Steven “Steve” Paul Jobs was born February 24, 1955, in San Francisco, California, and was adopted by Paul and Clara Jobs. He grew up with one sister, Patty. Currently, Jobs is an American business magnate and inventor. He is the co-founder and chief executive officer of Apple Inc. Jobs also previously served as chief executive of Pixar Animation Studios; he became a member of the board of directors of The Walt Disney Company in 2006, following the acquisition of Pixar by Disney.
"We don’t get a chance to do that many things, and every one should be really excellent. Because this is our life.
Life is brief, and then you die, you know?
And we’ve all chosen to do this with our lives. So it better be damn good. It better be worth it."

Steve Jobs and Cancer
In mid-2004, Jobs announced to his employees that he had been diagnosed with a cancerous tumor in his pancreas. The prognosis for pancreatic cancer is usually very grim; Jobs, however, stated that he had a rare, far less aggressive type known as islet cell neuroendocrine tumor. An islet cell neuroendocrine tumor is a mass of abnormal cells that forms in the endocrine (hormone-producing) tissues of the pancreas. Islet cell tumors may be benign (not cancer) or malignant (cancer).

Islet cells make and release hormones into the blood. Islet cell tumors may be functional (the hormones that are released cause symptoms) or nonfunctional (the hormones that are released do not cause symptoms) tumors. Because some tumors do not cause symptoms, a person might not know they have the cancer.
A non-functioning islet cell tumor may grow for a long time without causing symptoms. It may grow large or spread to other parts of the body before it causes symptoms, such as:
  • Diarrhea.
  • Indigestion.
  • A lump in the abdomen.
  • Pain in the abdomen or back.
  • Yellowing of the skin and whites of the eyes.

The symptoms of a functioning islet tumor depend on the type of hormone being made:
A tumor that makes pancreatic peptides (PPoma) often has no symptoms.
Too much gastrin may cause:
  • Stomach ulcers that keep coming back.
  • Pain in the abdomen, which may spread to the back. The pain may come and go and it may go away after taking an antacid.
  • The flow of stomach contents back into the esophagus (gastroesophageal reflux).
  • Diarrhea.
Too much insulin may cause:
  • Low blood sugar. This can cause blurred vision, headache, and feeling lightheaded, tired, weak, shaky, nervous, irritable, sweaty, confused, or hungry.
  • Feeling a fast heartbeat.
Too much glucagon may cause:
  • Skin rash on the face, stomach, or legs.
  • High blood sugar. This can cause headaches, frequent urination, dry skin and mouth, or feeling hungry, thirsty, tired, or weak.
  • Blood clots in the lung. This can cause shortness of breath, cough or pain in the chest. Blood clots in the arm or leg can cause pain, swelling, warmth, or redness of the arm or leg.
  • Diarrhea.
  • Weight loss for no known reason.
  • Sore tongue or sores at the corners of the mouth.
Too much vasoactive intestinal peptide (VIP) may cause:
  • Very large amounts of watery diarrhea.
  • Dehydration. This can cause feeling thirsty, making less urine, dry skin and mouth, feeling tired, headache, or dizziness.
  • Low potassium level in the blood. This can cause muscle weakness, aching, or cramps, numbness and tingling, frequent urination, and feeling a fast heartbeat, confused, or thirsty.
  • Cramps or pain in the abdomen.
  • Weight loss for no known reason.
Too much somatostatin may cause:
  • High blood sugar. This can cause headaches, frequent urination, dry skin and mouth, or feeling hungry, thirsty, tired, or weak.
  • Diarrhea.
  • Steatorrhea (very foul-smelling stool that floats).
  • Gallstones.
  • Yellowing of the skin and whites of the eyes.
  • Weight loss for no known reason.
Many of the risk factors that have been identified for pancreatic cancer (ductal adenocarcinomas of the pancreas) are not risk factors for islet cell tumors/pancreatic neuroendocrine neoplasms. For example, cigarette smoking doubles the risk of pancreatic cancer, but it does not appear to be a factor in the development of islet cell tumors/pancreatic endocrine neoplasms.

Several genetic (familial) syndromes predispose to pancreatic neuroendocrine neoplasms. These are important to recognize for three reasons. First, because these genetic syndromes are caused by genetic changes that can be inherited, other family members may be at risk. Second, these genetic syndromes predispose to (increase the risk of) more than one tumor type. Individuals with one of these syndromes therefore have an increased risk of developing pancreatic and extra-pancreatic neuroendocrine tumors. Finally, these syndromes are important because they provide insight into the biology of pancreatic neuroendocrine neoplasms. Because the genes that cause these genetic syndromes are known, scientists can understand the cellular pathways which lead to the development of pancreatic neuroendocrine neoplasms. The hope is that a better understanding of these pathways will lead to better treatments.

Multiple Endocrine Neoplasia Type 1, abbreviated MEN-1, is a familial syndrome caused by inherited mutations in the MEN1 gene on chromosome 11. The MEN-1 gene codes for the menin protein, and patients with an inherited mutation in the MEN1 are predisposed to develop tumors of the pituitary (the small "master" gland at the base of the brain), the parathyroids (four small glands in neck which help control blood calcium levels), and the pancreas.

von Hippel-Lindau Syndrome, abbreviated VHL, is a familial syndrome caused by inherited mutations in the VHL gene on chromosome3. Patients with von Hippel-Lindau are predisposed to developing tumors in a number of organs including the the brain (hemagioblastoma), the eye (hemagioblastoma), the kidney (renal cell carcinoma), and the adrenals (pheochromocytoma). Pancreatic disease may be the first manifestation of VHL, and most patients with VHL eventually develop a pancreatic tumor. The pancreatic tumors in patients with VHL are interesting because they can have unique appearances. Some have a "clear" appearance under the microscope, and others are mixed tumors.

