Pancreatic Cancer


Pancreatic cancer

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Pancreatic cancer

Classification and external resources

ICD-10

C25

ICD-9

157.0-157.9

OMIM

260350

DiseasesDB

9510

MedlinePlus

000236

eMedicine

med/1712

MeSH

D010190

Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas. The most common type of pancreatic cancer, accounting for 95% of these tumors, is adenocarcinoma (tumors exhibiting glandular architecture on light microscopy) arising within the exocrine component of the pancreas. A minority arise from islet cells, and are classified as neuroendocrine tumors. The signs and symptoms that eventually lead to the diagnosis depend on the location, the size, and the tissue type of the tumor, and may include abdominal pain, lower back pain, and jaundice (if the tumor compresses the bile duct).

Pancreatic cancer is the fourth most common cause of cancer-related deaths in the United States[1] and the eighth worldwide.[2] Pancreatic cancer has an extremely poor prognosis: for all stages combined, the 1- and 5-year relative survival rates are 25% and 6%, respectively;[3] for local disease the 5-year survival is approximately 20%[3][4] while the median survival for locally advanced and for metastatic disease, which collectively represent over 80% of individuals,[4] is about 10 and 6 months respectively.[5] Individuals vary, however – some are only diagnosed when they are terminally ill already and therefore only have a few days or weeks. Others have slower progression and may live a couple of years even if surgery is not possible.

Contents
[hide] 1 Signs and symptoms
2 Risk factors 2.1 Alcohol

3 Diagnosis
4 Pathophysiology 4.1 Exocrine pancreas cancers
4.2 Pancreatic cystic neoplasms
4.3 Pancreatic neuroendocrine tumors

5 Prevention 5.1 Screening

6 Treatment 6.1 Exocrine pancreas cancer

6.2 Pancreatic neuroendocrine tumors

7 Prognosis
8 See also
9 References
10 External links

Signs and symptoms [edit]

Early pancreatic cancer often does not cause symptoms,[6] and the later symptoms are usually nonspecific and varied.[6] Therefore, pancreatic cancer is often not diagnosed until it is advanced.[6] Common symptoms include:
Pain in the upper abdomen that typically radiates to the back[6] (seen in carcinoma of the body or tail of the pancreas)
Heartburn – acid stomach
Poor appetite or nausea and vomiting[6]
Diarrhea, loose stools.
Significant weight loss (cachexia)
Painless jaundice (yellow tint to whites of eyes (sclera) or yellowish skin, possibly in combination with darkened urine)[6] when a cancer of the head of the pancreas (75% of cases)[7] obstructs the common bile duct as it runs through the pancreas. This may also cause pale-colored stool and steatorrhea. The jaundice may be associated with itching as the salt from excess bile can cause skin irritation.
Trousseau sign, in which blood clots form spontaneously in the portal blood vessels, the deep veins of the extremities, or the superficial veins anywhere on the body, may be associated with pancreatic cancer.
Pulmonary embolisms due to pancreatic cancers producing blood clotting chemicals.
Diabetes mellitus, or elevated blood sugar levels. Many patients with pancreatic cancer develop diabetes months to even years before they are diagnosed with pancreatic cancer, suggesting new onset diabetes in an elderly individual may be an early warning sign of pancreatic cancer.[8]
Clinical depression has been reported in association with pancreatic cancer, sometimes presenting before the cancer is diagnosed. However, the mechanism for this association is not known.[9]
Symptoms of pancreatic cancer metastasis. Typically, pancreatic cancer first metastasizes to regional lymph nodes, and later to the liver or to the peritoneal cavity and, rarely, to the lungs;[10] it rarely metastasizes to bone or brain.[11]

Risk factors [edit]

Risk factors for pancreatic cancer may include:[6][12]
Family history: 5–10% of pancreatic cancer patients have a family history of pancreatic cancer. The genes have not been identified. Pancreatic cancer has been associated with the following syndromes: autosomal recessive ataxia-telangiectasia and autosomal dominantly inherited mutations in the BRCA2 gene and PALB2 gene, Peutz-Jeghers syndrome due to mutations in the STK11 tumor suppressor gene, hereditary non-polyposis colon cancer (Lynch syndrome), familial adenomatous polyposis, and the familial atypical multiple mole melanoma-pancreatic cancer syndrome (FAMMM-PC) due to mutations in the CDKN2A tumor suppressor gene.[13][14] There may also be a history of familial pancreatitis.[13]
Age. The risk of developing pancreatic cancer increases with age. Most cases occur after age 60, while cases before age 40 are uncommon.
Smoking. Cigarette smoking has a risk ratio of 1.74 with regard to pancreatic cancer; a decade of nonsmoking after heavy smoking is associated with a risk ratio of 1.2.[15]
Diets low in vegetables and fruits.[16]
Diets high in red meat. Processed meat consumption is positively associated with pancreatic cancer risk, and red meat consumption was associated with an increased risk of pancreatic cancer in men.[17]
Diets high in sugar-sweetened drinks (soft drinks).[18] In particular, the common soft drink sweetener fructose has been linked to growth of pancreatic cancer cells.[19]
Obesity[20]
Diabetes mellitus is both risk factor for pancreatic cancer, and, as noted earlier, new onset diabetes can be an early sign of the disease.[clarification needed how much]
Chronic pancreatitis has been linked, but is not known to be causal. The risk of pancreatic cancer in individuals with familial pancreatitis is particularly high.
Helicobacter pylori infection[21][22]
Gingivitis or periodontal disease[23]
Partial gastrectomy[24][25]

