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Esophageal cancerClassification and external resources

Endoscopic image of patient with esophageal adenocarcinoma seen at gastro-esophageal junction.

ICD-10 C15(http://apps.who.int/classifications/icd10/browse/2010/en#/C15)

ICD-9 150 (http://www.icd9data.com/getICD9Code.ashx?icd9=150)

OMIM 133239 (http://omim.org/entry/133239)

DiseasesDB 9150 (http://www.diseasesdatabase.com/ddb9150.htm)

MedlinePlus 000283(http://www.nlm.nih.gov/medlineplus/ency/article/000283.htm)

eMedicine article/277930 (http://emedicine.medscape.com/article/277930-overview) article/368206(http://emedicine.medscape.com/article/368206-overview)

MeSH D004938 (http://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?field=uid&term=D004938)

Esophageal cancerFrom Wikipedia, the free encyclopedia

Esophageal cancer (oroesophageal cancer) ismalignancy of the esophagus.There are various subtypes,primarily squamous cell cancer(approx 90-95% of all esophagealcancer worldwide) andadenocarcinoma (approx. 50-80%of all esophageal cancer in theUnited States). Squamous cellcancer arises from the cells thatline the upper part of theesophagus. Adenocarcinomaarises from glandular cells that arepresent at the junction of theesophagus and stomach.[1]

Esophageal tumors usually lead todysphagia (difficulty swallowing),pain and other symptoms, and arediagnosed with biopsy. Small andlocalized tumors are treatedsurgically with curative intent.Larger tumors tend not to beoperable and hence are treatedwith palliative care; their growthcan still be delayed withchemotherapy, radiotherapy or acombination of the two. In somecases chemo- and radiotherapy canrender these larger tumorsoperable. Prognosis depends onthe extent of the disease and othermedical problems, but is fairly poor.[2]

Contents1 Classification2 Signs and symptoms3 Causes

3.1 Increased risk3.2 Decreased risk

4 Diagnosis

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Micrograph of an esophagealadenocarcinoma (dark blue - upper-left of image) and normal squamousepithelium (upper-right of image).H&E stain.

4.1 Clinical evaluation5 Management

5.1 General approaches5.2 Follow-up

6 Prognosis7 Epidemiology8 References9 External links

ClassificationEsophageal cancers are typically carcinomas which arise from theepithelium, or surface lining, of the esophagus. Most esophagealcancers fall into one of two classes: squamous cell carcinomas, whichare similar to head and neck cancer in their appearance andassociation with tobacco and alcohol consumption, andadenocarcinomas, which are often associated with a history ofgastroesophageal reflux disease and Barrett's esophagus. A generalrule of thumb is that a cancer in the upper two-thirds is a squamouscell carcinoma and one in the lower one-third is an adenocarcinoma.Rare histologic types of esophageal cancer are different variants ofthe squamous cell carcinoma, and non-epithelial tumors, such asleiomyosarcoma, malignant melanoma, rhabdomyosarcoma,lymphoma and others.[3][4]

Signs and symptomsDysphagia (difficulty swallowing) and odynophagia (painful swallowing) are the most common symptomsof esophageal cancer. Dysphagia is the first symptom in most patients. Odynophagia may also be present.Fluids and soft foods are usually tolerated, while hard or bulky substances (such as bread or meat) causemuch more difficulty. Substantial weight loss is characteristic as a result of reduced appetite, poor nutritionand the active cancer. Pain behind the sternum or in the epigastrium, often of a burning, heartburn-likenature, may be severe, present itself almost daily, and is worsened by swallowing any form of food. Anothersign may be an unusually husky, raspy, or hoarse-sounding cough, a result of the tumor affecting therecurrent laryngeal nerve.

The presence of the tumor may disrupt normal peristalsis (the organized swallowing reflex), leading tonausea and vomiting, regurgitation of food, coughing and an increased risk of aspiration pneumonia. Thetumor surface may be fragile and bleed, causing hematemesis (vomiting up blood). Compression of localstructures occurs in advanced disease, leading to such problems as upper airway obstruction and superiorvena cava syndrome. Fistulas may develop between the esophagus and the trachea, increasing thepneumonia risk; this condition is usually heralded by cough, fever or aspiration.[2]

Most of the people diagnosed with esophageal cancer have late-stage disease, because people usually do nothave significant symptoms until half of the inside of the esophagus, called the lumen, is obstructed, by which

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Barrett's esophagus isconsidered to be a riskfactor for esophagealadenocarcinoma.

point the tumor is fairly large. [5]

If the disease has spread elsewhere, this may lead to symptoms related to this: liver metastasis could causejaundice and ascites, lung metastasis could cause shortness of breath, pleural effusions, etc.

