Pancreatic Cancer – Pancreatic Cancer: causes, Symptoms, Treatment, and Prevention

Pancreatic cancer: Malignancy of the pancreas. Pancreatic cancer has been called a “silent” disease because early pancreatic cancer usually does not cause symptoms. if the tumor blocks the common bile duct and bile cannot pass into the digestive system, the skin and whites of the eyes may become yellow (jaundiced), and the urine darker as a result of accumulated bile pigment called bilirubin.

Pancreatic Cancer Causes

The exact as to what damages DNA in the vast majority of cases of pancreatic cancer is not clear. In other words the exact pancreatic cancer causes are not clear. But it is known that a small percentage of people develop the disease as a result of a genetic predisposition. These people who have a close relative, such as a parent or sibling, with pancreatic cancer have a higher risk of developing pancreatic cancer themselves.

Age: is also a factor to be considered which increases the incidence of the disease. As age increases the probability of pancreatic cancer also increases. The incidence of Pancreatic Cancer is relatively low in individuals up to age 50, after which it increases significantly. The age group 65 – 79 has the highest incidence of Pancreatic Cancer.

Pancreatic Cancer Symptoms

In many cases, pancreatic cancer symptoms do not occur until the advanced stages. When pancreatic cancer symptoms do occur, they are often ignored because they are so vague and nonspecific. The first pancreatic cancer symptoms are usually pain in the abdomen and weight loss. Additional pancreatic cancer symptoms to look for include jaundice, fatigue, dizziness, weakness, diarrhea, chills, and muscle spasms.

Many of these pancreatic cancer symptoms are the result of a less serious ailment. However, only a doctor can accurately diagnosis whether or not your pancreatic cancer symptoms are the result of cancer.

Pancreatic cancer can cause pain and discomfort in your upper abdomen, which sometimes spreads to your back. at first, the pain may come and go, but as the cancer becomes larger, and more advanced, you may find that the pain is more constant, and lasts for longer.

The pain pancreatic cancer causes is often worse when you are lying down or eating. This type of pain tends to affect people whose tumour has formed in either the body or tail of the pancreas.

Pancreatic Cancer Treatment:

This cancer is difficult to diagnose because there are no symptoms in the early stages and because , when symptoms appear, they match other diseases. Depending on the stage and location of the cancer, surgery, chemotherapy and/or radiation therapy may be used. if the cancer has not spread beyond the pancreas, therapy can be successful, but, as stated earlier, it’s very unlikely to find pancreatic cancer in the early stages. In later stages, often the therapy concentrates on the comfort of the patient.

Obstruction of bile flow may be temporarily relieved by placement of a tube (stent) in the lower portion of the duct that drains bile from the liver and gallbladder. In most cases, however, the tumor eventually obstructs the duct above and below the stent. an alternative treatment method is the surgical creation of a channel that bypasses the obstruction. for example, an obstruction of the small intestine can be bypassed by a channel that connects the stomach with a portion of the small intestine that is beyond the obstruction.

Pancreatic cancer is the fourth leading cause of cancer deaths in the US, but receives extremely little federal funding to support research efforts. Dr. Randy Pausch, the Carnegie Mellon professor who has pancreatic cancer, has joined efforts with the Pancreatic Cancer Action Network to urge the federal government to provide critical funding to speed the cure for this horrible disease.

More : Pancreatic Cancer

In order to understand the causes of skin cancer, it is very important to analyze closely the disease cancer in itself. A normal alteration in the DNA of the cell results in abnormality within the cells. The malformed cells thereby start forming clusters and leads to tumor formation.

The controlled growth of the tumor is not that dangerous and does not lead to cancer. however, when the growth becomes uncontrolled and spreads to other tissues and cells cancer takes birth.

Skin cancer is one of the most common cancers in humans. This cancer affects the skin cells or the epithelial cells commonly. however, there are many variations of skin cancer and is normally caused by extreme exposure to sunlight.

