{"id":518486,"date":"2026-07-10T01:08:08","date_gmt":"2026-07-10T01:08:08","guid":{"rendered":"https:\/\/www.newsbeep.com\/nz\/518486\/"},"modified":"2026-07-10T01:08:08","modified_gmt":"2026-07-10T01:08:08","slug":"epigenomic-analysis-uncovers-new-aml-subgroups-and-drug-sensitivities","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/nz\/518486\/","title":{"rendered":"Epigenomic Analysis Uncovers New AML Subgroups and Drug Sensitivities"},"content":{"rendered":"

\"AML\"<\/a>AML has only a 29 percent survival rate, and it\u2019s a fast-growing cancer. It\u2019s often widespread in the bone marrow and the blood when it\u2019s first discovered in a patient, so being able to study the cancer, its progression, and its response to drugs in accurate and viable cell lines is crucial. [Toeytoey2530\/Getty Images]<\/p>\n

As one of the most aggressive blood cancers, the way acute myeloid leukemia (AML) is classified continues to shape every major clinical decision\u2014from risk stratification to the choice of targeted therapies. For decades, that classification has rested almost entirely on the gene mutations found in leukemic cells. But mutations alone have never fully explained why AML behaves so differently from patient to patient. A new study published in Nature now provides the missing layer: the epigenome.<\/p>\n

In the largest chromatin\u2011profiling effort ever conducted for any cancer, a research team led by Seishi Ogawa, MD, PhD, and Yotaro Ochi, MD, PhD, of Kyoto University, together with S\u00f6ren Lehmann, MD, PhD, of the Karolinska Institute, mapped the chromatin accessibility landscape of 1,563 AML patient samples. Their analysis\u2014built on ATAC\u2011seq, RNA\u2011seq, DNA methylation, ChIP\u2011seq, whole\u2011genome sequencing, and single\u2011cell multiomics\u2014reveals that AML can be classified into 16 distinct epigenomic subgroups, each defined by a characteristic chromatin state and its own regulatory wiring.<\/p>\n

As the authors wrote, \u201cATAC-seq\u2026show[s] that AML can be classified into 16 subgroups on the basis of chromatin accessibility profiles.\u201d This chromatin\u2011based structure was remarkably stable: single\u2011cell ATAC\u2011seq across more than 280,000 cells confirmed that each patient\u2019s leukemic population shares a conserved accessibility fingerprint.<\/p>\n

Each subgroup carries a unique combination of driver mutations, differentiation states, transcription\u2011factor networks, DNA methylation patterns, and super\u2011enhancer architecture. Many do not align cleanly with existing genomic classifications such as WHO or ICC, according to the researchers. In fact, the team found that even exhaustive decision\u2011tree analyses of known driver mutations could not explain most subgroup identities. As the paper noted, \u201cEvidence suggests that genetic alterations do not fully explain AML pathophysiology and heterogeneity.\u201d<\/p>\n

Clinically, chromatin information sharpened prognostic assessment in both Swedish and Japanese cohorts. Several subgroups also showed unexpected drug sensitivities. Three subgroups responded to MEK inhibitors despite lacking RAS\u2011pathway mutations. Another subgroup, enriched for RUNX1 mutations and marked by a chromatin profile resembling early B\u2011cell precursors, proved highly sensitive to ABL inhibitors.<\/p>\n

The study, \u201cChromatin landscape and epigenetic heterogeneity of acute myeloid leukemia<\/a>,\u201d positions chromatin architecture as a foundational dimension of AML biology. It also provides a practical path toward clinical adoption: the team distilled a 30\u2011gene expression signature capable of identifying high\u2011risk chromatin subgroups using standard sequencing workflows.<\/p>\n

Looking ahead, the group aims to develop lower\u2011cost diagnostic approaches and refine treatment strategies tailored to each epigenomic subgroup. The newly generated eCHROMA AML atlas is expected to serve as a resource for cancer epigenomics broadly, enabling discovery of new therapeutic targets and mechanistic insights.<\/p>\n","protected":false},"excerpt":{"rendered":"AML has only a 29 percent survival rate, and it\u2019s a fast-growing cancer. It\u2019s often widespread in the…\n","protected":false},"author":2,"featured_media":518487,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[10],"tags":[85567,2534,63590,7085,64963,2483,134,64621,111,43,139,69,6007,64622,2477,15284],"class_list":["post-518486","post","type-post","status-publish","format-standard","has-post-thumbnail","category-health","tag-acute-myeloid-leukemia","tag-cancer","tag-cancers","tag-dna-methylation","tag-epigenomics","tag-gene-expression","tag-health","tag-multiomics","tag-new-zealand","tag-news","tag-newzealand","tag-nz","tag-omics","tag-rna-sequencing-sequencing","tag-topics","tag-whole-genome-sequencing"],"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/posts\/518486","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/comments?post=518486"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/posts\/518486\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/media\/518487"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/media?parent=518486"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/categories?post=518486"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/nz\/wp-json\/wp\/v2\/tags?post=518486"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}