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In tumor samples from more than 200 patients across the U.S., Brazil, and Mexico, the same hidden switch kept appearing.<\/p>\n
Tracing that evidence, Pietro Berico, PhD, at NYU Grossman School of Medicine<\/a> linked a gene-controlling protein called HOXD13, which acts like a switch that turns other genes on or off, to faster tumor growth and weaker immune attack.<\/p>\n Tumors with higher HOXD13 activity had more blood supply and fewer immune cells inside, a combination that helps cancer survive and spread.<\/p>\n That pattern suggests HOXD13 is not just present but actively shaping how melanoma grows and avoids treatment, pointing toward therapies that may need to block both effects together.<\/p>\n Blood vessels answer<\/p>\n Growing tumors need oxygen and nutrients, and HOXD13 helped melanoma build extra blood vessels to deliver both.<\/p>\n That process, called angiogenesis, simply means creating new blood vessels where cancer cells need fuel to keep dividing.<\/p>\n HOXD13 boosted signals that tell the body to grow new blood vessels, giving tumors easier access to the bloodstream.<\/p>\n Other signals also reshaped those vessels in ways that may make them harder for treatments to fully block.<\/p>\n Immune cells excluded<\/p>\n Patients with higher HOXD13 activity had fewer cancer-fighting T cells, the immune cells that destroy abnormal cells, circulating in their blood.<\/p>\n Inside the tumors, those same cells showed up less often, leaving the cancer with fewer defenses to overcome.<\/p>\n That pattern matters because many melanoma treatments rely on these immune cells already being in place to do their job.<\/p>\n \u201cOur study provides new evidence that transcription factor HOXD13 is a potent driver of melanoma growth and that it suppresses the T cell<\/a> activity needed to fight the disease,\u201d Berico said.<\/p>\n Chemical signals from HOXD13<\/p>\n Beyond helping tumors grow, HOXD13 also increased a molecule called CD73, which helps produce a chemical that slows down the immune system.<\/p>\n That chemical, known as adenosine, can weaken nearby T cells and make it harder for them to attack cancer.<\/p>\n Earlier research<\/a> had already linked the CD73 molecule to weaker immune responses, which makes HOXD13\u2019s role more concerning.<\/p>\n When researchers turned off HOXD13 in experiments, more T cells were able to enter tumors and resume their attack.<\/p>\n Inside melanoma cells, HOXD13 changed which parts of DNA connect with genes that control growth and immune defense.<\/p>\n DNA can fold and loop, allowing distant sections to switch genes on or off when they come into contact.<\/p>\n HOXD13 strengthened those connections, turning on signals that support blood vessel growth and block immune activity.<\/p>\n That helps explain how a single protein can drive both faster tumor<\/a> growth and stronger resistance to the immune system.<\/p>\n Blocking both routes<\/p>\n Testing treatments in mice showed the strongest evidence yet that this switch could be directly targeted.<\/p>\n One drug blocked the signals that help tumors grow new blood vessels, while another blocked the chemical signal that slows down immune cells.<\/p>\n Using both together slowed tumor growth more than either treatment on its own.<\/p>\n This combined approach points to a potential treatment strategy that targets both tumor growth and immune suppression at the same time.<\/p>\n Patients guide choices<\/p>\n For patients, the finding points toward selection, not a single new treatment for everyone with melanoma.<\/p>\n In 2026, federal cancer statistics<\/a> estimated 112,000 new U.S. melanoma cases and 8,510 deaths.<\/p>\n Some patients with advanced melanoma receive immune checkpoint inhibitors (ICI<\/a>), drugs that remove signals from T cells.<\/p>\n Tumors with high HOXD13 activity may need extra support from treatment, because fewer immune cells reach the areas where those drugs need to work.<\/p>\n Wider cancer clues<\/p>\n Other cancers may also use this same switch, even though melanoma showed the clearest pattern in this research.<\/p>\n Scientists now plan to study glioblastomas, a fast-growing type of brain cancer, where HOXD13 levels can also be high.<\/p>\n They will also look at sarcomas, which are cancers that form in muscles, bones, and other support tissues.<\/p>\n Among these, osteosarcomas, a type of bone cancer, will only be relevant if they show the same pattern of growth and immune<\/a> evasion.<\/p>\n Limits still matter<\/p>\n Results in lab models do not mean a treatment targeting HOXD13 is ready for patients. Because HOXD13 works inside cells to control genes, it can be difficult to target safely with drugs.<\/p>\n Even treatments that block related pathways may cause side effects, since those same systems also support normal body functions.<\/p>\n Future clinical trials will need to identify which patients have high HOXD13 activity and test whether combined treatments improve outcomes.<\/p>\n This hidden switch now appears to coordinate how melanoma grows, avoids the immune system, and resists treatment.<\/p>\n Doctors cannot test for HOXD13 in routine care yet, but the finding gives researchers a clearer way to design treatments for the tumors most likely to evade current therapies.<\/p>\n The study is published in Cancer Discovery<\/a>.<\/p>\n \u2014\u2013<\/p>\n Like what you read? Subscribe to our newsletter<\/a> for engaging articles, exclusive content, and the latest updates.<\/p>\n Check us out on EarthSnap<\/a>, a free app brought to you by Eric Ralls<\/a> and Earth.com.<\/p>\n \u2014\u2013<\/p>\n","protected":false},"excerpt":{"rendered":"A new study has found that melanoma can use one protein, HOXD13, to grow new blood vessels while…\n","protected":false},"author":2,"featured_media":418465,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[10],"tags":[103,61,60],"class_list":{"0":"post-418464","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-health","8":"tag-health","9":"tag-ie","10":"tag-ireland"},"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/posts\/418464","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/comments?post=418464"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/posts\/418464\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/media\/418465"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/media?parent=418464"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/categories?post=418464"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/ie\/wp-json\/wp\/v2\/tags?post=418464"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}