What Types of Cancer Cause Blood Clots?

Pancreatic, stomach, brain, lung, and ovarian cancers carry some of the highest risks for blood clots, but virtually every cancer type raises the odds to some degree. Overall, people with cancer face roughly a fourfold increase in the risk of venous blood clots compared to the general population.¹ The relationship between cancer and clotting is not a simple one-to-one match, though. The type of tumor, its stage, the treatment being used, and the patient’s own body all push the risk up or down in ways that matter for real-world decisions.

The Highest-Risk Solid Tumors

Among solid tumors, pancreatic and stomach cancers consistently top the risk charts. Research evaluating clot risk across cancer types has found that cancers of the pancreas and stomach confer the highest thrombotic risk among all solid tumors.² Pancreatic cancer is especially notorious. One reason is that pancreatic tumors tend to be mucinous adenocarcinomas, meaning they secrete large amounts of abnormal mucin proteins into the bloodstream. These mucins interact with selectins on platelets and white blood cells, triggering clot formation even when no blood vessel injury has occurred. When purified carcinoma mucins were injected into mice, platelet-rich microthrombi formed rapidly, and the effect was dramatically reduced in mice lacking certain selectin receptors.³ This mucin-driven mechanism helps explain why cancers that produce mucin, including some colorectal and ovarian cancers, tend to be clot-prone.

Brain tumors, particularly glioblastoma, are among the most clot-prone cancers of all. Patients with glioblastoma face one of the highest rates of venous blood clots among all cancer types.⁴ In one study following glioblastoma patients, the one-year cumulative rate of venous clots was about 7.5%, and clot events were linked to higher mortality.⁵ Brain tumors create a particular clinical dilemma because anticoagulant treatment to prevent or dissolve clots also raises the risk of bleeding into the brain, making management tricky.

Lung and ovarian cancers sit in a clearly elevated risk tier as well. A prospective study tracking patients with breast, colorectal, lung, and ovarian cancers found that symptomatic venous blood clots occurred in about 8.5% of all patients studied.⁶ That rate may sound modest, but it is many times higher than what you would expect in people without cancer, and it translates to thousands of affected patients each year given how common these cancers are.

Blood Cancers Are Not Exempt

People sometimes assume that blood clots are mainly a solid-tumor problem, but blood cancers carry substantial clot risk too. Patients with lymphoma, multiple myeloma, and acute leukemia all face elevated thrombotic risk, particularly around the time of diagnosis and during chemotherapy.⁷ In fact, the clot rates associated with these blood cancers can exceed those of many solid tumors.⁸

Multiple myeloma is a standout example. Without preventive blood thinners, up to a third of myeloma patients may develop venous clots.⁹ What makes blood cancers interesting is that the clot risk often comes less from the cancer cells themselves and more from the treatments used against them. High-dose steroids, drugs like L-asparaginase used in leukemia treatment, and newer immunomodulatory agents used in myeloma all independently push up clot risk. Central venous catheters and growth factors used to support blood cell counts add further risk on top of that.⁸

Why Cancer Makes Blood Clot

The connection between cancer and clotting runs deep, involving several overlapping biological pathways. Understanding even the basics is useful because it explains why some cancers are worse offenders than others.

One of the most important drivers is a protein called tissue factor. In a healthy body, tissue factor sits on the outside of blood vessels and kicks off the clotting cascade when a vessel is damaged. Many tumor cells produce tissue factor on their surfaces and shed tiny membrane fragments called microparticles into the bloodstream. These microparticles are highly clot-promoting. In animal studies, higher levels of tumor-derived microparticles are associated with activated clotting, and these particles physically attach to sites of vascular injury and worsen clot formation.¹⁰ Cancers that express more tissue factor, like pancreatic and brain tumors, tend to have higher clot rates.

