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<\/p>\nCancer cachexia contender enters first pivotal trial<\/p>\n
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That all changed after he was diagnosed with pancreatic cancer<\/a> in 2010. Over the next seven years, as he endured intensive treatment, his love of food remained but his appetite dwindled. He lost muscle mass and became gaunt. Weakened and fatigued, he could no longer chop wood for the home\u2019s stove.<\/p>\n Kochanczyk\u2019s struggles were not only the result of the tumour and treatments waging war against one another in his body, but also due to cachexia, a cancer-linked syndrome<\/a> that causes reduced appetite and muscle wasting. \u201cIt\u2019s very hard to watch,\u201d recalls Dave\u2019s son Martin Kochanczyk. Since his father\u2019s death in 2017, Martin has become an advocate for cachexia awareness with the Cancer Cachexia Society, a community of scientists, people with the condition and others advancing research, awareness and treatment.<\/p>\n As Martin often explains to people with cancer and their families, his father was hardly an outlier. \u201cCachexia affects a lot of people,\u201d he says. Between 50% and 80% of people with cancer, depending on the tumour type and disease stage, experience cachexia.<\/p>\n \u201cI\u2019ve heard people describe it as lying down under a thousand-pound blanket,\u201d says sociologist Abigail Newell, senior director of research at the Cancer Support Community in Washington DC. \u201cSitting up feels like running a marathon.\u201d And it\u2019s more than a quality-of-life issue; cachexia affects survival. Exhaustion, hopelessness and other psychological symptoms can make people less willing to keep up with treatments. Severe cachexia can even make some therapies intolerable, or cause individuals to be excluded from clinical trials. Ultimately, 20\u201330% of cancer-associated deaths are attributable to cachexia, rather than the cancer itself.<\/p>\n Why are so many young people getting cancer? What researchers do and don\u2019t know<\/p>\n <\/a><\/p>\n Although cachexia was long considered an inescapable part of cancer\u2019s progression, it has now become a topic of study in its own right. In 2020, a global research initiative, Cancer Grand Challenges<\/a>, asked scientists to propose projects on cachexia.<\/p>\n The initiative ended up funding an international team of clinicians, scientists and advocates \u2014 16 research groups across 14 institutions \u2014 to the tune of \u00a320 million ($US25 million) to study cancer cachexia, its drivers, subtypes and potential treatments. Now in its fifth year, the project, known as CANCAN, has released about 30 papers, which have appeared alongside a rising tide of research from independent efforts.<\/p>\n With the influx of fresh studies, the very concept of cachexia is changing. Where scientists once saw simple malnutrition, muscle wasting and weight loss, they now see a whole-body syndrome of metabolism gone haywire. Studies reveal how cachexia is more than physical symptoms; it affects not just appetite and metabolism, but also motivation and behaviour. And a handful of companies, including pharmaceutical giant Pfizer, are testing medicines for cachexia<\/a> (see \u2018Fighting cachexia\u2019), raising hope that a treatment might be on the horizon.<\/p>\n Source: Ref. 10<\/p>\n \u201cIt\u2019s still an area of mystery,\u201d says Ryan Schoenfeld, chief executive of the Mark Foundation for Cancer Research in New York City, a grant-making organization. But the burst of activity over the past few years has made him optimistic. \u201cI feel confident in the future of the research here, that we\u2019ll uncover ways to treat cachexia that will make it more reversible than it is today,\u201d he says. \u201cIdeally, we\u2019ll prevent it.\u201d<\/p>\n Organ crosstalk<\/p>\n Cachexia has long been something of a paradox in cancer: widely prevalent and with a huge impact on people, it nevertheless existed beyond the gaze of many physicians and scientists. Specialists typically focused on the tumour, reasoning that eliminating the cancer would relieve the cachexia, says Schoenfeld. There are no approved medications for cancer cachexia in most parts of the world. The appetite stimulant anamorelin is available in Japan, but the US Food and Drug Administration and the European Medicines Agency found the evidence for its benefits to be insufficient for approval. Even if people with the condition force themselves to eat more, or are fed through a tube, it doesn\u2019t solve the problem.<\/p>\n With more people surviving for longer with cancer, the need for cachexia treatment is only growing, and funders and scientists have taken note. \u201cThere\u2019s a whole ecosystem of cachexia researchers now,\u201d says Tobias Janowitz, a physician-scientist at Cold Spring Harbor Laboratory in New York and co-principal investigator of CANCAN. Once a specialist topic relegated to niche conferences, cachexia has been on the programme of the annual meeting of the American Association for Cancer Research for the past several years, notes Mariam Jamal-Hanjani, a clinician-scientist at University College London and a CANCAN co-investigator.<\/p>\n Andrea Bonetto, a muscle physiologist at the University of Colorado Anschutz in Aurora, has been studying cachexia since before the field took off. When he began, the condition was considered mainly a case of muscle wasting. \u201cWhat is now clear, compared to 24 years ago, is that cachexia is not a single gene, a single-tissue disease, but it\u2019s multifaceted, it\u2019s multi-tissue, it\u2019s multi-systemic,\u201d he says. \u201cThere\u2019s huge crosstalk among different tissues and organs.