Alcohol [edit]

It is controversial whether alcohol consumption is a risk factor for pancreatic cancer. Overall, the association is consistently weak and the majority of studies have found no association.[26][27][28][29] Although drinking alcohol excessively is a major cause of chronic pancreatitis, which in turn predisposes to pancreatic cancer, chronic pancreatitis associated with alcohol consumption is less frequently a precursor for pancreatic cancer than other types of chronic pancreatitis.[30]

Some studies suggest a relationship,[31] the risk increasing with increasing amount of alcohol intake.[32][33] The risk is greatest in heavy drinkers,[34][35][36] mostly on the order of four or more drinks per day.[37] There appears to be no increased risk for people consuming up to 30g of alcohol a day,[29][38][39] which is approximately 2 alcoholic beverages/day,[39] so most people who take alcohol do so at a level that “is probably not a risk factor for pancreatic cancer”.[36] A pooled analysis concluded, “Our findings are consistent with a modest increase in risk of pancreatic cancer with consumption of 30 or more grams of alcohol per day”.[39]

Several studies caution that their findings could be due to confounding factors.[35][40] Even if a link exists, it “could be due to the contents of some alcoholic beverages”[41] other than the alcohol itself. One Dutch study even found that drinkers of white wine had lower risk.[42]

Diagnosis [edit]

Axial CT image with i.v. contrast. Macrocystic adenocarcinoma of the pancreatic head.
Most patients with pancreatic cancer experience pain, weight loss, or jaundice.[43]

Pain is present in 80% to 85% of patients with locally advanced or advanced metastatic disease. The pain is usually felt in the upper abdomen as a dull ache that radiates straight through to the back. It may be intermittent and made worse by eating. Weight loss can be profound; it can be associated with anorexia, early satiety, diarrhoea, or steatorrhea. Jaundice is often accompanied by pruritus and dark urine. Painful jaundice is present in approximately one-half of patients with locally unresectable disease, while painless jaundice is present in approximately one-half of patients with a potentially resectable and curable lesion.

The initial presentation varies according to location of the cancer. Malignancies in the pancreatic body or tail usually present with pain and weight loss, while those in the head of the gland typically present with steatorrhea, weight loss, and jaundice. The recent onset of atypical diabetes mellitus, a history of recent but unexplained thrombophlebitis (Trousseau sign), or a previous attack of pancreatitis are sometimes noted. Courvoisier sign defines the presence of jaundice and a painlessly distended gallbladder as strongly indicative of pancreatic cancer, and may be used to distinguish pancreatic cancer from gallstones. Tiredness, irritability and difficulty eating because of pain also exist. Pancreatic cancer is often discovered during the course of the evaluation of aforementioned symptoms.

Liver function tests can show a combination of results indicative of bile duct obstruction (raised conjugated bilirubin, γ-glutamyl transpeptidase and alkaline phosphatase levels). CA19-9 (carbohydrate antigen 19.9) is a tumor marker that is frequently elevated in pancreatic cancer. However, it lacks sensitivity and specificity. When a cutoff above 37 U/mL is used, this marker has a sensitivity of 77% and specificity of 87% in discerning benign from malignant disease. CA 19-9 might be normal early in the course, and could be elevated because of benign causes of biliary obstruction.[44] Imaging studies, such as computed tomography (CT scan) and endoscopic ultrasound (EUS) can be used to identify the location and form of the cancer. The definitive diagnosis is made by an endoscopic needle biopsy or surgical excision of the radiologically suspicious tissue. Endoscopic ultrasound is often used to visually guide the needle biopsy procedure.[45] Nonetheless, pancreatic cancer is usually staged using a CT scan. In fact, a histologic diagnosis is not usually required for resection of the tumor, rather histologic analysis helps determine which chemotherapeutic regimen to start.[46]

Pathophysiology [edit]

Micrograph of pancreatic ductal adenocarcinoma (the most common type of pancreatic cancer). H&E stain.
The development of pancreatic cancer may involve the over-expression of oncogenes, inactivation of tumor suppressor genes or the deregulation of various signaling proteins.[47] Mutations leading to carcinoma may be accelerated by genetic or environmental factors and other risk factors already described. Specific mutations vary among and even within the cyto-histologic categories discussed below.

Exocrine pancreas cancers [edit]

Micrographs of normal pancreas, pancreatic intraepithelial neoplasia (precursors to pancreatic carcinoma) and pancreatic carcinoma. H&E stain.
The most common form of pancreatic cancer (ductal adenocarcinoma) is typically characterized by moderately to poorly differentiated glandular structures on microscopic examination. Pancreatic cancer has an immunohistochemical profile that is similar to hepatobiliary cancers (e.g. cholangiocarcinoma) and some stomach cancers; thus, it may not always be possible to be certain that a tumour found in the pancreas arose from it.

Cross section of a human liver, taken at autopsy examination, showing multiple large pale tumor deposits. The tumor is an adenocarcinoma derived from a primary lesion in the body of the pancreas.
Pancreatic carcinoma is thought to arise from progressive tissue changes. Three types of precancerous lesion are recognised: pancreatic intraepithelial neoplasia – a microscopic lesions of the pancreas, intraductal papillary mucinous neoplasms and mucinous cystic neoplasms both of which are macroscopic lesions.[48] The cellular origin of these lesions is debated.

