Pancreatic Cancer: Is It Hereditary, How It Is Diagnosed and Why It Is Hard to Catch Early

A woman in her fifties sits across from her doctor with a folded piece of paper. On it, three names: her father, his sister, and a cousin. All three had pancreatic cancer. She wants to know whether the paper is a family tree or a forecast.

That question lands in clinics far more often than it used to, partly because genetic testing has become routine after a pancreatic cancer diagnosis, and partly because the disease has a reputation for arriving late and unannounced. Both parts of that reputation deserve a closer look. Fear tends to inflate the hereditary piece and flatten the nuance of why early detection is difficult.

So this article does three things. It separates inherited risk from ordinary bad luck. It walks through the tests that actually confirm the diagnosis, from a liver blood panel to an endoscopic ultrasound. And it explains, in plain anatomical terms, why a gland tucked behind the stomach is so good at hiding.

How common is pancreatic cancer, and who is most likely to get it?

The pancreas is a six-inch gland shaped a little like a flattened pear, lying crosswise behind the stomach. It makes digestive enzymes and the hormones insulin and glucagon. Cancer can start in either system, but about 95 percent of cases begin in the enzyme-producing cells and are called pancreatic ductal adenocarcinoma, according to Johns Hopkins and Cleveland Clinic patient information. The rarer neuroendocrine tumors, which arise from hormone cells, often behave quite differently and are covered here only briefly.

In the United States, pancreatic cancer accounts for roughly 3 percent of all new cancer diagnoses, based on the National Cancer Institute’s SEER program. That makes it far less common than breast, prostate, lung or colorectal cancer. Yet it sits near the top of the list for cancer deaths, a gap that says more about how late it is usually found than about how many people develop it.

Age is the dominant factor. Most people are diagnosed after 65, and the median age at diagnosis is around 70. Cases before age 50 are uncommon, and when they occur, doctors look harder for an inherited cause. Men are affected slightly more often than women, and Black Americans have higher rates than other groups, for reasons that likely mix genetics, smoking history, diabetes prevalence and access to care.

That framing matters for the hereditary question. If someone’s grandfather was diagnosed at 78, that fits the ordinary age pattern and says little about the family’s genes. Two relatives diagnosed in their fifties tells a different story.

Is pancreatic cancer hereditary? What the one-in-ten figure really means

Here is the number that does most of the work: about 10 percent of pancreatic cancers are thought to have a hereditary component, either an identified inherited gene change or a pattern of cases in close relatives, according to the National Cancer Institute’s genetics summary and Cleveland Clinic. Flip it around and the message is calmer than most people expect. Roughly nine in ten cases arise in people with no inherited predisposition at all.

Hereditary in this context means something specific. Everyone is born with two copies of thousands of genes that repair DNA damage or control cell division. If a person inherits one faulty copy of certain repair genes from a parent, every cell in the body starts life one step closer to losing that safeguard. The faulty copy is present in eggs or sperm, so it can be passed to children, each of whom has a 50 percent chance of inheriting it.

Two things follow. First, inheriting a gene change is not inheriting the cancer. Most carriers of even the higher-risk genes never develop pancreatic cancer; the change raises probability, sometimes substantially, but does not guarantee anything. Second, a family cluster can exist without any known gene being found. Doctors call this familial pancreatic cancer, and it is discussed in its own section below because it is managed differently from a confirmed gene change.

There is a third, more subtle category. Families share more than DNA. Smoking habits, diet patterns and the tendency toward type 2 diabetes cluster in households too, and each of those independently raises pancreatic cancer risk. Sorting inherited from shared-environment risk is one of the jobs of a genetic counselor.

Which inherited genes raise the risk of pancreatic cancer?

A handful of genes account for most confirmed hereditary cases. Several are better known for other cancers, which is why a family history of breast, ovarian, melanoma or colon cancer can be relevant to a pancreatic cancer conversation. The table below summarizes the main ones described in the National Cancer Institute’s genetics summary.