Causes

Increased risk

There are a number of risk factors for esophageal cancer.[2] Some subtypes ofcancer are linked to particular risk factors:

Age - most patients are over 60, and the median in US patients is 67.[2]

Sex - the disease is more common in men.Heredity - it is more likely in people who have close relatives with cancer.Tobacco smoking and heavy alcohol use increase the risk, and togetherappear to increase the risk more than either individually. Tobacco and/oralcohol account for approximately 90% of all esophageal squamous cellcarcinomas. Tobacco smoking is also linked to esophagealadenocarcinoma though no scientific evidence has been found betweenalcohol and esophageal adenocarcinoma.[citation needed]

Gastroesophageal reflux disease (GERD) and its resultant Barrett'sesophagus increase esophageal cancer risk due to the chronic irritation ofthe mucosal lining. Adenocarcinoma is more common in this condition.[6]

Human papillomavirus (HPV)[7]

Corrosive injury to the esophagus by swallowing strong alkalines (lye) or acidsParticular dietary substances, such as nitrosaminesA medical history of other head and neck cancers increases the chance of developing a second cancerin the head and neck area, including esophageal cancer.Plummer-Vinson syndrome (anemia and esophageal webbing)Tylosis and Howel-Evans syndrome (hereditary thickening of the skin of the palms and soles)Radiation therapy for other conditions in the mediastinum[2]

Coeliac disease predisposes towards squamous cell carcinoma.[8]

Obesity increases the risk of adenocarcinoma fourfold.[9] It is suspected that increased risk of refluxmay be behind this association.[6][10]

Thermal injury as a result of drinking hot beverages[11][12]

Alcohol consumption in individuals predisposed to alcohol flush reaction[13]

Achalasia[14]

Decreased risk

Risk appears to be less in patients using aspirin or related drugs (NSAIDs).[15]

The role of Helicobacter pylori in progression to esophageal adenocarcinoma is still uncertain, but, onthe basis of population data, it may carry a protective effect.[16][17] It is postulated that H. pyloriinduces chronic gastritis, which is a risk factor for reflux, which in turn is a risk factor for esophagealadenocarcinoma.[18]

According to the National Cancer Institute, "diets high in cruciferous (cabbage, broccoli/broccolini,

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Endoscopy and radial endoscopicultrasound images of submucosaltumor in mid-esophagus.

Cancer of the esophagus, CT withcontrast, axial image.

cauliflower, Brussels sprouts) and green and yellow vegetables and fruits are associated with adecreased risk of esophageal cancer."[19]

Moderate coffee consumption is associated with a decreased risk.[20]

According to one Italian study of "diet surveys completed by 5,500 Italians"—a study which hasraised debates questioning its claims among cancer researchers cited in news reports about it—eatingpizza more than once a week appears "to be a favorable indicator of risk for digestive tract neoplasmsin this population."[21]

Diagnosis

Clinical evaluation

Although an occlusive tumor may be suspected on a barium swallowor barium meal, the diagnosis is best made withesophagogastroduodenoscopy (EGD, endoscopy); this involves thepassing of a flexible tube down the esophagus and examining thewall. Biopsies taken of suspicious lesions are then examinedhistologically for signs of malignancy.

Additional testing is usually performed to estimate the tumor stage.Computed tomography (CT) of the chest, abdomen and pelvis canevaluate whether the cancer has spread to adjacent tissues or distantorgans (especially liver and lymph nodes). The sensitivity of a CTscan is limited by its ability to detect masses (e.g. enlarged lymphnodes or involved organs) generally larger than 1 cm. Positronemission tomography is also used to estimate the extent of thedisease and is regarded more precise that CT alone. Esophagealendoscopic ultrasound can provide staging information regarding thelevel of tumor invasion, and possible spread to regional lymph nodes.

The location of the tumor is generally measured by the distance fromthe teeth. The esophagus (25 cm or 10 inches long) is commonlydivided into three parts for purposes of determining the location.Adenocarcinomas tend to occur distally and squamous cellcarcinomas proximally, but the converse may also be the case.