The second most common type of exocrine pancreas cancer is mucinous.Empty citation‎ (help) [discuss] The prognosis is slightly better. Empty citation‎ (help) [discuss]

Other exocrine cancers include adenosquamous carcinomas, signet ring cell carcinomas, hepatoid carcinomas, colloid carcinomas, undifferentiated carcinomas, and undifferentiated carcinomas with osteoclast-like giant cells.[49]

Pancreatic cystic neoplasms [edit]

Pancreatic cystic neoplasms are a broad group of pancreas tumors that have varying malignant potential.[discuss]

Pancreatic neuroendocrine tumors [edit]

Main article: Neuroendocrine tumor

Endocrine pancreatic tumors have been variously called islet cell tumors, pancreas endocrine tumors (PETs), and pancreatic neuroendocrine tumors (PNETs).[50] The annual clinically recognized incidence is low, about five per one million person-years.[49] However, autopsy studies incidentally identify PETs in up to 1.5%[5] most of which would remain inert and asymptomatic.[5]

The majority of PNETs are usually categorized as benign[51][52][53] but the definition of malignancy in pancreas endocrine tumors has been ambiguous. A small subset of endocrine pancreatic tumors are incontrovertible pancreatic endocrine cancers, that make up about 1% of pancreas cancers.[49][50] Low- to intermediate-grade neuroendocrine carcinomas of the pancreas may be called islet cell tumors. Some sources have also termed these pancreatic carcinoid,[50] a practice that has sometimes been strongly condemned.[citation needed] Definitional migration has caused some complexity of PNET classification,[50] which has adversely affected what is known about the epidemiology and natural history of these tumors.[50] It is probable that some of these tumors have been included in ICD-O-3 histology classifications 8240–8245, in that they were labeled pancreatic carcinoid tumours[50][54] but most islet cell carcinomas have been coded as ICD-O-3 system 8150–8155.[50]

The more aggressive endocrine pancreatic cancers are known as pancreatic neuroendocrine carcinomas (PNEC). Similarly, there has likely been a degree of admixture of PNEC and extrapulmonary small cell carcinoma.[citation needed]

Prevention [edit]

According to the American Cancer Society, there are no established guidelines for preventing pancreatic cancer, although cigarette smoking has been reported as responsible for 20–30% of pancreatic cancers.[55]

The ACS recommends keeping a healthy weight, and increasing consumption of fruits, vegetables, and whole grains, while decreasing red meat intake, although there is no consistent evidence this will prevent or reduce pancreatic cancer specifically.[56][57] In 2006, a large prospective cohort study of over 80,000 subjects failed to prove a definite association.[58] The evidence in support of this lies mostly in small case-control studies.[16]

A long-term study found that people who consumed in the range of 300 to 449 international units (IU) of vitamin D daily had a 43% lower risk of pancreatic cancer than those who took less than 150 IU per day;[59][60] 150 IU is appreciably less than what was then, or is now, recommended.[61] The World Health Organization (WHO) International Agency for Research on Cancer (IARC), concluded that there were insufficient studies in pancreatic cancer, and while it found evidence for an inverse association between vitamin D and colorectal cancer to be persuasive, it found evidence for a causal link to be limited, and also found that randomized controlled trials (RCTs) were inconclusive.[62] Taking too much vitamin D may be harmful.[61] Poor general diet, obesity, and relative physical inactivity can be risk factors in some cancers, so the role of vitamin D itself is not certain.[63]

A Harvard study from 2007 showed a modest inverse trend between blood circulation of B vitamins, such as B12, B6, and folate and pancreatic cancer incidence, but not when the vitamins were ingested in tablet form.[64] However, the results of a meta-analysis of randomised trials by Rothwell and colleagues indicate that taking a daily low dose aspirin regimen for more than five years decreases the risk of developing pancreatic adenocarcinoma (ductal pancreatic cancer) by 75%. [65]

Screening [edit]

People who may have a high risk of pancreatic cancer due to a family history can be followed, but there is no consensus on what constitutes optimal monitoring. Several small studies have shown promising preliminary results for new biomarkers, but further validation on a larger scale is needed. People with pancreatic cancer themselves, or family members, may wish to participate in the activities at a research facility, or identify a pancreas tumor registry.

A possible ‘dipstick screen’, developed by 15 year old Jack Andraka, with the collaboration of John Hopkins University detects the level of a protein called mesothelin in the urine, or blood, which is a biomarker for pancreatic cancer. Experts believe it stands a chance of becoming a cheap test for the disease but will take years to develop. [66]

Treatment [edit]

Exocrine pancreas cancer [edit]

Surgery [edit]

Treatment of pancreatic cancer depends on the stage of the cancer.[67] Although only localized cancer is considered suitable for surgery with curative intent at present, only ~20% of cases present with localised disease at diagnosis.[68] Surgery can also be performed for palliation, if the malignancy is invading or compressing the duodenum or colon. In such cases, bypass surgery might overcome the obstruction and improve quality of life but is not intended as a cure.[45]

The Whipple procedure is the most common attempted curative surgical treatment for cancers involving the head of the pancreas. This procedure involves removing the pancreatic head and the curve of the duodenum together (pancreato-duodenectomy), making a bypass for food from stomach to jejunum (gastro-jejunostomy) and attaching a loop of jejunum to the cystic duct to drain bile (cholecysto-jejunostomy). It can be performed only if the patient is likely to survive major surgery and if the cancer is localized without invading local structures or metastasizing. It can, therefore, be performed in only the minority of cases.