Gene or syndrome	Better known for	What it means for the pancreas
BRCA2, BRCA1, PALB2	Breast and ovarian cancer	Moderately raised pancreatic risk, higher for BRCA2 than BRCA1
ATM	Breast cancer	Moderately raised risk; commonly found on tumor-related testing
CDKN2A (familial atypical multiple mole melanoma)	Melanoma	Among the highest lifetime pancreatic risks of any single gene
STK11 (Peutz-Jeghers syndrome)	Gut polyps, freckling around lips	Very high lifetime risk; surveillance often starts earlier
MLH1, MSH2, MSH6, PMS2 (Lynch syndrome)	Colorectal and uterine cancer	Modestly raised risk; tumors may respond differently to some therapies
PRSS1, SPINK1 (hereditary pancreatitis)	Recurrent pancreatitis from childhood	Risk rises through decades of inflammation, higher still in smokers
TP53 (Li-Fraumeni syndrome)	Many early cancers	Pancreatic cancer is one of several raised risks

Notice how different these are. A CDKN2A change carries a lifetime pancreatic risk that can exceed one in ten, while a Lynch syndrome change nudges risk up only modestly. That spread is why a genetic result should never be read as a single verdict; the specific gene, the family history and the person’s age all shape what a clinician recommends next.

Notice too what is missing. Most people with a family history who undergo testing receive a negative result. That does not close the file. It simply moves them into the familial category described next.

What is familial pancreatic cancer, and does one relative count?

Clinicians use a precise definition. Familial pancreatic cancer describes a family with at least two first-degree relatives (a parent, sibling or child of each other) who have had the disease, without a known gene change to explain it, per the National Cancer Institute’s genetics summary. About half or more of families that meet this definition test negative for every currently known gene, which tells researchers there are inherited factors still to be discovered.

What about a single relative? The evidence summarized by the NCI suggests that one affected first-degree relative roughly doubles a person’s risk compared with the general population. Because the baseline lifetime risk is low, doubling it still leaves the absolute risk small. With two affected first-degree relatives the estimated increase is several-fold, and with three it climbs steeply. Younger age at diagnosis in relatives, generally under 50, adds weight to the family history.

A practical way to think about it:

• One relative diagnosed late in life: worth mentioning to a doctor, rarely a reason for testing on its own.
• One relative plus a family history of breast, ovarian, melanoma or colon cancer: a reasonable trigger for a genetics referral.
• Two or more first-degree relatives, or one diagnosed before 50: meets common criteria for counseling and possible surveillance.

Family history also has a habit of being incomplete. A grandmother who died of a vaguely described stomach or liver cancer decades ago may have had pancreatic disease that was never confirmed. Genetic counselors are used to working with fuzzy pedigrees, and they will often ask for whatever records exist rather than dismissing an uncertain story.

Should I get genetic testing if a parent had pancreatic cancer?

The answer has shifted over the past decade. Major US cancer guidelines now recommend that everyone diagnosed with pancreatic cancer be offered germline genetic testing, regardless of age or family history, because an inherited change is found in a meaningful minority and can influence both treatment planning and advice for relatives. Cleveland Clinic and Mayo Clinic patient information both reflect that shift.

For healthy relatives, the logic runs in a specific order. The most informative person to test is the one who had cancer. If a parent tested positive for, say, a PALB2 change, then their children can be tested for that exact change, and a negative result is genuinely reassuring. If the affected parent was never tested and has died, a child can still be tested, but a negative result is harder to interpret, because it might mean no hereditary factor exists or that the family carries a gene not yet identified.

Testing itself is a blood or saliva sample analyzed on a multi-gene panel. The harder part is the conversation before and after. A genetic counselor will map the family tree, estimate the likelihood of finding something, explain what each possible result would change in practice, and discuss insurance protections and implications for siblings and children.

Two honest caveats belong here. Results sometimes return a variant of uncertain significance, a change whose effect is not yet known and which should not be acted on as if it were harmful. And a positive result can raise as many questions as it answers, since surveillance for the pancreas remains imperfect. Deciding whether that information is wanted is a personal choice, and a good counselor will respect either answer.

Can people at high risk be screened for pancreatic cancer?

There is no screening test for the general population. US preventive guidelines advise against routine screening in people at average risk, because the available tests generate false alarms and unnecessary procedures without evidence that they save lives in that group. That position is unlikely to change until a reliable blood test emerges, and none has yet met that bar.

