![\"Sylvester](\"https:\/\/www.europesays.com\/ie\/wp-content\/uploads\/2026\/01\/img-rna-dna-mutation.jpg\")
<\/p>\n
Summary<\/p>\n
- \n
- A new study from\u00a0Sylvester Comprehensive Cancer Center reveals how two mutations cooperate to erroneously splice RNA messages and disrupt the cell\u2019s identity.<\/li>\n
- The genes IDH2 and SRSF2 affect two key systems: the chemical signals that control gene\u00a0expression\u00a0and the way RNA is spliced. Understanding both could help\u00a0improve\u00a0treatments for AML.<\/li>\n
- The findings, published in\u00a0Science Advances,\u00a0provide a mechanistic map that could inform future therapies.<\/li>\n<\/ul>\n
Picture a film editor piecing together a blockbuster. Each scene must flow seamlessly to tell the story. In our cells, RNA plays that script editing role, splicing together genetic \u201cscenes\u201d so proteins know their lines.<\/p>\n
But in acute myeloid leukemia (AML),<\/a> two genetic mutations, IDH2 and SRSF2, throw the editor off script, creating a chaotic plot that drives disease.<\/p>\n
A new study from\u00a0Sylvester Comprehensive Cancer Center,<\/a> part of the University of Miami Miller School of Medicine,\u00a0reveals how these mutations cooperate to erroneously splice RNA messages and disrupt the cell\u2019s identity. The findings, published in\u00a0Science Advances,<\/a>\u00a0provide a mechanistic map that could inform future therapies. The study was written\u00a0by\u00a0first author\u00a0Aristeidis Telonis, Ph.D.,<\/a> with\u00a0senior author Maria \u201cKen\u201d Figueroa, M.D.<\/a><\/p>\n
What\u2019s Happening Inside the Cell<\/p>\n
In healthy cells, splicing trims and joins RNA segments to produce accurate instructions for making proteins. Think of it as cutting and pasting dialogue\u00a0to make\u00a0the movie make sense. The SRSF2 gene acts like a casting director, choosing which lines stay. IDH2, meanwhile, influences the chemical \u201cstage,\u201d the epigenetic marks that guide those choices.\u00a0Scientists\u00a0at Sylvester discovered that the two mutations team up to cause trouble.<\/p>\n
![\"Dr.](\"https:\/\/www.europesays.com\/ie\/wp-content\/uploads\/2026\/01\/img-Aristeidis-Telonis.jpg\")
Dr. Aristeidis Telonis is studying how mutations cooperate to erroneously splice RNA messages.<\/p>\n\u201cWhen those two forces collide, the editing room becomes chaos,\u201d said\u00a0Dr.\u00a0Telonis, assistant\u00a0professor of\u00a0biochemistry and\u00a0molecular\u00a0biology at the Miller School.<\/p>\n
The study shows this synergy leads to mis-splicing of key transcriptional regulators\u2014the master switches that determine cell identity.<\/p>\n
Why It Matters<\/p>\n
Treating AML depends on knowing what goes wrong inside cells. IDH2 and SRSF2 affect two key systems: the chemical signals that control gene\u00a0expression\u00a0and the way RNA is spliced. Understanding both could help\u00a0improve\u00a0treatments.<\/p>\n
\u201cThese mutations don\u2019t act alone. They reshape the cell\u2019s blueprint,\u201d said Dr. Figueroa. \u201cWhen structure and chemical signals work together in the wrong way, the cell\u2019s identity\u00a0changes. Understanding that process gives us a roadmap for better, more precise treatments.\u201d<\/p>\n
![\"Miller](\"https:\/\/www.europesays.com\/ie\/wp-content\/uploads\/2026\/01\/img-maria-figueroa.jpg\")
Dr. Maria \u201cKen\u201d Figueroa says understanding cell changes can lead to more effective treatments for AML.<\/p>\nThe urgency for understanding is there. AML\u00a0is a fast-growing cancer that starts in the bone marrow, where blood cells are made. In 2025, more than 22,000 people\u00a0were\u00a0diagnosed\u00a0with AML. It mostly affects older adults, but it can occur in younger people\u00a0as well.<\/p>\n
AML happens when immature white blood cells grow out of control and crowd out healthy cells. Standard treatments include chemotherapy, targeted drugs and sometimes stem cell transplants.<\/a> While these treatments can help, AML is hard to cure because the cancer cells often change and resist therapy. Each patient\u2019s disease can look different at the genetic level, which makes finding the right treatment challenging.<\/p>\n