A second pathway involves a protein called podoplanin, which appears on the surface of certain tumor cells and their shed vesicles. Podoplanin activates platelets by binding to a receptor on the platelet surface, causing them to clump together. This mechanism has been studied in ovarian cancer, where both the cancer cells and the tiny vesicles they release cause platelet clumping.¹¹ Podoplanin is also implicated in cancer spread, which helps explain why clotting and metastasis are often linked.¹²

A third and more recently appreciated mechanism involves neutrophils, a type of white blood cell. When neutrophils encounter threats, they can expel their own DNA and proteins outward in web-like structures called neutrophil extracellular traps. These structures act as physical scaffolds that capture platelets and red blood cells, accelerating clot formation.¹³ In cancer, neutrophils infiltrating the tumor environment release these traps at abnormally high rates, contributing to both clotting and disease progression.¹⁴ This process links the immune system and the clotting system in ways researchers are still working out.

How Cancer Treatment Itself Raises Clot Risk

It is not just the tumor driving clots. Many cancer treatments independently increase clotting risk, sometimes substantially. This is a crucial point for patients because it means even cancers not traditionally considered “high risk” for clots can become so once aggressive treatment begins.

Chemotherapy damages blood vessel linings, reduces natural anticoagulant proteins, and can make the blood stickier. Drugs that block blood vessel growth, known as antiangiogenesis agents, are used in many cancers, and both arterial and venous blood clots have emerged as significant side effects of these drugs.¹⁵

Immune checkpoint inhibitors, a newer class of cancer drugs that unleash the immune system against tumors, carry their own clotting burden. In one study, the rate of venous clots was over 22-fold higher in patients receiving these drugs compared to the general population, and rates of heart attack and stroke were also elevated.¹⁶ A large analysis of over 10,000 patients without prior clot history found that one in roughly 13 developed a venous clot within six months of starting checkpoint inhibitor therapy, and the 12-month rate climbed to about one in nine.¹⁷ These numbers are striking and are changing how oncologists think about clot prevention in immunotherapy patients.

Central venous catheters, the intravenous lines often placed in cancer patients for chemotherapy delivery, are another independent risk factor. One large review found a clot rate of about 3.6% across all central line types, with clots developing a median of 12 days after insertion. Peripherally inserted central catheters, or PICC lines, carried the highest risk among catheter types.¹⁸ The risk is highest in the first couple of weeks after the line goes in.¹⁹

Venous Clots Versus Arterial Clots

Most of the conversation about cancer and blood clots focuses on venous clots, meaning clots in the veins, which include deep vein thrombosis in the legs and pulmonary embolism in the lungs. But cancer also increases the risk of arterial clots, which cause heart attacks and strokes. The rate of arterial clots within six months of a cancer diagnosis ranges from roughly 1% to 5%.²⁰

Arterial and venous clots form through somewhat different processes. Arterial clots are driven primarily by platelet activation under high blood-flow conditions, while venous clots depend more on the coagulation cascade and slower-flowing blood.²⁰ This distinction matters for treatment because drugs that work well against one type may be less effective against the other. It also helps explain why some cancer treatments, particularly antiangiogenesis drugs, seem to disproportionately increase arterial clot risk. When an arterial clot does occur in a cancer patient, the outlook is serious: recurrence within six months is reported at about 37%, and mortality increases substantially.²⁰

How Clots Affect Cancer Survival

Developing a blood clot during cancer treatment is not just a temporary complication; it worsens outcomes in a measurable way. A large population-based study found that cancer patients who developed venous clots had a one-year mortality of 45%, compared to 38% in matched cancer patients without clots. By five years, the difference widened further.²¹ After adjusting for age, race, and cancer stage, a clot diagnosis was a significant predictor of death within one year across all cancer types studied, with the increased risk ranging from 1.6- to 4.2-fold depending on the cancer.²²

Part of this is because clots often signal more aggressive disease. Patients whose cancer had already spread at the time of diagnosis were more likely to develop clots, and metastatic disease itself was the strongest predictor of death.²² But the clot itself also causes direct harm. It can interrupt cancer treatment while the patient is treated with blood thinners, increase hospitalization, and carry its own risk of death from pulmonary embolism. Beyond survival statistics, patients who develop clots report meaningful reductions in quality of life, with measurable drops in health-related well-being scores.