When the skin is exposed to the harsh UV rays for a long duration of time, the harmful rays can easily initiate alteration of the cells. Invisible radiations coming from the sun is responsible for the destruction of the DNA and thereby results into skin cancer.

Cancer is an entirely cellular problem and spreads through the blood from tissues to tissues. Thus, genetic constitution can primarily be held responsible for the problem when a strict history of cancer runs down the family. normally, you will not try to consider certain eruptions on your skin as important and would just ignore them.

However, small eruptions on the skin or some kind of mole formation or even a bruise can give rise to cancer overtime.However, there is not much of a chance of the moles or eruptions to take the shape of cancer. Nevertheless, taking precautions will help you keep the chances at a distance and thereby help you stay secured.

Continuous exposure of the skin to any kind of synthetic harmful radiations can also lead to skin cancer by simple alteration of the cells.Skin cancer though can be treated if diagnosed at an early stage, but once the cancer travels locations and reaches other parts of the body it becomes disastrous.

Normally skin rashes, incurable eruptions or some kind of discoloration and rough patches signals the alteration of cells. when these notable signs do not fade away within a few days, consultation of the doctor is a must.

As we know, this killer disease has no symptoms and only diagnose when it's too late. what could be done to avoid this or what to do to find out if you are not getting this? does it start by having stomach aches or similar to indigestion or colon cancer symptoms?

It isn't just pancreatic cancer that has no symptoms until it is advanced . . that is true of all most every single cancer . . and there are over 200 different types and just as many rare subtypes. Cancer is a progressive disease which means it start out microscopic and grows indefinitely. Tiny. big. Bigger. Large. Enormous. When it is tiny no one can find it in a body . . it is too small to be noticed . . cancer is not something foreign . . it is your own DNA that has mutated . . so the body considers a cancer just another part of the body. Small cancer can co-incide quite nicely inside the body . . it isn't until the cancer begins to invade surrounding tissue at the Bigger or Large stage that it may be noticed.

So . . no cancer does not 'start' by having stomach aches or similar indigestion . . by the time you feel any of that . . the cancer is advanced. you literally . . feel nothing . .when cancer first starts. and the rest will depend on how aggressive the type of tumor you have .. some grow very fast and can take days or weeks . . but some grow very slowly and can take years. If you have a fast growing tumor than the cancer may be noticable sooner but it is hard to get into treatment quick enough to stop it or slow it down . . if the tumors are slower growing than you may have more 'time' to make decisions about treatment. This fact is often confusing to people . . they do not realize that many cancers are aggressive and fast growing and that time is critical (you don't have time to 'experiment' with treatments to see what will work – you might only get one chance to control the disease). and, than there are other types of slower growing cancers in which people do have more time to try out treatments. Treatment for cancer can be complicated by many factors . . which is why it is difficult to treat and why there is no 'cure' for all cancers at this moment. There is treatment though for all cancer types and that treatment could lead to an individual remission or 'cure'. . no guarantee though.

A well known survivor of pancreatic cancer is Steven Jobs, the founder of the Apple Computer who was diagnosed in 2004 and is doing very well.

My aunt unfortunately has this. she started having problems with her stomach, like bad indigestion and pain in the stomach. she had tests, barium meal which showed up nothing. Then a year ago, she developed jaundice, which after that they discovered it was pancreatic cancer. she is now really thin, but getting chemotherapy, and has gained a few pounds. she has been told there is no cure and all they can do is try and shrink the tumour.

the classical sign of pancreatic ca is migratory thrombophlebitis.. although rarely seen..
unfortunately as u have correctly put … diagnosis is usually late…
anorexia is one of the earliest signs.
sometimes patient may present with features of obstructive jaundice..
they may even present with features of acute pancreatitis….
rarely.. an asymptomatic lump in the upper abdomen

Posted on: Thursday, 19 August 2010, 15:12 CDT

LEIDEN, The Netherlands, Aug. 19 /PRNewswire-USNewswire/ — nearly two decades after they identified the specific genetic flaw that causes a common type of muscular dystrophy, scientists believe they have figured out how that flaw brings about the disease. The finding by an international team of researchers settles a longstanding question about the roots of facioscapulohumeral muscular dystrophy or FSHD. The work is published in the August 20 issue of Science.