Management

General approaches

The treatment is determined by the cellular type of cancer(adenocarcinoma or squamous cell carcinoma vs other types), thestage of the disease, the general condition of the patient and otherdiseases present. On the whole, adequate nutrition needs to beassured, and adequate dental care is vital.

If the patient cannot swallow at all, an esophageal stent may be

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Esophageal cancer, CT scan withcontrast, coronal image.

Self-expandable metallic stents areused for the palliation of esophagealcancer.

Esophageal cancer affecting the loweresophageus. Insets show the tumor inmore detail both before and afterplacement of a stent.

inserted to keep the esophagus patent; stents may also assist inoccluding fistulas. A nasogastric tube may be necessary to continuefeeding while treatment for the tumor is given, and some patientsrequire a gastrostomy (feeding hole in the skin that gives directaccess to the stomach). The latter two are especially important if thepatient tends to aspirate food or saliva into the airways, predisposingfor aspiration pneumonia.

Esophagectomy is the removal of a segment of the esophagus; as thisshortens the length of the remaining esophagus, some other segmentof the digestive tract (typically the stomach or part of the colon orjejunum) is pulled up to the chest cavity and interposed.[22] If thetumor is unresectable or the patient is not fit for surgery, palliativeesophageal stenting can allow the patient to tolerate soft diet.

Types of esophagectomy:

The thoracoabdominal approach opens the abdominal andthoracic cavities together.The two-stage Ivor Lewis (also called Lewis-Tanner) approachinvolves an initial laparotomy and construction of a gastrictube, followed by a right thoracotomy to excise the tumor andcreate an esophagogastric anastomosis.The three-stage McKeown approach adds a third incision in theneck to complete the cervical anastomosis.

Data are accumulating to indicate endoscopic therapy is a safe, lessinvasive, and effective therapy for very early esophageal cancer. Thecandidates for endoscopic therapy are Stage 1 patients with tumorsinvading into the lamina propria (T1 mucosal) or submucosa (T1submucosal) that do not have regional or distant metastasis. Patientswith carcinoma in situ or high-grade dysplasia can also be treatedwith endoscopic therapy. Submucosal cancers with increased risk ofnodal metastases may not be as amenable to curative therapy.

Two forms of endoscopic therapy have been used for Stage 0 and Idisease: endoscopic mucosal resection (EMR) and mucosal ablationusing photodynamic therapy, Nd-YAG laser, or argon plasmacoagulation.

EMR has been advocated for early cancers (that is, those that aresuperficial and confined to the mucosa only) and has been shown tobe a less invasive, safe, and highly effective nonsurgical therapy forearly squamous cell esophageal cancer. Preliminary reports alsosuggest its safety and efficacy for early adenocarcinoma arising inBarrett’s esophagus. The prognosis after treatment with EMR iscomparable to surgical resection. This technique can be attempted inpatients, without evidence of nodal or distant metastases, withdifferentiated tumors that are slightly raised and less than 2 cm in

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diameter, or in differentiated tumors that are ulcerated and less than 1 cm in diameter. The most commonlyemployed modalities of EMR include strip biopsy, double-snare polypectomy, resection with combined useof highly concentrated saline and epinephrine, and resection using a cap.

The strip biopsy method for endoscopic mucosal resection of esophageal cancer is performed with a double-channel endoscope equipped with grasping forceps and snare. After marking the lesion border with anelectric coagulator, saline is injected into the submucosa below the lesion to separate the lesion from themuscle layer and to force its protrusion. The grasping forceps are passed through the snare loop. The mucosasurrounding the lesion is grasped, lifted, and strangulated and resected by electrocautery. The endoscopicdouble-snare polypectomy method is indicated for protruding lesions. Using a double-channel scope, thelesion is grasped and lifted by the first snare and strangulated with the second snare for complete resection.

Endoscopic resection with injection of concentrated saline and epinephrine is carried out using a double-channel scope. The lesion borders are marked with a coagulator. Highly concentrated saline and epinephrineare injected (15–20 ml) into the submucosal layer to swell the area containing the lesion and elucidate themarkings. The mucosa outside the demarcated border is excised using a high-frequency scalpel to the depthof the submucosal layer. The resected mucosa is lifted and grasped with forceps, trapping and strangulatingthe lesion with a snare, and then resected by electrocautery.

