ARTicle Gallery

This artwork illustrates resistance to therapy emerging from seeds present at leukeima diagnosis. Each leaf here is a leukemic clone; its shape reflects expansion, contraction and new feature gain during the course of therapy and disease progression.

Read the original article "Mutational Landscape and Patterns of Clonal Evolution in Relapsed Pediatric Acute Lymphoblastic Leukemia" Esmé Waanders, Zhaohui Gu, Stephanie M. Dobson, Željko Antić et al. Fig 2B from the article was used as a theme for the artwork

Natural patterns are amazingly similar across scales, from molecular to cosmic. In this artwork, the prototype of a moon terrain is a cell monolayer grown in a culture dish (Fig 4J), and the spectrum of transcription factor TFEB activity in leukemia cells (Fig 4M) becomes mountain peaks and aurora borealis lights.

Read the article "TFEB Links MYC Signaling to Epigenetic Control of Myeloid Differentiation and Acute Myeloid Leukemia" by Seongseok Yun et al.

Within the complex engine that is cellular metabolism, some high-speed gears are optional for normal cells but essential for AML. In the article, Dongqing Yan et al uncover leukemic cells dependence on SIRT5-geared metabolism (Fig S7B) and design a small molecule inhibitor of SIRT5 (Fig 7A) to throw into it as a monkey wrench.

Read the article "SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia" by Dongqing Yan et al.

What can artificial intelligence (AI) help us see in a bone marrow histology image? A lot of clinically and biological features, including patient age and gender, myelodysplastic syndrome subtype, and even specific genetic lesions, as shown in the article.

Read the article "Machine Learning of Bone Marrow Histopathology Identifies Genetic and Clinical Determinants in Patients with MDS" by Oscar Brück et al. Supplementary Fig 9a was used as a theme for the artwork.

Chromosomes literally mean “colored bodies”. Seeing chromosomes in color here helps to imagine how in cancer cells these skeins of DNA get tangled, torn and wound up in wrong places. In the article Rustad et al unravel complex ways in which chromosomal fragment mix-up contributes to myeloma progression and outcome. In the example above (Fig 1A), nine different chromosomes exchanged pieces.

Read the original article "Revealing the Impact of Structural Variants in Multiple Myeloma" by Even H. Rustad et al.

This article characterizes PE, an enhancer element crucial for PTEN expression in T cells and for leukemia suppression. The artwork shows PTEN as a tumor-suppressing "genie" arising from PE "lamp". Leukemia cells can escape PTEN control by breaking PE. The genie shape is inspired by the tSNE plot of Fig 4E, and the desert landscape by the violon plots in Fig 4F.

Read the article "A Tumor Suppressor Enhancer of PTEN in T-cell Development and Leukemia" by Luca Tottone et al.

DNA methylation patterns reflect the cell’s proliferative history, like the tree’s age can be deduced from its growth rings. In the article, Roels et al decoded methylation patterns of T-ALL cell genomes into insights about biological age and tissue of origin of this leukemia type.

Read the article "Aging of Preleukemic Thymocytes Drives CpG Island Hypermethylation in T-cell Acute Lymphoblastic Leukemia" by Juliette Roels et al.

A keen eye can see meaningful patterns in seemingly random scatter. As reported in the article, resistance to type 1 inhibitors is most common in Ras pathway, whereas resistance to type 2 inhibitors arises by new mutations in Flt3.

Read the article "Patterns of Resistance Differ in Patients with Acute Myeloid Leukemia Treated with Type I versus Type II FLT3 Inhibitors" by Ahmad S. Alotaibi et al.

Fig. 1B was used as a theme for the artwork.

The opener art illustrates how increased temperature destabilizes an oncoprotein, causing its aggregation and inactivation. The background color depicts temperature gradient.

Read the article "Hyperthermia Destabilizes PML/RARα Oncofusion in Acute Promyelocytic Leukemia" by Yasen Maimaitiyiming et al.

This artwork illustrates a complex interplay during mRNA transcription elongation in myeloma cells. When RNA pol II (big fish) makes mRNA transcript, it moves along H3K4me3 marks (shown as fish eggs) of histone tails (shown as seaweed). These H3K4me3 marks are removed by KDM5A (small green fish). When KDM5A is kept inactive by a drug, there is so much H3K4me3 that RNA pol II is caught up in one place, and does not elongate the mRNA.

Read the article "Lysine Demethylase 5A Is Required for MYC-Driven Transcription in Multiple Myeloma" by Hiroto Ohguchi et al.

Fig 6H was used as a theme for the artwork.