ARTicle Showcase

Artist: Sichkarenko

The transformation of indolent chronic lymphocytic leukemia (CLL) into aggressive Richter syndrome (RS) is an outstanding clinical challenge, in part because of difficulty modeling the conditions in tractable experimental systems. A novel mouse model allows unprecedented insight into the universe of CLL and RS clonal dynamics, dysregulated signaling pathways, and therapeutic vulnerabilities.

Artist: Sichkarenko

Clusters of stars in the night sky have been mapped, given names, and even linked to human destinies by myths and legends. Today, advanced single-cell multiomics technology is allowing us to map the intricate world inside our bodies, uncovering cell clusters associated with health and disease, in the quest to predict clinical outcomes.

Artist: Vavryk

Stem cells produce different types of blood cells folowing instructions written in specific genes. Changes in these instructions, like adding 5hmC with the help of TET2, control which type of blood cell is made. TET enzymes are often dysfunctional in myeloid neoplasms that overproduce myeloid cells a the expense of erythroid cells, but TET substrate vitamin C can help balance things out.

Artist: Petrova

Targeted therapies work for only a portion of leukemia patients. Instead of targeting patients directly, 45 drugs targeting a specific genetic lesion (arrows) are individually tested on each child's leukemia cells in a lab (balloons) to pinpoint the most effective options. Successful hits on the right side indicating drug sensitivity and misses on the left side indicating drug resistance.

Artist: Vavryk

In the cellular transcription factory, NOTCH1, SIRT1, and KAT7 proteins are assembly line robots acting on DNA molecules (the conveyor belt). They coordinate each other's activity by adding or removing acetyl groups - pins - that act as molecular switches.

Artist: Radyanskaya

Chronic leukemia cells shed a lot of exosomes, tiny cellular samples of themselves. This may be a strategy to exhaust anti-leukemia immunity: when T-cells are bombarded with leukemic exosomes, their cancer-fighting ability quicky fades.

Artist: Vitanovskyj

A fierce battle rages in the bone marrow of multiple myeloma patients receiving CAR T cell therapy: cancerous myeloma cells, the transfused CAR T cells, and the patient’s normal immune cells are locked in battle. Assessing the phenotypes of the various combatants reveals characteristics that correlate with the duration of patients’ response to the therapy.

Artist: Gennert

Lineage-ambiguous leukemias often occur with rearrangement of ZNF384, resulting in fusion proteins involving various partner genes. These gene fusions corrupt the normal roles of their constituent proteins as regulators of gene expression networks, unleashing oncogenic genetic programs upon the cell in a cascade of dysregulated cellular processes.

Artist: Sichkarenko

Stepping back through time, the chronologic acquisition of driver mutations in classic Hodgkin lymphoma (cHL) can be inferred from whole genome sequencing of Hodgkin and Reed Sternberg (HRS) cells.

Artist: Slavneisheva; SayoStudio

Leukemia cells dwell in the bone marrow, but some of their descendants take off to distant shores. This study dissects molecular features of leukemic cells in both locations, identifying traits of successful colonists, enriched in leukemic subclones which entered and settled in the central nervous system.

Artist: Vavryk

Age-related clonal hematopoiesis is highly associated with TET2 loss-of-function mutations, but the mechanisms underlying leukemic transformation are unclear. The combination of Tet2 deficiency and deletion of a PU.1 regulatory region in progenitor cells leads to dysregulated chromatin, impaired PU.1 target genes, and acquired myeloid leukemia only during aging.

Artist: Vavryk

A laundry bag (human cell) supposedly contains 23 pairs of socks (chromosomes). But when the laundry is sorted, some socks are unmatched or damaged, and some pairs are missing, a state called hypoploidy. The illustration shows 23 pairs of fluorescently painted chromosomes as socks with unique stripe patterns, presenting a low-hypodiploid karyotype typical for p53-deficient ALL subset.

Artist: Slavneisheva

DNMT3A-mutant hematopoietic stem cells beat out the competition by co-opting IFNγ signaling. Like in the Olympic Games, friendly competition can lead to a toxic (micro-)environment when under stress.

Artist: SayoStudio

Polycomb proteins limit growth-promoting gene activity by transcriptional silencing: binding to their DNA and keeping it tight like closed lips. Cancer cells often break this silence by mutating Polycomb components BCOR1 and 2. This artwork illustrates how cancer genes "get loud" when BCOR is not around.

Artist: Sichkarenko

The COVID-19 pandemic thrust vaccine responses in immunocompromised patients into the spotlight. Patients with B-cell malignancies experienced depressed anti-spike antibody levels, but T cell responses were not suppressed. Vaccine responses continue to be shown to be a complex, multilayered process involving more than antigen-specific antibody production.