A fourth method of EMR employs the use of a clear cap and prelooped snare inside the cap. After insertion,the cap is placed on the lesion and the mucosa containing the lesion is drawn up inside the cap by aspiration.The mucosa is caught by the snare and strangulated, and finally resected by electrocautery. This is called the"band and snare" or "suck and cut" technique. The resected specimen is retrieved and submitted formicroscopic examination for determination of tumor invasion depth, resection margin, and possible vascularinvolvement. The resulting "ulcer" heals within three weeks.

Although most lesions treated in the esophagus have been early squamous cell cancers, EMR can also beused to debulk or completely treat polypoid dysplastic or malignant lesions in Barrett’s esophagus. In apreliminary report from Germany, EMR was performed as primary treatment or adjunctive therapyfollowing photodynamic therapy for early adenocarcinomas in Barrett's esophagus. The "suck and cut"technique (with and without prior saline injection) was used, as well as the "band and cut" technique.Although all tumors were resected without difficulty, 12.5% developed bleeding (which was managedsuccessfully by endoscopic therapy). Eighty-one percent of the lesions were completely resected. The otherlesions were also treated with other endoscopic techniques. While this report suggests it is feasible tocompletely resect local, circumscribed, early adenocarcinomas arising in Barrett's esophagus, the relativesafety and efficacy of EMR in conjunction with photodynamic therapy is unknown.

The major complications of endoscopic mucosal resection include postoperative bleeding, perforation andstricture formation. During the procedure, an injection of 100,000 times diluted epinephrine into themuscular wall, along with high-frequency coagulation or clipping can be applied to the bleeding point forhemostasis. It is important to administer acid-reducing medications to prevent postoperative hemorrhage.Perforation may be prevented with sufficient saline injection to raise the mucosa containing the lesion. The"non-lifting sign" and complaints of pain when the snare strangulates the lesion are contrainidications ofEMR. When perforation is recognized immediately after a procedure, the perforation should be closed byclips. Surgery should be considered in cases of endoscopic closure failure. The incidence of complicationsranges from 0–50% and squamous cell recurrence rates range from 0–8%.

Laser therapy is the use of high-intensity light to destroy tumor cells; it affects only the treated area. This istypically done if the cancer cannot be removed by surgery. The relief of a blockage can help to reduce

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Age-standardized death fromesophagus cancer per100,000 inhabitants in 2004[25]

no data

dysphagia and pain. Photodynamic therapy, a type of laser therapy, involves the use of drugs that areabsorbed by cancer cells; when exposed to a special light, the drugs become active and destroy the cancercells.

Chemotherapy depends on the tumor type, but tends to be cisplatin-based (or carboplatin or oxaliplatin)every three weeks with fluorouracil (5-FU) either continuously or every three weeks. In more recent studies,addition of epirubicin was better than other comparable regimens in advanced nonresectable cancer.[23]

Chemotherapy may be given after surgery (adjuvant, i.e. to reduce risk of recurrence), before surgery(neoadjuvant) or if surgery is not possible; in this case, cisplatin and 5-FU are used. Ongoing trials comparevarious combinations of chemotherapy; the phase II/III REAL-2 trial – for example – compares fourregimens containing epirubicin and either cisplatin or oxaliplatin, and either continuously infusedfluorouracil or capecitabine.

Radiotherapy is given before, during or after chemotherapy or surgery, and sometimes on its own to controlsymptoms. In patients with localised disease but contraindications to surgery, "radical radiotherapy" may beused with curative intent.

Follow-up

Patients are followed up frequently after a treatment regimen has been completed. Frequently, othertreatments are necessary to improve symptoms and maximize nutrition.

PrognosisIn general, the prognosis of esophageal cancer is quite poor, because most patients present with advanceddisease. By the time the first symptoms such as dysphagia start manifesting themselves, the cancer hasalready well progressed. The overall five-year survival rate (5YSR) is approximately 15%, with mostpatients dying within the first year of diagnosis.[24]

Individualized prognosis depends largely on stage. Those with cancer restricted entirely to the esophagealmucosa have about an 80% 5YSR, but submucosal involvement brings this down to less than 50%.Extension into the muscularis propria (muscular layer of the esophageus) has meant a 20% 5YSR andextension to the structures adjacent to the esophagus results in a 7% 5YSR. Patients with distant metastases(who are not candidates for curative surgery) have a less than 3% 5YSR. .