The picture is different for people whose risk is clearly elevated. International expert consensus, summarized in the National Cancer Institute’s genetics review, supports surveillance for people who carry a high-risk gene change plus a family history, or who meet the familial definition of two or more affected first-degree relatives. Surveillance typically uses one of two tools:

• MRI with MRCP (magnetic resonance cholangiopancreatography), which maps the pancreatic ducts without radiation.
• Endoscopic ultrasound (EUS), in which a thin scope carrying an ultrasound probe is passed through the stomach so the pancreas can be imaged from a few millimeters away.

Programs often alternate the two, usually once a year, starting around age 50 or ten years before the youngest affected relative’s diagnosis. For CDKN2A carriers and people with Peutz-Jeghers syndrome, expert groups suggest starting earlier, typically in the thirties or forties. Those ages are starting points for discussion, not rules, and the surveillance team sets the schedule.

What surveillance can and cannot do deserves plain statement. It finds precancerous cysts and small tumors more often than chance would, and observational studies suggest cancers found this way are more often operable. Whether that translates into fewer deaths is still being studied, and a normal scan does not eliminate risk. People in surveillance should still report new symptoms between visits rather than waiting for the next appointment.

What are the early signs of pancreatic cancer?

Early pancreatic cancer is often silent, which is the central problem of this disease. When symptoms do appear, they depend heavily on where in the gland the tumor sits. The pancreas has a head, body and tail, and about two-thirds of adenocarcinomas start in the head, right next to the bile duct.

That location explains the most recognizable sign. A tumor in the head can pinch the bile duct, so bile backs up into the blood. The result is jaundice: yellowing of the skin and the whites of the eyes, urine that turns dark like strong tea, stools that become pale or clay-colored, and skin itching that can be intense. The NHS and Mayo Clinic both list this cluster as a reason to seek prompt assessment.

Tumors in the body or tail cause fewer early signals, and the ones they do cause are frustratingly ordinary:

• A dull ache in the upper abdomen that bores through to the back, sometimes worse after eating or when lying flat.
• Unintentional weight loss and loss of appetite.
• Feeling full quickly, nausea, or indigestion that does not settle.
• Greasy, floating, foul-smelling stools, because fewer enzymes reach the gut.
• New fatigue that is out of proportion to activity.

Two less obvious clues can matter. New diabetes in someone over 50 without the usual risk factors, or existing diabetes that suddenly becomes hard to control, is discussed in its own section below. Unexplained blood clots in the legs or lungs can also occasionally be an early feature, since some tumors make the blood more prone to clotting.

None of these symptoms is specific. Each is far more likely to have a benign cause. The pattern that raises concern is persistence, combination, and appearance in someone over 60 or with a relevant family history.

Why is pancreatic cancer so hard to catch early?

Consider where the gland lives. The pancreas sits in the retroperitoneum, the space behind the abdominal lining, pressed against the spine and shielded in front by the stomach, liver and loops of bowel. A doctor cannot feel a small pancreatic tumor during an examination the way a breast or thyroid lump can be felt. A patient cannot see it, as one might notice a changing mole.

Then there is the matter of nerves. The pancreas has few pain receptors of its own. Early tumors grow without triggering the sharp, localizing pain that sends people to an emergency department. By the time pain arrives, it usually means the tumor has reached nerves running behind the gland, which is also when it has often reached nearby blood vessels.

The symptoms it does produce borrow from everyday complaints. Back ache, indigestion, tiredness and modest weight loss are among the most common reasons people visit primary care, and the vast majority of them have nothing to do with cancer. Testing everyone with those symptoms for a rare disease would do more harm than good, so clinicians rely on pattern recognition and persistence.

Biology adds a final layer. Pancreatic adenocarcinoma tends to spread to lymph nodes and the liver while the primary tumor is still small, sometimes under two centimeters. A cancer that has already traveled cannot be caught early by finding the original lump.

The consequence shows up in national statistics. According to the NCI’s SEER program, fewer than one in five cases are diagnosed while the cancer is still confined to the pancreas. Most are found after it has reached lymph nodes or distant organs. That single fact, more than any feature of the tumor itself, drives the disease’s outcomes.

Can new diabetes be a sign of pancreatic cancer?

Diabetes and pancreatic cancer are linked in both directions, and untangling them is one of the more interesting frontiers in early detection.

Long-standing type 2 diabetes is an established risk factor. Mayo Clinic lists it alongside smoking, obesity and chronic pancreatitis, and the mechanism is thought to involve years of raised insulin levels and low-grade inflammation acting on pancreatic cells. The increase in risk is modest, and the overwhelming majority of people with diabetes never develop pancreatic cancer.