Cancers of the tail of the pancreas can be resected using a procedure known as a distal pancreatectomy.[67] Recently, localized cancers of the pancreas have been resected using minimally invasive (laparoscopic) approaches.[69]

After surgery, adjuvant chemotherapy with gemcitabine has been shown in several large randomized studies to significantly increase the 5-year survival (from approximately 10 to 20%), and should be offered if the patient is fit after surgery (Oettle et al. JAMA 2007, Neoptolemos et al. NEJM 2004, Oettle et al. ASCO proc 2007).

Radiation [edit]

Principles of radiation therapy in pancreas adenocarcinoma are reviewed extensively in guidelines by the National Comprehensive Cancer Network.[70] Radiation can be considered in several situations. One situation is the addition of radiation therapy after potentially curative surgery. Groups in the US have been more apt to use adjuvant radiation therapy than groups in Europe.[71]

Chemotherapy [edit]

In patients not suitable for resection with curative intent, palliative chemotherapy may be used to improve quality of life and gain a modest survival benefit. Gemcitabine was approved by the United States Food and Drug Administration in 1998, after a clinical trial reported improvements in quality of life and a 5-week improvement in median survival duration in patients with advanced pancreatic cancer. This marked the first FDA approval of a chemotherapy drug primarily for a nonsurvival clinical trial endpoint. Gemcitabine is administered intravenously on a weekly basis.

A Canadian-led Phase III randomised controlled trial, reported in 2005, involved 569 patients with advanced pancreatic cancer, led the US FDA in 2005 to license erlotinib (Tarceva) in combination with gemcitabine as a palliative regimen for pancreatic cancer. This trial compared the outcome of gemcitabine/erlotinib to gemcitabine/placebo, and demonstrated improved survival rates, improved tumor response and improved progression-free survival rates.[72][73] Other trials are now investigating the effect of the above combination in the adjuvant (post surgery) and neoadjuvant (pre-surgery) settings.

Addition of oxaliplatin to Gemcitabine (Gem/Ox) was shown to confer benefit in small trials, but is not yet standard therapy.[74]

Pancreatic neuroendocrine tumors [edit]

Main article: Neuroendocrine tumor

The majority of these tumors are histologically benign. Treatment of pancreatic endocrine tumors, including the less common malignant tumors, may include:
Watchful waiting: incidentally identified small tumors, for example on a computed tomography (CT) scan performed for other purposes, may conceptually not always need intervention, but criteria for watchful waiting are unclear.
Surgery: tumors within the pancreas only (localized tumors), or with limited metastases, may be removed. For localized tumors, the surgical procedure is much less extensive than the types of surgery used to treat pancreatic adenocarcinoma.
Hormone therapy: if the tumor is not amenable to surgical removal and is causing symptoms by secreting functional hormones, a synthetic hormone analog medication, octreotide, may lessen the symptoms, and sometimes also slows tumor growth.
Radiation therapy: occasionally used if there is pain due to anatomic extension, such as metastasis to bone.
Radiolabeled hormone: some PNETs absorb a hormone called norepinephrine and these may respond to nuclear medicine medication, radiolabeled MIBG therapy (or, experamentally, other hormones), given intravenously.
Radiofrequency ablation (RFA), cryoablation, hepatic artery embolization
Chemotherapy and targeted medication for PNETs receive Wikipedia discussion in the relevant section of that article.

Prognosis [edit]

Age-standardized death from pancreatic cancer per 100,000 inhabitants in 2004.[75]

no data

10

Exocrine pancreatic cancer (adenocarcinoma and less common variants) typically has a poor prognosis, partly because the cancer usually causes no symptoms early on, leading to locally advanced or metastatic disease at time of diagnosis.

Pancreatic cancer may occasionally result in diabetes. Insulin production is hampered, and it has been suggested the cancer can also prompt the onset of diabetes and vice versa.[76] It can be associated with pain, fatigue, weight loss, jaundice, and weakness. Additional symptoms are discussed above.

For pancreatic cancer:
For all stages combined, the 1-year relative survival rate is 25%, and the 5-year survival is estimated as less than 5% [77] to 6%.[3]
For local disease, the 5-year survival is approximately 20%.[3][4]
For locally advanced and for metastatic disease, which collectively represent over 80%[4] to 85-90%[13] of individuals, the median survival is about 10 and 6 months, respectively.[5] Without active treatment, metastatic pancreatic cancer has a median survival of 3–5 months;[13] complete remission is rare.[13]

Outcomes with pancreatic endocrine tumors, many of which are benign and completely without clinical symptoms, are much better, as are outcomes with symptomatic benign tumors; even with actual pancreatic endocrine cancers, outcomes are rather better, but variable.[50][78]

In 2010, an estimated 43,000 people in the US were diagnosed with pancreas cancer[3] and almost 37,000 died from the disease;[3] pancreatic cancer has one of the highest fatality rates of all cancers, and is the fourth-highest cancer killer among both men and women worldwide.[79] Although it accounts for only 2.5% of new cases, pancreatic cancer is responsible for 6% of cancer deaths each year.[80]

See also [edit]
Category:Deaths from pancreatic cancer
Category:Pancreatic cancer survivors
Gastrointestinal cancer
Pancreatic Cancer Action (organisation in the UK)
Lustgarten Foundation for Pancreatic Cancer Research (organization in the US)

References [edit]