Unraveling how the genetic defect causes FSHD has been especially challenging for scientists. Unlike with many genetic diseases, their identification of the mutation that is the basis of FSHD did not quickly lead to a deeper understanding of how the disease actually comes about. The lack of clarity has posed a significant barrier to researchers hoping to turn the knowledge of the genetic flaw into significant progress for patients.

The latest findings clarify the picture significantly. Scientists have discovered that several deleted versions of a gene trigger the remaining copies of that gene to be much more active than usual. That’s because the DNA that codes for the gene is not as tightly coiled or elusive to the body’s molecular machinery as usual when some copies are missing, and so the gene – known as DUX4, which makes a protein harmful to muscle cells – is more active than it should be.

The work offers up a new therapeutic target to scientists aiming to develop a treatment or cure for the disease.

The research was led by genetics researchers at the University of Leiden in the Netherlands, working together with scientists at the University of Rochester Medical Center, the Fred Hutchinson Cancer Research Center in Seattle, and other investigators. The research was funded by several organizations, including the Fields Center for FSHD and Neuromuscular Research, based at Rochester and at Leiden (urmc.rochester.edu/fields-center/).

“It is amazing to realize that a long and frustrating journey of almost two decades now culminates in the identification of a single small DNA variant that differs between patients and people without the disease. we finally have a target that we can go after,” said Silvere van der Maarel, Ph.D., professor of medical epigenetics at Leiden and the corresponding author of the paper. Working closely with van der Maarel was the first author of the paper, Richard Lemmers of Leiden.

FSHD is an inherited disorder that usually makes its presence felt in the teen years. First symptoms usually are weakness in the upper body; a person might have trouble lifting the arms, for example. Weakness of the facial muscles is also common, for instance, difficulty smiling or whistling, closing the eyelids completely, or even sipping through a straw. Later on, the condition affects the lower body – the muscles of the feet, legs, and hips. Patients usually live a normal life span, but around 20 percent of patients end up using a wheelchair.

Doctors estimate that about 1 in 20,000 people worldwide, including about 15,000 Americans, have FSHD, which is the third most common type of muscular dystrophy.

It was 18 years ago, in 1992, that a team from the same laboratory in Leiden identified the genetic defect at the root of the disease. The scientists found that in healthy people there are 11 or more copies of a certain DNA sequence dubbed D4Z4 near the tip on chromosome 4. nearly all FSHD patients have too-few copies – 10 or fewer of the D4Z4 repeat.

Since then the team has worked to understand how that defect translates into the disease. Meanwhile, the University of Rochester built on its history as a powerhouse of leading muscular dystrophy research and treatment worldwide; Rochester’s studies of FSHD were wide ranging and included both clinical and translational research. The University created the National Registry of Myotonic and FSHD Patients and Family Members, which includes information on hundreds of patients who volunteer for research. The FSHD team at Rochester has also established the world’s largest repository of biological samples, such as blood, skin and muscle specimens, from individuals with FSHD, a resource that has proven to be crucial in advancing knowledge of the disease.

The groups began collaborating, and their interactions accelerated three years ago, thanks to a gift from new York developer and philanthropist Richard T. Fields.

Now, the team has worked out a crucial step in how the defect leads to disease. The finding draws on the genetics expertise at Leiden, the clinical research experience with FSHD patients at Rochester, and epigenetics knowledge in Seattle.

“In most patients with FSHD, a piece of DNA is missing,” said Rabi Tawil, M.D., an author of the Science paper and the neurologist who leads Rochester’s FSHD team and the Fields Center. “For a long time it was thought that this was simply junk DNA that was missing, and that the missing material must affect the function of a nearby gene on chromosome 4.”