Tuberous Sclerosis Complex (TSC) is a third genetic syndrome which predisposes to pancreatic neuroendocrine neoplasms. Tuberous sclerosis complex is caused by inherited mutations in one of two genes- TSC1 or TSC2. The TSC1 gene is on chromosome 9 and it codes for the protein hamartin. The TSC2 gene is on chromosome 16 and it codes for the protein tuberin. Patients with tuberous sclerosis complex can suffer from developmental delay, mental retardation and even autism, and they are predisposed to develop a number of different tumors. They are predisposed to develop three different brain lesions- "tubers," subependymal giant cell astrocytomas and subependymal nodules. In fact, the name tuberous sclerosis comes from the brain lesions that these patients develop- Tuber in Latin means swelling and skleros in Greek means hard. They also can develop distinctive lesions of the skin (hypomelanotic macules and facial angiofibromas), kidney (angiomyolipomas), lungs (lymphangioleiomatosis), heart (rhabdomyomas), and eye tumors ( hamartomas). Most of these are entirely benign growths, but they can cause symptoms depending on their location. Although less common than the other manifestations of tuberous sclerosis, several patients with tuberous sclerosis complex have been reported who developed pancreatic neuroendocrine neoplasms.

Neurofibromatosis type 1, also known as von Recklinghausen disease, is a familial syndrome caused by inherited mutations in the NF1 gene on chromosome 17. The NF1 gene codes for the protein neurofibromin. Patients with neurofibromatosis develop dark patches of skin (café-au-lait spots), and benign (non-cancerous) and malignant (cancerous) tumors of the nervous system. The benign nerous system tumors include neurofibromas, and the malignant the "malignant peripheral nerve sheath tumor." They can also develop distinctive eye lesions called Lisch nodules, and a small percentage develop somatostatinomas of the pancreas/duodenum.
Reports often indicate that there are about two to three thousand cases diagnosed in the U.S. each year - although autopsy indicates that there may be a higher incidence of these islet cell tumors than are diagnosed.
Age-Adjusted SEER Incidence Rates, 2004-2008
Age at Diagnosis
All Races
Both Sexes
All ages
Under 65
65 and over
All ages (IARC world std)
There are quite a few tests that can be used to test for an islet cell tumor, including...
Treatment will depend on the type of tumor and whether the tumor is noncancerous (benign) or cancerous (malignant). Malignant tumors can spread to other organs, grow aggressively, and may not be treatable. Tumors are usually removed with surgery, if possible.
If malignant cancer cells spread (metastasize) to the liver, a portion of the liver may also be removed, if possible. If the cancer is widespread, various forms of chemotherapy may be used to try and shrink the tumors.
If the abnormal production of hormones is causing problems, you may receive medications to counteract their effects. For example, with gastrinomas, the overproduction of gastrin leads to too much acid in the stomach. Medications that block acid release can reduce symptoms.
Surgical removal of non-functioning islet cell tumors is often curative. Patients are evaluated for surgery and all attempts are made to try and completely remove the tumor. The type of surgery depends on the location of the tumor. These tumors typically tend to be large and therefore enucleation of the tumor is usually not possible.
For tumors located in the head of the pancreas, a Whipple operation is usually indicated whereas for tumors in the tail of the pancreas a distal pancreatectomy is required. For very small tumors, organ preservation procedures such as a pancreatic head resection or a spleen preserving distal pancreatectomy may be possible options.
The approach to remove these tumors preferentially is by laparoscopic surgery. An open procedure is usually offered to the patient if there is presence of metastases, for very large tumors (greater than 10 centimeters), if there is invasion of the major blood vessels around the pancreas by the tumor, and by patient preference. For all other patients, the laparoscopic procedure is offered as the treatment of choice.
Functional islet cell tumors often present in a dramatic fashion due to secretion of excessive amounts of hormones such as insulin, gastrin, or glucagon. These tumors tend to present at a very early stage when the tumor is tiny and is often not readily detectable.
Localization of these tumors is an important consideration since the tumors may be very small, only a few millimeters in size, when the patient presents with major symptoms related to over secretion of the hormones.
The different types of functioning neuroendocrine tumors require special consideration for surgery. Surgery is tailored to the type of the tumor. For further details click on the following links:
Any Hope?
Islet cell tumors can often be cured. The prognosis (chance of recovery) and treatment options depend on the following:
  • The type of cancer cell.
  • Where the tumor is found in the pancreas.
  • Whether the tumor has spread to more than one place in the pancreas or to other parts of the body.
  • Whether the patient has MEN1 syndrome.
  • The patient's age and general health.
  • Whether the cancer has just been diagnosed or has recurred (come back).

You may be cured if the tumors are surgically removed before they have spread to other organs. If tumors are cancerous, chemotherapy may be used, but it usually cannot cure patients. However, life-threatening problems (such as very low blood sugar) can occur due to excess hormone production, or if the cancer spreads throughout the body.


Back to You, Steve
After initially resisting the idea of conventional medical intervention and embarking on a special diet to thwart the disease, Jobs underwent a pancreaticoduodenectomy (or "Whipple procedure") in July 2004 that appeared to successfully remove the tumor. Jobs apparently did not require nor receive chemotherapy or radiation therapy.
"Reports of my death are greatly exaggerated."
In April 2009, Jobs underwent a liver transplant at Methodist University Hospital Transplant Institute in Memphis, Tennessee. Jobs' prognosis was "excellent."

As for history, Jobs had no clear indicators as to why he got cancer in the first place. Because the type of cancer is so rare, it is possible that the causes for this specific type aren't know.

Unfortunately, Jobs has not invested in any Cancer societies. Neither has his family, nor the company Apple.

Thanks To....

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