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43.^ Bakkevold KE, Arnesjø B, Kambestad B (April 1992). “Carcinoma of the pancreas and papilla of Vater: presenting symptoms, signs, and diagnosis related to stage and tumour site. A prospective multicentre trial in 472 patients. Norwegian Pancreatic Cancer Trial”. Scandinavian Journal of Gastroenterology 27 (4): 317–25. doi:10.3109/00365529209000081. PMID 1589710.
44.^ Frank J. Domino M.D. (2007). 5 minutes clinical suite version 3. Philadelphia, PA: Lippincott Williams & Wilkins.[page needed]
45.^ a b Philip Agop, “Pancreatic Cancer”. ACP PIER & AHFX DI Essentials. American College of Physicians. 4 Apr 2008. Accessed 7 Apr 2009.[page needed]
46.^ Tempero MA, Arnoletti JP, Behrman S, et al. (September 2010). “Pancreatic adenocarcinoma”. J Natl Compr Canc Netw 8 (9): 972–1017. PMC 3135380. PMID 20876541.
47.^ Sarkar FH, Banerjee S, Li Y (November 2007). “Pancreatic cancer: pathogenesis, prevention and treatment”. Toxicol. Appl. Pharmacol. 224 (3): 326–36. doi:10.1016/j.taap.2006.11.007. PMC 2094388. PMID 17174370.
48.^ Delpu Y, Hanoun N, Lulka H, Sicard F, Selves J, Buscail L, Torrisani J, Cordelier P (2011). “Genetic and epigenetic alterations in pancreatic carcinogenesis”. Curr Genomics 12 (1): 15–24.
49.^ a b c Johns Hopkins Medicine; The Sol Goldman Pancreas Cancer Research Center. Types of Pancreas Tumors. http://pathology.jhu.edu/pancreas/BasicTypes1.php
50.^ a b c d e f g h Yao, J. C.; Eisner, M. P.; Leary, C.; Dagohoy, C.; Phan, A.; Rashid, A.; Hassan, M.; Evans, D. B. (2007). “Population-Based Study of Islet Cell Carcinoma”. Annals of Surgical Oncology 14 (12): 3492–3500. doi:10.1245/s10434-007-9566-6. PMC 2077912. PMID 17896148. edit
51.^ “The prognosis of patients with PENs is difficult to predict, in part because the definition of malignancy in PENs has been ambiguous. By some, PENs have been defined as malignant only when lymph nodes are involved or liver metastases are documented. Other investigators have included vascular invasion or invasion of adjacent structures as evidence of malignancy. However, the concept that a PEN removed successfully without recurrence was therefore biologically benign could be challenged. In fact, strict separation of PENs into benign and malignant groups may be less clinically useful than the definition of prognostic factors.”Hochwald, S. N.; Zee, S.; Conlon, K.; Colleoni, R.; Louie, O.; Brennan, M.; Klimstra, D. (2002). “Prognostic Factors in Pancreatic Endocrine Neoplasms: An Analysis of 136 Cases with a Proposal for Low-Grade and Intermediate-Grade Groups”. Journal of Clinical Oncology 20 (11): 2633–2642. doi:10.1200/JCO.2002.10.030. PMID 12039924. edit
52.^ “One of the most controversial aspects of PENs has been the prediction of prognosis.”Klimstra, D. S. (2007). “Nonductal neoplasms of the pancreas”. Modern Pathology 20: S94–S112. doi:10.1038/modpathol.3800686. PMID 17486055. edit
53.^ “The classification of these tumors remains controversial, and prognosis is difficult to predict” Wendy L. Frankel (2006) Update on Pancreatic Endocrine Tumors. Archives of Pathology & Laboratory Medicine: July 2006, Vol. 130, No. 7, pp. 963–966. http://www.archivesofpathology.org/doi/full/10.1043/1543-2165(2006)130%5B963:UOPET%5D2.0.CO;2
54.^ Modlin http://onlinelibrary.wiley.com/doi/10.1002/cncr.11105/pdf
55.^ “Can Cancer of the Pancreas Be Prevented?”. American Cancer Society. Archived from the original on October 12, 2007. Retrieved 2007-12-13.
56.^ Coughlin SS, Calle EE, Patel AV, Thun MJ (December 2000). “Predictors of pancreatic cancer mortality among a large cohort of United States adults”. Cancer Causes & Control 11 (10): 915–23. doi:10.1023/A:1026580131793. ISSN 0957-5243. PMID 11142526.
57.^ Zheng W, McLaughlin JK, Gridley G, et al. (September 1993). “A cohort study of smoking, alcohol consumption, and dietary factors for pancreatic cancer (United States)”. Cancer Causes & Control 4 (5): 477–82. doi:10.1007/BF00050867. PMID 8218880.
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59.^ “Health | Vitamin D ‘slashes cancer risk'”. BBC News. 2006-09-15. Retrieved 2009-09-15. The BBC quoted the lead researcher: “I would make no specific recommendation for vitamin D supplementation to prevent pancreatic cancer until we can carry out a trial to determine definitively who might benefit from such an intervention.” The BBC quoted Henry Scowcroft, science information officer at the charity Cancer Research UK: “The results of this study don’t mean that people should take vitamin D supplements to ward off pancreatic cancer, especially as vitamin D can be harmful in large quantities…As the authors themselves point out, this is the very first study to find any association between the disease and vitamin D intake…So this result needs to be repeated in other large studies, and scientists need to show exactly how vitamin D might prevent pancreatic cancer before we could issue any specific lifestyle advice.”
60.^ “Vitamin D May Cut Pancreatic Cancer”. Webmd.com. 2006-09-12.
61.^ a b Institute of Medicine. Dietary Reference Intakes for Calcium and Vitamin D. http://www.iom.edu/Reports/2010/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D.aspx Dietary Reference Intakes for Calcium and Vitamin D IOM, November 30, 2010: “The IOM finds that the evidence supports a role for vitamin D and calcium in bone health but not in other health conditions. Further, emerging evidence indicates that too much of these nutrients may be harmful, challenging the concept that “more is better.”
62.^ World Health Organization; International Agency for Research on Cancer (IARC). Vitamin D and Cancer. IARC Working Group Reports Vol.5, International Agency for research on Cancer, Lyon, 25 November 2008
63.^ Lipson P. Vitamin D: Still more questions than answers. http://blogs.forbes.com/sciencebiz/2010/08/18/vitamin-d-still-more-questions-than-answers/ “Vitamin D deficiency is common in people with poor diets (including obese people) and in people who are relatively inactive. These are independent risk factors for… …some cancers. And while some cellular mechanisms have been discovered that may lend plausibility to a vitamin D hypothesis, there are as of yet no convincing data that allow us to draw conclusions about vitamin D and these diseases.”
64.^ Schernhammer E, Wolpin B, Rifai N, et al. (June 2007). “Plasma folate, vitamin B6, vitamin B12, and homocysteine and pancreatic cancer risk in four large cohorts”. Cancer Research 67 (11): 5553–60. doi:10.1158/0008-5472.CAN-06-4463. PMID 17545639.
65.^ Rothwell P, Fowkes F, Belch, J.n B, Rifai N, et al. (Jan 2011). “Effect of daily aspirin on long term risk of death due to cancer: analysis of individual patient data from randomised trials”. Lancet 337 (9759): 31–41. doi:10.1016/S0140-6736(10)62110-1. Text “21144578” ignored (help)
66.^ The Independent, 5 May 2013 [1]
67.^ a b “Surgical Treatment of Pancreatic Cancer”. Johns Hopkins University. Retrieved 5 September 2009.
68.^ Corbo V, Tortora G, Scarpa A (2012) Molecular pathology of pancreatic cancer: from bench-to-bedside translation. Curr Drug Targets
69.^ “Laparoscopic Pancreas Surgery”. Johns Hopkins University. Retrieved 5 September 2009.
70.^ Pancreatic Adenocarcinoma (access to the guideline section of the website is free, but may require registration; see sections “PANC-F” and “MS”) http://www.nccn.org/professionals/physician_gls/pdf/pancreatic.pdf
71.^ Neoptolemos JP, Stocken DD, Friess H, et al. (March 2004). “A randomized trial of chemoradiotherapy and chemotherapy after resection of pancreatic cancer”. The New England Journal of Medicine 350 (12): 1200–10. doi:10.1056/NEJMoa032295. PMID 15028824.
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External links [edit]