The reverse relationship is the one worth understanding. A tumor growing in the pancreas can disrupt insulin production and interfere with how the body uses insulin, so diabetes sometimes appears as a consequence of the cancer, often one to three years before diagnosis. Studies summarized by cancer institutes suggest that a small proportion of people who develop diabetes after age 50 will be diagnosed with pancreatic cancer within three years. The proportion is small, roughly under one percent, but it is many times higher than in the general population of the same age.

Certain features make the pattern more suspicious. Diabetes that begins in a person who is losing weight rather than gaining it is unusual, because type 2 diabetes normally travels with weight gain. Diabetes that appears without a family history or obesity, or existing diabetes that abruptly becomes hard to control without any change in habits, also warrants a second look.

Researchers are developing risk scores that combine age, weight change and blood glucose trends to flag who might benefit from imaging. These are still being validated and are not yet standard practice. For now, the practical advice is simple: mention new or worsening diabetes to a doctor alongside any other symptoms, especially unexplained weight loss.

How is pancreatic cancer diagnosed? Blood tests, scans and biopsy

Diagnosis usually unfolds in stages, each one asking a narrower question than the last.

Blood tests come first. A liver panel can reveal the pattern of bile duct blockage that causes jaundice, with raised bilirubin and certain liver enzymes. A tumor marker called CA 19-9 is often measured, but it needs careful interpretation. It can be elevated by benign conditions such as gallstones or pancreatitis, it is normal in a meaningful minority of people with pancreatic cancer, and roughly one person in ten lacks the enzyme needed to produce it at all. Mayo Clinic describes it as useful for tracking known disease rather than for making the diagnosis.

Imaging does the heavy lifting. The standard first scan is a contrast-enhanced CT performed with a pancreatic protocol, meaning images are timed to catch the moment the gland and its surrounding arteries and veins fill with contrast dye. This shows the tumor, its relationship to major blood vessels, and any spread to the liver or lymph nodes. MRI with MRCP is an alternative that images the ducts particularly well and is often used when a CT result is unclear or a person cannot receive iodine contrast.

Endoscopic ultrasound is the closest look available. A flexible scope with an ultrasound tip is passed into the stomach and duodenum, placing the probe within millimeters of the pancreas. It detects small tumors that CT can miss and, crucially, allows a fine needle to be guided into the mass to collect cells or a tissue core for the pathologist. That biopsy confirms the diagnosis and, increasingly, provides material for tumor genetic testing.

Less often, doctors use ERCP, which combines endoscopy with X-ray imaging of the bile duct and can place a stent to relieve a blockage during the same procedure, or PET-CT to search for distant spread. Which tests are used, and in what order, depends on the initial findings and the local team’s judgment.

What does staging mean, and why does it drive every decision?

Once cancer is confirmed, the next question is how far it has traveled. Staging answers that, and in pancreatic cancer it determines almost everything about what can be offered.

Doctors use the TNM system: T describes the tumor’s size and whether it has grown into nearby structures, N describes lymph node involvement, and M records distant spread, most commonly to the liver, lungs or the lining of the abdomen. These are combined into stages 0 through IV, with stage 0 meaning abnormal cells confined to the duct lining and stage IV meaning distant spread.

Surgeons add a second, more practical language. They describe tumors as resectable, borderline resectable, locally advanced or metastatic. The distinction hinges on blood vessels. The pancreas is wrapped around the superior mesenteric artery and vein, the portal vein and the celiac artery, vessels that supply the liver and intestines. A tumor that has grown around these cannot always be removed safely. Roughly speaking, only a minority of people have disease that is resectable at diagnosis, which is the direct consequence of the late detection discussed earlier.

Staging is done mostly through the same CT or MRI used for diagnosis, sometimes supplemented by EUS, PET-CT or a small keyhole procedure called laparoscopy to check the abdominal lining for tiny deposits that scans cannot see.

Patients often ask why a stage cannot be given the day of the scan. The honest answer is that the picture is assembled from several sources, then reviewed by a multidisciplinary team of surgeons, oncologists, radiologists and pathologists who look at the images together. That meeting, not any single test, produces the plan.

When should you see a doctor about possible pancreatic cancer symptoms?