\u201d Each region of the body might receive signals that cause it to alter its metabolism or activities, and to send signals that influence cachexia pathways in other parts.<\/p>\n The path starts with the cancer. The immune system might respond to the presence of abnormal cells, resulting in inflammation. But cachexia-associated signalling spreads widely. Bonetto\u2019s group found, for example, that tumours that neither originate in nor infiltrate bone can, nonetheless, cause cell death and breakdown in bones1<\/a>. Antibodies that block a regulator of bone remodelling and muscle structure called RANKL, which is made by bone and by several tumour types, minimized bone and muscle loss and preserved strength in a mouse model of ovarian cancer2<\/a>. Bisphosphonate drugs used to treat osteoporosis had similar benefits, suggesting that these medications might have a place in treating cachexia, too.<\/p>\n The liver also seems to have a key role in cachexia signalling. For one, its secretions seem to worsen the breakdown of muscle and bone, Bonetto says. A contribution from this organ makes sense, says Mauricio Berriel Diaz, a biologist at the Helmholtz Centre Munich in Germany, because the liver is a major regulator of metabolism. He and his colleagues reported that liver cells respond to cachexia by secreting a handful of specific compounds3<\/a>. In lab dishes, these compounds cause heart cells to shrink and fat cells to break down fat. Levels of these secretions were also elevated in people with cachexia3<\/a>.<\/p>\n Another study, in mouse models of cachexia, linked liver problems to the vagus nerve<\/a>, which runs between the brain and other organs. Vagus dysfunction caused the liver to alter its metabolism, adopting a pro-inflammatory, cachexia-promoting state. Blocking vagal activity minimized weight loss and improved appetite and activity level in these mice4<\/a>.<\/p>\n A disease of the brain<\/p>\n The brain<\/a> ultimately becomes a key orchestrator of cachexia, says Adam Kepecs, a neuroscientist at Washington University in St. Louis, Missouri. It is the only place in the body that can integrate the various inflammatory, metabolic and hormonal elements of such a complex condition, Kepecs says. And it\u2019s where cachexia becomes not just physical, but also psychological.<\/p>\n US cancer deaths are falling \u2014 but not fast enough<\/p>\n <\/a><\/p>\n Right now, much of the excitement around drug development for cachexia has to do with the action of the stress hormone GDF15 in the brain. GDF15 activates a signalling pathway that diminishes appetite and creates a sense of satiety. If you eat something that doesn\u2019t agree with you, GDF15 sounds the alarm, so you don\u2019t eat it again. The hormone is a well-known contributor to the appetite loss seen in cachexia, but scientists don\u2019t fully understand where it comes from or how it participates in the condition.<\/p>\n At the University of Oklahoma in Oklahoma City, cancer biologist Min Li and his colleagues have identified GDF15\u2019s role in a three-way conversation between the tumour, the brain and the immune system. Tumour cells alone don\u2019t cause much cachexia in the mice that he and his colleagues used, Li says. But they release signals that cause immune cells to produce GDF15. When GDF15 reaches the brain, the brain then signals back to the tumours, causing them to recruit further immune cells. These then become additional GDF15 producers, creating a vicious cycle. Eliminating or blocking GDF15 reduced cachexia in the mice5<\/a>.<\/p>\n Immune signals and the inflammation they cause are well-known contributors to cachexia, but Kepecs and his colleagues found that at least one immune molecule has an influence well beyond affecting appetite and wasting. When the researchers did behavioural tests on mice with cachexia, they found that the animals were less likely to put in extra effort to obtain food or water \u2014 even beyond expectations for mice with low appetite and reduced energy levels6<\/a>. They seemed to have low motivation.<\/p>\n","protected":false},"excerpt":{"rendered":"Mealtimes were always a family affair for the Kochanczyks of Indiana. Dave Kochanczyk loved barbecuing, cooking Polish fare…\n","protected":false},"author":2,"featured_media":703749,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[10],"tags":[847,5389,59,102,4230,5898,4231,90,56,54,55],"class_list":["post-703748","post","type-post","status-publish","format-standard","has-post-thumbnail","category-health","tag-cancer","tag-drug-discovery","tag-gb","tag-health","tag-humanities-and-social-sciences","tag-medical-research","tag-multidisciplinary","tag-science","tag-uk","tag-united-kingdom","tag-unitedkingdom"],"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/posts\/703748","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/comments?post=703748"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/posts\/703748\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/media\/703749"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/media?parent=703748"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/categories?post=703748"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/tags?post=703748"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}![\"\"](\"https:\/\/www.newsbeep.com\/uk\/wp-content\/uploads\/2026\/07\/d41586-026-02228-7_52987964.jpg\"\/)
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