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Categories: Digestive system neoplasia
Pancreas disorders

Caffeic Acid phenethyl ester inhibits epithelial-mesenchymal transition of human pancreatic cancer cells.

Chen MJ, Shih SC, Wang HY, Lin CC, Liu CY, Wang TE, Chu CH, Chen YJ.

Source

Division of Gastroenterology, Department of Internal Medicine, Mackay Memorial Hospital, Taiwan ; Mackay Medicine, Nursing and Management College, Taipei, Taiwan.

Abstract

Background. This study aimed to investigate the effect of propolis component caffeic acid phenethyl ester (CAPE) on epithelial-mesenchymal transition (EMT) of human pancreatic cancer cells and the molecular mechanisms underlying these effects. Methods. The transforming growth factor β (TGF-β-) induced EMT in human pancreatic PANC-1 cancer cells was characterized by observation of morphology and the expression of E-cadherin and vimentin by western blotting. The migration potential was estimated with wound closure assay. The expression of transcriptional factors was measured by quantitative RT-PCR and immunocytochemistry staining. The orthotopic pancreatic cancer xenograft model was used for in vivo assessment. Results. The overexpression of vimentin was attenuated by CAPE, and the alteration in morphology from polygonal to spindle shape was partially reversed by CAPE. Furthermore, CAPE delayed the TGF-β-stimulated migration potential. CAPE treatment did not reduce the expression levels of Smad 2/3, Snail 1, and Zeb 1 but inhibited the expression of transcriptional factor Twist 2. By using an orthotopic pancreatic cancer model, CAPE suppressed the expression of Twist 2 and growth of PANC-1 xenografts without significant toxicity. Conclusion. CAPE could inhibit the orthotopic growth and EMT of pancreatic cancer PANC-1 cells accompanied by downregulation of vimentin and Twist 2 expression.

PMID: 23662124 [PubMed – in process]

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Overexpression of regenerating islet-derived 1 alpha and 3 alpha genes in human primary liver tumors with beta-catenin mutations.

Cavard C, Terris B, Grimber G, Christa L, Audard V, Radenen-Bussiere B, Simon MT, Renard CA, Buendia MA, Perret C
Département GDPM, INSERM U-567, CNRS UMR 8104, Institut Cochin, Université Paris 5, France. cavard@cochin.inserm.fr

The Wnt/beta-catenin signaling pathway is activated in many human hepatocellular carcinomas (HCC). We tried to identify the genes involved in carcinogenesis and progression of HCC with beta-catenin mutations. We used PCR-based subtractive hybridization to compare gene expression between malignant and benign components of a human HCC occurring in pre-existing adenoma activated for beta-catenin. Two of the genes identified belong to the Regenerating gene (REG) family. They encode the Regenerating islet-derived 3 alpha (REG3A/HIP/PAP/REG-III) and 1 alpha (REG1A) proteins, both involved in liver and pancreatic regeneration and proliferation. Using siRNA directed against beta-catenin, we demonstrated that REG3A is a target of beta-catenin signaling in Huh7 hepatoma cells. The upregulation of REG3A and REG1A expression is significantly correlated to the beta-catenin status in 42 HCC and 28 hepatoblastomas characterized for their beta-catenin status. Thus, we report strong evidence that both genes are downstream targets of the Wnt pathway during liver tumorigenesis.