EpidemiologyEsophageal cancer is a relatively rare form of cancer, but some worldareas have a markedly higher incidence than others: Belgium, China,Iran, Iceland, India, Japan, the United Kingdom appear to have ahigher incidence, as well as the region around the Caspian Sea.[26]

The American Cancer Society estimated that during 2007,approximately 15,560 new esophageal cancer cases will be diagnosedin the United States.[27]

In the United States, squamous cell carcinoma of the esophagususually affects African American males with a history of heavy

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less than 3

3-6

6-9

9-12

12-15

15-18

18-21

21-24

24-27

27-30

30-35

more than 35

smoking or alcohol use. Until the 1970s, squamous cell carcinomamade up the vast majority of esophageal cancers in the United States.In recent decades, incidence of adenocarcinoma of the esophagus(which is associated with Barrett's esophagus) steadily rose in theUnited States to the point that it has now surpassed squamous cellcarcinoma in this country. In contrast to squamous cell carcinoma,esophageal adenocarcinoma is more common in Caucasian men (overthe age of 60) than it is in African Americans. Multiple reportsindicate esophageal adenocarcinoma incidence has increased duringthe past 20 years, especially in non-Hispanic white men. Esophagealadenocarcinoma age-adjusted incidence increased in New Mexicofrom 1973 to 1997. This increase was found in non-Hispanic whitesand Hispanics and became predominant in non-Hispanic whites.[28]

Esophageal cancer incidence and mortality rates for AfricanAmericans continue to be higher than the rate for Causasians.However, incidence and mortality of esophageal cancer hassignificantly decreased among African Americans since the early1980s, whereas with Caucasians, it has slightly increased.[29]

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4. ^ Halperin, Edward C.; Perez, A. Brady, Luther W. (2008). Perez and Brady's principles and practice of radiationoncology (http://books.google.com/books?id=NyeE6-aKnSYC&pg=PA1137) . Lippincott Williams & Wilkins.p. 1137. ISBN 978-0-7817-6369-1. http://books.google.com/books?id=NyeE6-aKnSYC&pg=PA1137.

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9. ^ Merry AH, Schouten LJ, Goldbohm RA, van den Brandt PA (2007). "Body Mass Index, height and risk ofadenocarcinoma of the oesophagus and gastric cardia: a prospective cohort study"(//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2095659) . Gut 56 (11): 1503–11.DOI:10.1136/gut.2006.116665 (http://dx.doi.org/10.1136%2Fgut.2006.116665) . PMC 2095659

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(//www.ncbi.nlm.nih.gov/pmc/articles/PMC2095659/?tool=pmcentrez) . PMID 17337464(//www.ncbi.nlm.nih.gov/pubmed/17337464) . //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2095659.

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12. ^ Whiteman DC (2009). "Hot tea and increased risk of oesophageal cancer."(http://www.bmj.com/cgi/content/full/338/mar26_2/b610?view=long&pmid=19325178) . BMJ 338: b610.DOI:10.1136/bmj.b610 (http://dx.doi.org/10.1136%2Fbmj.b610) . PMID 19325178(//www.ncbi.nlm.nih.gov/pubmed/19325178) . http://www.bmj.com/cgi/content/full/338/mar26_2/b610?view=long&pmid=19325178.

13. ^ Brooks PJ, Enoch MA, Goldman D, Li TK, Yokoyama A (2009). "The alcohol flushing response: Anunrecognized risk factor for esophageal cancer from alcohol consumption"(//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2659709) . PLOS Medicine 6 (3): 191–5.DOI:10.1371/journal.pmed.1000050 (http://dx.doi.org/10.1371%2Fjournal.pmed.1000050) . PMC 2659709(//www.ncbi.nlm.nih.gov/pmc/articles/PMC2659709/?tool=pmcentrez) . PMID 19320537(//www.ncbi.nlm.nih.gov/pubmed/19320537) . //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2659709.

14. ^ Park W, Vaezi M (2005). "Etiology and pathogenesis of achalasia: the current understanding". Am J Gastroenterol100 (6): 1404–14. DOI:10.1111/j.1572-0241.2005.41775.x (http://dx.doi.org/10.1111%2Fj.1572-0241.2005.41775.x) . PMID 15929777 (//www.ncbi.nlm.nih.gov/pubmed/15929777) .

