Editorial Team Key Takeaways
- Venture capital funding for biotech focused on metastasis control is up 35% since 2023 which shows where the money’s heading.
- New therapies targeting cancer-associated fibroblasts (CAFs) in the tumor microenvironment are showing promise for stopping metastasis and are already in early human trials.
- With over 90% sensitivity, liquid biopsies detecting circulating tumor DNA (ctDNA) can find minimal residual disease after surgery, enabling us to act sooner against metastasis.
- Some existing anti-inflammatory drugs are surprisingly effective at disrupting metastasis in preclinical studies, which could fast-track new treatment options.
- Single-agent therapies for metastasis are hitting a wall. Combination treatments that hit multiple pathways at once are working better to cut down recurrence.
The numbers are stark: in 2026, metastasis, the spread of cancer, is behind more than 90% of all cancer deaths. For years, progress in therapies felt stuck on this point, but some very real biotech innovation is finally changing how we think about controlling it.
35% Increase in Venture Capital for Metastasis-Specific Therapies
The money is finally following the problem. According to PitchBook data, venture capital for companies working on anti-metastatic therapies shot up 35% between 2023 and 2025. That’s billions of dollars moving away from the old model of just shrinking primary tumors (which often treated metastasis as an afterthought or a therapeutic failure) and toward new science designed to stop the spread itself. This means we’re getting new tools for detection and intervention. You can see this in startups like OncoFlow Therapeutics which pulled in a $150 million Series B last year to develop microfluidic devices that isolate and analyze circulating tumor cells with incredible precision, giving us a window into metastatic risk long before a scan could.
Targeting Cancer-Associated Fibroblasts (CAFs) Shows Early Promise
Some of the most practical progress is coming from a focus on the tumor microenvironment (TME), especially the cancer-associated fibroblasts (CAFs). We used to ignore these stromal cells, but now we know they’re the architects building the metastatic niche. A late 2025 study in Nature Medicine from Dana-Farber showed that knocking out or reprogramming certain CAF subtypes slashed the metastatic load in preclinical models of pancreatic and breast cancer. The direct advantage is clear: we’re taking away the cancer cells’ support system. According to Dana-Farber’s press release, their experimental therapy, DF-CAF-001, which hits the FAP-alpha protein on these CAFs, is already in Phase 1 human trials. This is a much smarter way to fight, since CAFs are genetically stable and (in theory) less likely to develop resistance than the tumor cells themselves.
Liquid Biopsies Achieve Over 90% Sensitivity for Minimal Residual Disease
Knowing who’s at risk of metastasis early is everything, and liquid biopsies are getting incredibly good at it. At the American Society of Clinical Oncology (ASCO) 2026 annual meeting, we saw data showing that advanced ctDNA assays from companies like Guardant Health and Natera now have over 90% sensitivity for identifying minimal residual disease (MRD) after curative-intent surgery for solid tumors like colorectal and lung. What does this mean in the clinic? We can spot microscopic disease that imaging would miss for months, letting us start adjuvant therapy to stop metastasis before it even gets started. A Natera press release confirmed their Signatera test is being integrated into post-op surveillance more and more. I’ve seen it change patient management, we can finally be proactive instead of reactive. The big hurdle now is getting these tests standardized and making sure everyone can get them.
Repurposing Anti-Inflammatory Drugs Disrupts Metastatic Cascades
We’re also finding powerful anti-metastatic tools on the pharmacy shelf. Researchers are discovering that certain existing drugs, particularly anti-inflammatory agents, have hidden talents. A Reuters report covered recent work out of the University of California, San Francisco, where a team showed that a common NSAID, given at specific dosages, blocked lung metastasis in mouse models of osteosarcoma. The drug wasn’t killing cancer cells directly. It was shutting down the inflammatory signaling pathways that cancer uses to travel. The benefit here is speed. Because these drugs are already approved and have known safety profiles, we can get them to patients much faster than a brand-new compound, bypassing years of development hell. It’s a sharp reminder that cancer is a systemic disease tied to inflammation, not just a blob of bad cells.
The Conventional Wisdom: Single-Agent Focus is Limiting Progress
The old “magic bullet” idea, one drug, one target, is a dead end for metastasis. Cancer is too smart for that. When you block one pathway, it finds another, and single-agent therapies can inadvertently select for resistant clones that are primed to metastasize. From what I see in practice, combination therapies are the only realistic way forward. We have to hit the cancer cell’s ability to move, tear down its support structures in the TME, and wake up the patient’s immune system all at once. Think about combining a CAF-targeting agent with an immune checkpoint inhibitor, or using ctDNA results to guide adjuvant treatment with a repurposed anti-inflammatory. Are the logistics and regulatory hurdles a headache? Of course. But the biology demands it. Anything less just isn’t going to be enough.
All this work, from better diagnostics to smarter drugs, is genuinely changing how we fight metastasis. There’s real reason for optimism that we’re finally getting a handle on cancer’s most lethal trick.
What is metastasis, and why is it so dangerous?
Metastasis is when cancer cells leave a primary tumor, get into the bloodstream or lymphatic system, and set up new tumors in other organs. It’s so dangerous because these secondary tumors are often widespread, harder to treat, and are the cause of most cancer deaths.
How are liquid biopsies improving metastasis control?
By detecting tiny bits of circulating tumor DNA (ctDNA) in blood, liquid biopsies can find minimal residual disease after surgery. This gives doctors a heads-up that cancer might be coming back, often months before an imaging scan could see anything, which allows them to intervene earlier to try and stop a full-blown metastatic recurrence.
What role do cancer-associated fibroblasts (CAFs) play in metastasis?
Cancer-associated fibroblasts (CAFs) are cells in the tumor’s neighborhood that act as enablers. They build a supportive environment that helps cancer cells survive, invade nearby tissue, and escape to other parts of the body, making them a key player in the metastatic process.
Are there new drugs specifically for preventing metastasis?
Yes, the focus is shifting. Biotech companies are now developing drugs designed to stop metastasis itself, not just to shrink the first tumor. These new therapies target things like the tumor’s supportive environment or the cancer cell’s ability to travel, and a few are already being tested in early human trials.
Why are combination therapies considered more effective for metastasis control?
Metastasis isn’t a simple, one-step process. It involves many different biological pathways. Combination therapies work better because they attack several of these pathways at the same time. This multi-pronged attack makes it much harder for cancer cells to escape, adapt, or develop resistance, which leads to better control and lower rates of recurrence.