Oncogene (2006)
PMID: 16314847 Fulltext – Related articles – Download citation

University of Texas MD Anderson Cancer Center
Gastroenterology Services

MD Anderson’s Gastrointestinal Cancer Center diagnoses, treats and manages cancers of the digestive system and allied diseases. This multidisciplinary facility has specialized teams of oncologists to handle malignancies of the liver, pancreas, bowels, stomach and esophagus. Endocrine tumors in the pancreas, adrenal glands, thyroid and parathyroid are also treated here. Specialized services at the Gastrointestinal Cancer Center include video endoscopy for diagnosis and treatment, and photodynamic therapy for esophageal cancer and Barrett’s esophagus. Ongoing clinical trials at the Center cover a wide range of gastrointestinal cancers, including gene-based therapies for treatment of pancreatic cancer.

2.

Memorial Sloan Kettering Cancer Center
Gastroenterology Services

At Memorial Sloan-Kettering Cancer Center, our doctors are working to improve the understanding and treatment of neuroendocrine tumors of the gastrointestinal system. Neuroendocrine tumors act quite differently — and, as a result, are managed differently — than other types of tumors. Making an accurate diagnosis before treatment begins is crucial to ensuring the best outcome for patients with these uncommon tumors. Our neuroendocrine tumor experts — a team that includes medical oncologists, gastroenterologists, gastrointestinal cancer surgeons, endocrinologists, pathologists, and other specialists — have the experience needed to evaluate neuroendocrine tumors and select the appropriate treatment plan for each patient. The team treats hundreds of patients with neuroendocrine tumors each year.

3.

Mayo Clinic
Gastroenterology Services

Gastroenterology and Hepatology at Mayo Clinic specializes in the prevention, diagnosis and treatment of diseases of the digestive tract and liver. It is the largest practice of its kind in the United States. In any given year, members of the Division perform approximately 30,000 minimally invasive, endoscopic procedures in state-of-the-art facilities. Through a divisional infrastructure organized around interest groups oriented toward disease processes, organ systems, procedures or patient groups, clinical expertise is integrated with the newest forms of established and experimental diagnostic and therapeutic methods. Outpatients and patients in the hospital are cared for by teams of physicians and allied health personnel with broad expertise in all forms of gastroenterological and hepatobiliary diseases. Because of our recognition that high-quality care depends upon scientific discovery, major research programs at the basic, applied, and translational levels exist to generate new knowledge that ultimately benefits patients.

4.

Johns Hopkins Hospital
Gastroenterology Services

At the Johns Hopkins Hospital Division of Gastroenterology & Hepatology, our dedicated team of physicians, nurses, scientists, and staff collaborate to provide patients with expert care and treatment options to fit their needs, improve their health, and enhance their quality of life. By offering comprehensive gastroenterology care, research and access to leading experts in the field, we have been ranked among the nation’s top three GI programs by U.S. News & World Report since 1999. Our mission is to advance the understanding, diagnosis, treatment and prevention of gastrointestinal and liver disease through patient care, education and research. Reflective of this mission, our web site offers comprehensive information for patients and physicians, including:
•An in-depth digestive disease library in several languages, including a user-friendly glossary of medical terms
•Overview of our programs and services and information on how to refer a patient, make an appointment, and prepare for a procedure
•Podcasts, videos, and animations to enhance awareness of GI conditions and treatment options
•Information about upcoming and ongoing clinical trials
•Free Continuing Medical Education (CME) resources online, including Grand Rounds

5.

University of Washington Medical Center
Gastroenterology Services

Our Division is deeply and passionately committed to the missions of academic medicine. We provide the highest quality patient care for a wide spectrum of gastrointestinal and liver diseases. The faculty in our five teaching hospitals possess both depth and expertise in a variety of disorders, including AIDS, inflammatory bowel diseases, liver transplantation, bone marrow transplantation, and cancer of the gastrointestinal tract. Our many innovative and pioneering clinical research programs allow our patients to access highly promising and exciting treatment protocols. Our patient care program includes several major components. Gastrointestinal pathology services assist patients and their physicians in the correct diagnosis of GI symptoms; therapeutic endoscopy provides patients with avenues for treatment of pre-cancerous bowel diseases; and our hepatology and liver transplant services provide clinical services for patients with hepatitis and other chronic liver diseases. Our faculty conduct research, perform and supervise clinical procedures, and see patients in five area teaching hospitals.

6.

Dan-Farber Cancer Institute
Gastroenterology Services

The Center for Gastrointestinal Oncology focuses on the care of patients with abnormalities (polyps, tumors, and cancers) of the digestive system, specifically the esophagus, stomach, liver, biliary tract (gallbladder, bile ducts, ampulla of vater), pancreas, colon, rectum, and anus. This care involves prevention, treatment, and research services offered for:
•Individuals at risk of developing these cancers, focusing on early detection and prevention;
•Individuals with family histories of digestive system cancers who may want genetic counseling; or
•Individuals already diagnosed with a cancer of the digestive system looking for treatment opportunities.