15. ^ Corley DA, Kerlikowske K, Verma R, Buffler P. Protective association of aspirin/NSAIDs and esophageal cancer:a systematic review and meta-analysis. Gastroenterology 2003;124:47–56. PMID 12512029. See also NCI -"Esophageal Cancer (PDQ): Prevention"(http://www.cancer.gov/cancertopics/pdq/prevention/esophageal/healthprofessional#Section_57) .

16. ^ Wong A, Fitzgerald RC (2005). "Epidemiologic risk factors for Barrett's esophagus and associatedadenocarcinoma". Clin. Gastroenterol. Hepatol. 3 (1): 1–10. DOI:10.1016/S1542-3565(04)00602-0(http://dx.doi.org/10.1016%2FS1542-3565%2804%2900602-0) . PMID 15645398(//www.ncbi.nlm.nih.gov/pubmed/15645398) .

17. ^ Ye W, Held M, Lagergren J, et al. (2004). "Helicobacter pylori infection and gastric atrophy: risk ofadenocarcinoma and squamous-cell carcinoma of the esophagus and adenocarcinoma of the gastric cardia"(http://jnci.oxfordjournals.org/cgi/content/full/96/5/388) . J. Natl. Cancer Inst. 96 (5): 388–96.DOI:10.1093/jnci/djh057 (http://dx.doi.org/10.1093%2Fjnci%2Fdjh057) . PMID 14996860(//www.ncbi.nlm.nih.gov/pubmed/14996860) . http://jnci.oxfordjournals.org/cgi/content/full/96/5/388.

18. ^ Nakajima S, Hattori T (2004). "Oesophageal adenocarcinoma or gastric cancer with or without eradication ofHelicobacter pylori infection in chronic atrophic gastritis patients: a hypothetical opinion from a systematic review"(http://www.blackwell-synergy.com/doi/full/10.1111/j.1365-2036.2004.01975.x) . Aliment. Pharmacol. Ther. 20Suppl 1: 54–61. DOI:10.1111/j.1365-2036.2004.01975.x (http://dx.doi.org/10.1111%2Fj.1365-2036.2004.01975.x) .PMID 15298606 (//www.ncbi.nlm.nih.gov/pubmed/15298606) . http://www.blackwell-synergy.com/doi/full/10.1111/j.1365-2036.2004.01975.x.

19. ^ NCI (2002). "Prevention: Dietary Factors, based on Chainani-Wu N. Diet and oral, pharyngeal, and esophagealcancer" (http://www.cancer.gov/cancertopics/pdq/prevention/esophageal/healthprofessional#Section_57) . NutrCancer 44 (2): 104–26. PMID 12734057 (//www.ncbi.nlm.nih.gov/pubmed/12734057) .http://www.cancer.gov/cancertopics/pdq/prevention/esophageal/healthprofessional#Section_57.

20. ^ Tavani, A; Bertuzzi M, Talamini R, Gallus S, Parpinel M, Franceschi S, Levi F, La Vecchia C. (10 2003). "Coffeeand tea intake and risk of oral, pharyngeal and esophageal cancer". Oral Oncol. 39 (7): 695–700.DOI:10.1016/S1368-8375(03)00081-2 (http://dx.doi.org/10.1016%2FS1368-8375%2803%2900081-2) .PMID 12907209 (//www.ncbi.nlm.nih.gov/pubmed/12907209) .

21. ^ Gallus S, Bosetti C, Negri E, Talamini R, Montella M, Conti E, Franceschi S, La Vecchia C. Does pizza protectagainst cancer? Int J Cancer 2003;107:283–4. PMID 12949808. Cited and qtd. by WebMD(http://www.webmd.com/content/article/71/81291.htm) and BBC News (http://news.bbc.co.uk/2/3086013.stm) .

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22. ^ Deschamps C, Nichols FC, Cassivi SD, et al. (2005). "Long-term function and quality of life after esophagealresection for cancer and Barrett's". Surgical Clinics of North America 85 (3): 649–56.DOI:10.1016/j.suc.2005.01.018 (http://dx.doi.org/10.1016%2Fj.suc.2005.01.018) . PMID 15927658(//www.ncbi.nlm.nih.gov/pubmed/15927658) .