Predicting Who Will Get a Clot

Given that clots worsen outcomes, oncologists have tried to develop scoring systems to identify the patients most at risk. The most widely used is the Khorana score, which assigns points based on cancer type, pre-treatment blood counts, and body mass index. In a meta-analysis, patients with a high Khorana score had an 11% rate of venous clots within six months, compared to 5% for those with a low score.²³ However, the score’s ability to sort patients is imperfect. Only about 23% of patients who actually developed clots had been flagged as high risk by the score, meaning most clots occurred in patients classified as low or intermediate risk.²³

This limitation is especially pronounced in patients with metastatic cancer, where a blood marker called D-dimer has shown better predictive accuracy than the Khorana score. In one study comparing the two approaches in metastatic patients, D-dimer had a markedly higher ability to discriminate who would develop a clot.²⁴ Other biomarkers like soluble fibrin are also being studied. Research in Japanese cancer patients found that elevated soluble fibrin at baseline and rising D-dimer levels over time were both associated with later clot events, and having pancreatic cancer was independently linked to a roughly threefold increase in clot risk even after adjusting for other factors.²⁵ The field is moving toward combining tumor type, blood markers, and treatment type into better prediction tools, but no single test reliably identifies every patient who will clot.

Treating and Preventing Clots in Cancer Patients

For decades, the standard treatment for blood clots in cancer patients was injectable low-molecular-weight heparin, given by daily shots for months. Oral blood thinners called direct oral anticoagulants have now become a viable alternative. A randomized trial found that oral anticoagulants were noninferior to heparin injections for preventing recurrent clots, with recurrence rates of about 6% versus 9% over six months.²⁶ For most cancer patients, swallowing a pill is far more practical than daily injections, which has been a meaningful quality-of-life improvement.

The choice is not always straightforward, though. Cancers in or near the gastrointestinal tract pose a higher bleeding risk with oral anticoagulants, and brain tumors raise the specter of intracranial bleeding with any blood thinner. A real-world analysis of patients with brain metastases from various primary cancers found that oral anticoagulants were associated with a lower risk of intracranial bleeding in patients with breast cancer or melanoma brain metastases, but no clear difference was seen for lung, colorectal, or renal cell carcinoma.²⁷ The bottom line is that anticoagulant choice in cancer increasingly depends on the specific tumor type, its location, and its tendency to bleed.

Preventive blood thinners for patients who have not yet clotted are more controversial. Guidelines generally recommend considering prophylaxis for high-risk outpatients starting chemotherapy, especially those with pancreatic or lung cancer and a high Khorana score, as well as for cancer patients who are hospitalized or undergoing surgery. But for many patients, the risk of treatment-related bleeding has to be weighed against the clot-prevention benefit, and that calculation varies case by case.

Clots in Children and Young Adults with Cancer

Blood clots are not just an adult problem. In children with cancer, clotting complications occur at notable rates, driven by an interaction between the cancer itself, the effects of treatment, and sometimes an underlying inherited tendency toward clotting. Recognized risk factors in pediatric cancer include very young age, adolescence, non-O blood group, the type and location of cancer, the presence of central venous catheters, and the specific chemotherapy regimen. In children, clots most commonly occur in the extremities rather than the lungs. The risk profile differs enough from adults that pediatric oncology teams use separate protocols for prevention and monitoring.

When a Clot Is the First Sign of Cancer

Sometimes a blood clot appears before anyone knows cancer is present. An unexplained deep vein thrombosis or pulmonary embolism, particularly in a younger person without obvious risk factors like recent surgery or prolonged immobility, can prompt doctors to look for a hidden malignancy. The term Trousseau syndrome, named after the nineteenth-century French physician who described the link between migratory blood clots and occult cancer, is still used to describe this clinical situation. Mucinous adenocarcinomas of the pancreas, stomach, and ovary are the most commonly associated cancers, which fits with the mucin-driven clotting mechanism described earlier.

How aggressively doctors should screen for cancer after an unprovoked clot remains debated. Some guidelines recommend basic bloodwork, age-appropriate cancer screening, and a careful physical exam. Others have tested more extensive imaging. The yield is modest in absolute numbers: most people who get an unprovoked clot do not have an underlying cancer. But when a cancer is found this way, it is sometimes caught earlier than it would have been otherwise, which can make a real difference for cancers where early detection improves survival.