The Science Behind the Scenes<\/p>\n
The team studied patient samples and lab models using advanced tools to read RNA and map chemical changes in DNA. Here\u2019s what they found:<\/p>\n
\u2022\u00a0When both mutations are present, cells make more splicing\u00a0errors than when only one mutation\u00a0is present.<\/p>\n
\u2022\u00a0These mistakes often\u00a0occur\u00a0near sites where DNA\u2019s chemical tags have changed, suggesting a link between splicing errors and epigenetic changes.<\/p>\n
\u2022\u00a0The genes most affected are long and complex, which makes them easier to disrupt.<\/p>\n
Researchers used artificial intelligence to predict splicing mistakes based on DNA\u2019s chemical patterns.<\/p>\n
\u201cOur model shows that methylation patterns alone can predict splicing outcomes,\u201d said Dr.\u00a0Telonis. \u201cThis link opens the doors for future trials to explore the use of epigenetic therapies in AMLs with these two mutations.\u201d<\/p>\n
Implications for Future Cancer Therapies<\/p>\n
The study hints that targeting epigenetic modifiers and splicing regulators together might offer new treatment strategies. In lab tests, cells carrying both mutations showed heightened sensitivity to\u00a0romidepsin, a drug that inhibits chromatin-modifying enzymes. That finding suggests a potential therapeutic angle.<\/p>\n
\u201cWe\u2019re beginning to see how these vulnerabilities could be exploited,\u201d\u00a0said Dr.\u00a0Figueroa, Sylvester\u2019s associate director of translational research and a professor of\u00a0biochemistry and molecular biology<\/a>\u00a0at the Miller School. \u201cIt\u2019s early, but this mechanistic clarity gives us a foundation for combination approaches.\u201d<\/p>\n
Cells rely on precise RNA editing to stay on script. In AML with IDH2 and SRSF2 mutations, the epigenetic notes and the editing machine reinforce each other\u2019s mistakes, disrupting the very regulators that keep identity intact. Mapping that error pathway is a critical step toward therapies that restore the right messages or silence the wrong ones.<\/p>\n
Tags:<\/strong> Acute Myeloid Leukemia<\/a>, AI<\/a>, AML<\/a>, artificial intelligence<\/a>, biochemistry and molecular biology<\/a>, cancer research<\/a>, chemotherapy<\/a>, Dr. Aristeidis Telonis<\/a>, Dr. Maria Figueroa<\/a>, gene editing<\/a>, Leukemia<\/a>, Sylvester Comprehensive Cancer Center<\/a>, technology<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"By: Staff Writer | January 02, 2026 | 7 min. read\u00a0|\u00a0 Share Summary A new study from\u00a0Sylvester Comprehensive…\n","protected":false},"author":2,"featured_media":264462,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[78],"tags":[119815,291,135585,289,135586,2566,4144,135587,135588,18,1278,135,19,17,20800,12261,82],"class_list":{"0":"post-264461","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-health","8":"tag-acute-myeloid-leukemia","9":"tag-ai","10":"tag-aml","11":"tag-artificial-intelligence","12":"tag-biochemistry-and-molecular-biology","13":"tag-cancer-research","14":"tag-chemotherapy","15":"tag-dr-aristeidis-telonis","16":"tag-dr-maria-figueroa","17":"tag-eire","18":"tag-gene-editing","19":"tag-health","20":"tag-ie","21":"tag-ireland","22":"tag-leukemia","23":"tag-sylvester-comprehensive-cancer-center","24":"tag-technology"},"share_on_mastodon":{"url":"https:\/\/pubeurope.com\/@ie\/115828878431826652","error":""},"_links":{"self":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/posts\/264461","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/comments?post=264461"}],"version-history":[{"count":0,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/posts\/264461\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/media\/264462"}],"wp:attachment":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/media?parent=264461"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/categories?post=264461"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/tags?post=264461"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}