23. ^ Ross P, Nicolson M, Cunningham D, et al. (April 2002). "Prospective randomized trial comparing mitomycin,cisplatin, and protracted venous-infusion fluorouracil (PVI 5-FU) With epirubicin, cisplatin, and PVI 5-FU inadvanced esophagogastric cancer.". Journal of clinical oncology : official journal of the American Society of ClinicalOncology 20 (8): 1996–2004. DOI:10.1200/JCO.2002.08.105 (http://dx.doi.org/10.1200%2FJCO.2002.08.105) .PMID 11956258 (//www.ncbi.nlm.nih.gov/pubmed/11956258) .

24. ^ Polednak AP (May 2003). "Trends in survival for both histologic types of esophageal cancer in US surveillance,epidemiology and end results areas". Int. J. Cancer 105 (1): 98–100. DOI:10.1002/ijc.11029(http://dx.doi.org/10.1002%2Fijc.11029) . PMID 12672037 (//www.ncbi.nlm.nih.gov/pubmed/12672037) .

25. ^ "WHO Disease and injury country estimates"(http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html) . World HealthOrganization. 2009. http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html.Retrieved Nov. 11, 2009.

26. ^ Stewart, Bernard W.; Kleihues, P. (2003). World cancer report. Lyon: IARC Press. ISBN 92-832-0411-5.27. ^ "What Are the Key Statistics About Cancer of the Esophagus?"

(http://web.archive.org/web/20070929091631/http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_are_the_key_statistics_for_esophagus_cancer_12.asp?sitearea=cri) . Detailed Guide: Esophagus Cancer. American CancerSociety. August 2006. Archived from the original(http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_are_the_key_statistics_for_esophagus_cancer_12.asp?sitearea=cri) on 2007-09-29.http://web.archive.org/web/20070929091631/http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_are_the_key_statistics_for_esophagus_cancer_12.asp?sitearea=cri. Retrieved 2007-03-21.

28. ^ Kenneth J. Vega, M.D., M. Mazen JamaM.D.l (September 2000). "Changing pattern of esophageal cancerincidence in New Mexico" (http://www.blackwell-synergy.com/doi/abs/10.1111/j.1572-0241.2000.02329.x?cookieSet=1&journalCode=ajg) . Changing pattern of esophageal cancer incidence in New Mexico. The AmericanJournal of Gastroenterology. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1572-0241.2000.02329.x?cookieSet=1&journalCode=ajg. Retrieved 2007-03-21.

29. ^ "Incidence and Mortality Rate Trends"(http://web.archive.org/web/20070316171346/http://planning.cancer.gov/disease/Esophageal-Snapshot.pdf) (PDF). ASnapshot of Esophageal Cancer. National Cancer Institute. September 2006. Archived from the original(http://planning.cancer.gov/disease/Esophageal-Snapshot.pdf) on 2007-03-16.http://web.archive.org/web/20070316171346/http://planning.cancer.gov/disease/Esophageal-Snapshot.pdf. Retrieved2007-03-21.

External linksNCI Esophageal Cancer Home Page (http://cancer.gov/cancerinfo/types/esophageal)Cancer.Net: Esophageal Cancer (http://www.cancer.net/patient/Cancer+Types/Esophageal+Cancer)Barrett's Oesophagus Campaign - Working to prevent oesophageal cancer / cancer of the gullet(http://www.barrettscampaign.org.uk/)MedlinePlus: Esophageal Cancer (http://www.nlm.nih.gov/medlineplus/esophagealcancer.html)Esophageal Cancer (http://www.cancernetwork.com/cancer-management-11/chapter12/article/10165/1405663) From Cancer Management: A Multidisciplinary Approach(http://www.cancernetwork.com/cancer-management-11)Learn More about Esophageal Cancer (http://massgeneral.org/cancer/crr/types/gi/eso_gi.asp)Oesophageal Cancer at Cancer Research UK (http://www.cancerhelp.org.uk/help/default.asp?page=4478)Oesophageal Cancer Facts/ Resources (BBC) (Last updated: 30 January 2004)(http://news.bbc.co.uk/2/hi/health/medical_notes/3244469.stm)

6/29/12 6:02 AMEsophageal cancer - Wikipedia, the free encyclopedia

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Esophageal Cancer Awareness Association Home Page (http://ecaware.org)Esophageal Cancer Action Network Home Page (http://ecan.org)

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