The single most useful rule is this: jaundice is never something to watch and wait on. If the whites of the eyes turn yellow, urine becomes dark and stools become pale, seek medical assessment the same day or within a day or two, as the NHS advises. Painless jaundice in an adult over 40 is one of the few symptom patterns that prompts doctors to move quickly toward pancreatic imaging.

Other red-flag combinations that warrant a prompt appointment rather than a routine one:

• Unexplained weight loss of more than a few pounds together with new upper abdominal or back pain.
• New diabetes after 50 in someone who is losing weight, or existing diabetes that suddenly becomes hard to control.
• Persistent indigestion, nausea or loss of appetite lasting more than a few weeks, especially in someone over 60.
• Greasy, pale, floating stools that continue for more than a couple of weeks.
• An unexplained blood clot in the leg or lung.
• Any of the above in a person with two or more close relatives who have had pancreatic cancer, or a known inherited gene change.

Seek emergency care for severe abdominal pain with vomiting, fever with jaundice, signs of internal bleeding such as black stools or vomiting blood, or sudden breathlessness with chest pain, which can signal a clot in the lung.

For most people, these symptoms will turn out to have another cause, and a doctor’s job includes ruling out common explanations first. Blood tests and an ultrasound are usually where the process starts. What matters is not to let vague symptoms drift for months. Writing down when each symptom began, what makes it better or worse, and any relevant family history turns a hard-to-describe complaint into something a clinician can act on.

What lifestyle factors actually change pancreatic cancer risk?

Genes cannot be changed. Several other risk factors can, and the evidence for them is stronger than for most cancer prevention advice.

Smoking sits at the top. Cleveland Clinic and Mayo Clinic identify it as the most important avoidable cause, with smokers carrying roughly double the risk of people who have never smoked. Cigarettes deliver carcinogens into the blood, and the pancreas, with its rich blood supply, is exposed to them constantly. The good news is that risk falls after quitting and approaches that of never-smokers over one to two decades. For people with hereditary pancreatitis or a high-risk gene, quitting smoking is the single most powerful step available, since tobacco and inherited susceptibility compound each other.

Body weight and metabolism come next. Obesity, particularly excess fat around the abdomen, is linked to higher risk, and the mechanism overlaps with type 2 diabetes: chronically raised insulin and inflammatory signaling that act on pancreatic tissue. Maintaining a healthy weight and staying physically active address both.

Chronic pancreatitis, long-term inflammation of the gland, raises risk substantially, and heavy alcohol use is its most common cause. Moderating alcohol protects the pancreas through that route.

What about diet? Evidence linking specific foods to pancreatic cancer is weaker and often inconsistent. Diets high in processed and red meat show modest associations in some studies; diets rich in fruit, vegetables and whole grains show modest protective associations in others. No supplement has been shown to prevent pancreatic cancer, and the NIH Office of Dietary Supplements cautions against assuming that antioxidant or vitamin supplements lower cancer risk in general.

The realistic message: not smoking, keeping weight and blood sugar in a healthy range, and drinking alcohol moderately or not at all are the changes with evidence behind them. They will not eliminate risk, and they matter most for people who already carry an inherited one.

What treatment questions do patients ask first after a diagnosis?

Treatment is beyond the scope of this article in detail, and the specifics always sit with the treating team. Still, a few questions come up almost immediately, and understanding the shape of the answers helps people prepare for the conversation.

Can it be removed? Surgery is the only approach with the potential to remove the cancer entirely, and it is possible only when imaging shows the tumor has not spread distantly or wrapped around critical vessels. For tumors in the head of the pancreas, the operation is called a pancreaticoduodenectomy, often known as the Whipple procedure. It removes the head of the pancreas, the duodenum, the gallbladder and part of the bile duct, then reconnects the digestive tract. Tumors in the body or tail are treated with a distal pancreatectomy, which often includes removal of the spleen. Both are major operations with a recovery measured in weeks, and Mayo Clinic notes they are generally performed at centers that do them regularly.

What if surgery is not possible? Chemotherapy, sometimes combined with radiation, is used to control the cancer, relieve symptoms and, in borderline cases, shrink a tumor enough to make surgery feasible. Increasingly, chemotherapy is given before surgery even for resectable tumors. If an inherited BRCA or related gene change is found, that result can influence which drug classes the oncology team considers, which is one reason germline testing is now offered to everyone diagnosed.