The center is staffed with medical, radiation, and surgical oncologists, gastroenterologists, radiologists, pathologists, nurses, and social workers. Patients have easy access to the multidisciplinary team in a one-day evaluation where the team will discuss with the patient and family the available treatment options for their situation. This collaboration among patients, referring physicians, and the clinicians is dedicated to providing the very best care for our patients.

7.

Massachusetts General Hospital
Gastroenterology Services

The Massachusetts General Hospital Division of Gastroenterology offers comprehensive, cutting-edge, and coordinated care for patients with all types of digestive diseases, from heartburn to organ failure. Our collaborative practice of gastroenterologists and endoscopists are dedicated to the prevention, diagnosis, treatment and management of these digestive diseases. Possessing expertise in all aspects of digestive health, our multidisciplinary team of specialists offers patients the benefit of an individualized treatment plan. The Division of Gastroenterology was ranked fourth in the country by U.S. News and World Report in 2010 and is part of the hospital’s Digestive Healthcare Center. The division’s specialists are among the best in New England, and many are consistently recognized in Boston Magazine’s Best Doctors survey.

8.

University of California, San Francisco Medical Center
Gastroenterology Services

UCSF gastroenterology services specialize in the prevention, diagnosis and treatment of diseases of the liver and digestive tract, including the stomach, duodenum, gallbladder, biliary tract, pancreas, small intestine and colon. Our team offers expertise in general gastroenterology as well as: gastrointestinal cancers, gastrointestinal motility, inflammatory bowel disease, liver transplants and viral hepatitis. We strive to provide patients with thoughtful, compassionate and timely care as well as the most advanced procedures such as photodynamic therapy and those involving endoscopic techniques.

9.

Cleveland Clinic
Gastroenterology Services

Gastroenterologists and hepatologists at Cleveland Clinic offer expert diagnosis and medical treatment for patients with disorders of the esophagus, liver, gallbladder, stomach, pancreas, small intestine and colon. Cleveland Clinic Gastroenterologists use the latest endoscopic advances to perform tens of thousands of minimally invasive procedures each year. These include colonoscopy, sigmoidoscopy and state-of-the-art procedures such as capsule endoscopy, endoscopic ultrasound (EUS) and endoscopic retrograde cholangiopancreatography (ERCP). Other innovative treatments options and procedures include:
•Cryoablation for Barrett’s Esophagus
•Endoscopic Pancreatic Function Test
•Extracorporeal and intraductal Lithotripsy
•Endoscopy Therapy for IBD

10.

Ronald Reagan UCLA Medical Center
Gastroenterology Services Overview

The Digestive Disease Center provides consultation for patients with liver and gastrointestinal disorders and operates special clinics for inflammatory bowel disease, functional bowel disorders, and abdominal pain, pancreatic and biliary diseases, familial Mediterranean fever, hepatic disorders, and gastrointestinal and hepatic histopathology. The Gastroenterology Procedures Unit (an integral part of the Digestive Disease Center) performs a full spectrum of tests and therapies including diagnostic endoscopy, neuromuscular diagnostic tests, endoscopic therapy, and gastrointestinal neuromuscular disease therapy.

Note: Everist Genomics has no relationship with U.S. News and does not endorse any specific healthcare organizations.

http://health.usnews.com/best-hospitals/rankings/cancer?page=90

Identification of Pancreatic Cancer Stem Cells

Chenwei Li1,
David G. Heidt1,
Piero Dalerba4,
Charles F. Burant2,3,
Lanjing Zhang3,
Volkan Adsay4,
Max Wicha3,
Michael F. Clarke5, and
Diane M. Simeone1,2

+ Author Affiliations

Departments of 1Surgery, 2Molecular and Integrative Physiology, and 3Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan; 4Department of Pathology, Karmanos Cancer Center, Detroit, Michigan; and 5Department of Internal Medicine, Stanford University School of Medicine, Palo Alto, California

Requests for reprints:
Diane M. Simeone, Departments of Surgery and Molecular and Integrative Physiology TC 2922D, University of Michigan Medical Center, Box 0331, 1500 East Medical Center Drive Ann Arbor, MI 48109. Phone: 734-615-1600; Fax: 734-936-5830; E-mail: simeone@umich.edu.

Abstract

Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA). Pancreatic cancer cells with the CD44+CD24+ESA+ phenotype (0.2–0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44+CD24+ESA+ cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44+CD24+ESA+ pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44+CD24+ESA+ pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation. [Cancer Res 2007;67(3):1030–7]
pancreatic cancer
stem cells
niche
CD44
ESA
CD24

Footnotes
Received June 2, 2006.
Revision received October 18, 2006.
Accepted November 21, 2006.
•©2007 American Association for Cancer Research.

Content referenced by
http://en.wikipedia.org/wiki/Pancreatic_cancer
http://www.ncbi.nlm.nih.gov/pubmed?term=pancreatic%20cancer
http://www.ihop-net.org/UniPub/iHOP/index.html?search=pancreatic+&field=all&ncbi_tax_id=0&organism_syn=http://www.everistgenomics.com/content/patient-resources/colorectal/top-ranked-hospitals.htm
http://scholar.google.ca/scholar?hl=en&q=pancreatic+cancer&btnG=&as_sdt=1%2C5&as_sdtp=

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About garyskeete

ASHWORTH MEDICINE-Professional Medical Assisting, Doctor of Science,Legal Assistant Diploma BSc Criminal Justice PhD Computational Neuroscience MD DSC Epigenetics
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