insights to refine the risk stratification in T-ALL. Notably, genomic complexity (≥ 15 genomic imbalances) and chromothripis demonstrated an association with an inferior outcome in terms of EFS and CIR in pediatric and adult T-ALL.

It demonstrated a statistically significant coexisting with t (11; 14) (p<0.001), complex karyotypes (involves at least 6 chromosomes) (p<0.001), high plasma cell ratio in bone marrow (p=0.001) and poor response to VRD (bortezomib, lenalidomide, dexamethasone) treatment (p<0.001), but mutually exclusive with monosome 13, del(13q14), dup1q21 and t (4; 14). Gain of 11q13.3-q25 is a reproducible chromosomal copy number abnormality in NDMM characterized by coexisting with t (11; 14), complex karyotypes, higher plasma cell ratio in bone marrow and poor treatment response to VRD. t(11; 14) patients with 11q gain had a poorer PFS compared to patients with t(11; 14) only, mPFS was only 9 months for TIE patients. t(11; 14) with 11q gain NDMM patients needs to be considered as high risk and ASCT could improve patients' survival.

A transcriptome risk score utilizing novel SPECTRA variables identified a substantial subset of CLL patients with IGHV-mutated status and presence of del(13q) who have uncharacteristically short TTFT, but who would be classified as favorable risk under current best practice stratification. Future directions include validating our results with external patient cohorts from Mayo Clinic and investigating the genetic and transcriptomic profile of SPECTRA low- and high-risk cohorts to determine targetable pathways for treatment.

At relapse they received daratumumab based salvage in combination with lenalidomide and then pomalidomide...The first profiled bone marrow was collected during leukapheresis for cilta-cel but due to progressive disease the patient received an FCRL5 directed bispecific, and a second sample was collected at progression after a brief sCR to this agent... This case represents the first known bi-allelic loss of CD38 and acquired loss of FCRL5 expression. These events, along with the loss of BCMA highlight the need for more advanced clinical testing to assess the actionability of the diverse therapeutic targets available to treat patients today.