It turns out that each of the D4Z4 repeats contains a copy of a gene known as DUX4, but scientists have not known until recently that DUX4 is a functional gene. When a critical number of copies are missing, the structure of the tip of chromosome 4 becomes more open, making the DUX4 gene more accessible for transcription.

When crucial pieces of DNA that introduce and conclude the repetitive string are composed of certain sequences, the ingredients for molecular mischief are in place, making the remaining copies of DUX4 much more stable than they normally are.

“This provides a new and unifying model for FSHD because it will focus future research on determining whether the DUX4 protein causes FSHD, as indicated by our consortium’s genetic analysis,” said Stephen Tapscott, M.D., Ph.D., a member of the Human Biology Division at the Fred Hutchinson Cancer Research Center and one of the authors of the Science paper. The team is currently studying how active DUX4 is in patients in FSHD compared to people who do not have the disease.

In previous research, other investigators had identified a nearby gene known as FRG1 as central to the development of FSHD. The teams in Leiden, Rochester and Seattle teams were unable to reproduce those results and instead point to DUX4.

Currently there is no treatment for FSHD that slows the disease or addresses the underlying problem. Typically patients are treated with medications to alleviate their pain, and are given supportive treatment, such as braces and other aids for their arms and legs to help them deal with weakness. there have been a few studies investigating possible treatments – drugs on the market for other conditions – but those haven’t turned up anything that works in FSHD patients.

“Interventions tried thus far haven’t been based on the science underlying the disease,” said Tawil, a professor in the Department of Neurology. “That’s why this is such an exciting step. instead of guesswork, we now have one unified hypothesis, and one target. This marks the first time we can work solidly from basic science to seek a treatment for FSHD.”

The team plans to screen existing compounds in a search for one that inhibits DUX4. The group also plans to develop rigorous techniques for measuring the effects of test medications on FSHD patients, and to continue to try to understand how DUX4 damages muscles. Early research indicates that DUX4 hinders the body’s ability to regenerate muscle and makes muscles more susceptible to oxidative stress.

In addition to van der Maarel, Lemmers, Tapscott and Tawil, the authors of the Science paper include:

• From Leiden University Medical Center: Patrick van der Vliet, Rinse Klooster, Johannes Dauwerse, Kirsten Straasheijm, Gert Jan van Ommen, and Rune Frants.
• From the Fred Hutchinson Cancer Research Center in Seattle: Lauren Snider.
• From Nice University in France: Sabrina Sacconi.
• From the BioDonostia Health Research Institute in San Sebastian, Spain, as well as the Centro Investigacion Biomedica en Red para Enfermedades Neurodegenerativas: Pilar Camano.
• From Radboud University Nijmegen Medical Center the Netherlands: George Padberg.
• From the University of Washington: Daniel Miller.

Funding to conduct the work came from several organization, including the Fields Center, the Netherlands Organization for Scientific Research, the Netherlands Genomic Initiative NOW, the U.S. National Institutes of Health, the Muscular Dystrophy Assn., the Shaw Family Foundation, a Marjorie Bronfman Fellowship grant from the FSH Society, the Pacific Northwest Friends of FSH Research, the Centro Investigacion Biomedica en Red para Enfermedades Neurodegenerativas, the Basque Government, and the Instituto Carlos III.

One of the nation’s top academic medical centers, the University of Rochester Medical Center (urmc.rochester.edu) forms the centerpiece of the University’s health research, teaching, patient care, and community outreach missions. The Medical Center receives more than $240 million in external research funding per year and the University of Rochester School of Medicine and Dentistry ranks in the top one-quarter of U.S. medical centers in federal research funding. The University’s health care delivery network is anchored by Strong Memorial Hospital – a 754-bed, University-owned teaching hospital. As upstate new York’s premier health care delivery network, patients benefit from the Medical Center’s robust teaching and biomedical research programs.

SOURCE University of Rochester Medical Center

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