What about symptoms? Supportive care runs alongside every plan. A stent placed in a blocked bile duct relieves jaundice. Enzyme replacement helps digestion when the gland cannot supply enough. Pain management, nutritional support and psychological care are part of standard treatment, not afterthoughts.

Should I ask about clinical trials? Yes. Trials are how the evidence base for this disease improves, and eligibility is worth raising at the first oncology visit.

Frequently asked questions

Is pancreatic cancer hereditary?

Usually not. About one in ten cases is linked to an inherited gene change or a pattern of cases in close relatives, according to the National Cancer Institute and Cleveland Clinic. The other nine in ten occur in people with no inherited predisposition. Inheriting a gene change raises risk but does not mean cancer will develop; most carriers never get pancreatic cancer.

If my mother had pancreatic cancer, what is my risk?

Having one first-degree relative roughly doubles the risk compared with the general population, but because the baseline lifetime risk is low, the absolute risk stays small. Risk rises more sharply with two or more affected close relatives, a relative diagnosed before 50, or a family history of breast, ovarian, melanoma or colon cancer. Those situations are worth discussing with a genetic counselor.

Which genes cause hereditary pancreatic cancer?

The main ones are BRCA2, BRCA1, PALB2 and ATM, the melanoma gene CDKN2A, STK11 in Peutz-Jeghers syndrome, the Lynch syndrome genes MLH1, MSH2, MSH6 and PMS2, TP53 in Li-Fraumeni syndrome, and PRSS1 or SPINK1 in hereditary pancreatitis. Each carries a different level of risk, with CDKN2A and STK11 among the highest and Lynch syndrome among the more modest.

Should everyone with pancreatic cancer have genetic testing?

Yes, major US cancer guidelines now recommend offering germline genetic testing to everyone diagnosed with pancreatic cancer, regardless of age or family history. An inherited change is found in a meaningful minority, and the result can influence treatment options and tell relatives whether they should consider testing. A genetic counselor explains what each possible result would mean before the sample is taken.

Is there a screening test for pancreatic cancer?

Not for the general population. Routine screening of average-risk adults is advised against because current tests produce false alarms without proven benefit. People at high risk, meaning carriers of certain gene changes or those with two or more affected first-degree relatives, may be offered yearly surveillance with MRI/MRCP or endoscopic ultrasound, usually starting around age 50 or ten years before the youngest relative’s diagnosis.

What are the first signs of pancreatic cancer?

Early disease is often silent. When signs appear, the most recognizable is jaundice: yellow eyes and skin, dark urine, pale stools and itching, caused by a tumor blocking the bile duct. Other early clues include upper abdominal pain that spreads to the back, unexplained weight loss, loss of appetite, greasy stools, new diabetes after 50, and occasionally unexplained blood clots.

Why is pancreatic cancer usually found late?

The pancreas sits deep behind the stomach, cannot be felt on examination and has few pain nerves, so small tumors cause no symptoms. When symptoms arrive, they resemble indigestion, back strain or tiredness, which are common and usually benign. The cancer also tends to spread while the primary tumor is still small. Fewer than one in five cases are found while still confined to the gland.

Can a blood test detect pancreatic cancer?

No single blood test can diagnose it. Liver tests can show the pattern of bile duct blockage, and the marker CA 19-9 is often measured, but CA 19-9 can be raised by benign conditions and is normal in some people with cancer. It is mainly used to track known disease. Diagnosis relies on CT or MRI imaging and, usually, an endoscopic ultrasound-guided biopsy.

Does new diabetes mean I might have pancreatic cancer?

Almost always not. Only a small fraction of people who develop diabetes after 50 are diagnosed with pancreatic cancer within the following few years, though the rate is higher than in the general population. The features that prompt a closer look are diabetes appearing alongside weight loss rather than weight gain, no family history or obesity, or existing diabetes that suddenly becomes difficult to control.

How can I lower my risk of pancreatic cancer?

Not smoking is the most powerful step; smokers have roughly double the risk, and it falls after quitting. Keeping weight and blood sugar in a healthy range, staying active and limiting alcohol, which protects against chronic pancreatitis, also help. No supplement has been shown to prevent pancreatic cancer. These measures matter most for people who already carry an inherited risk.

References

• Pancreatic Cancer – NHS
• Pancreatic Cancer – Cleveland Clinic

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.