IN THE NAME OF GOD GI CANCER

ESOPHAGEAL CANCER INCIDENCE AND ETIOLOGY 4.5:100,000 people , mortality4.4:100,000 It is about 10 times less common than CRC but kills about one-quarter as many patients Rare but increasingly common and extremely lethal malignancy

They are either squamous cell carcinomas or adenocarcinomas; the two histologic subtypes have a similar clinical presentation but different causative factors One notable shift of dominant esophageal cancer type from SCC to adenocarcinoma, strongly linked to reflux disease and Barrett’s metaplasia

Other distinctions between cell types are: Adenocarcinoma to affect the distal esophagus in white males Squamous cell to affect the more proximal esophagus in black males with the added risk factors of smoking, alcohol consumption, caustic injury, and human papilloma virus infection

SCC is more common cell type, rises incidence strikingly in association with geographic location … extending from the southern shore of the Caspian Sea on the west to northern China on the east, encompassing parts of Iran, central Asia, Afghanistan, Siberia, and Mongolia Familial increased risk has been observed in high incidence regions , gene associations are not yet defined

It is more common in blacks than whites ,in males than females; most often after age 50 and associated with a lower socioeconomic status Such cancers generally arise in the cervical and thoracic portions of the esophagus

Causative factors :excess alcohol consumption and/or cigarette smoking ,these factors acting synergistically The whiskey is higher incidence than wine or beer SCC : ingestion of nitrates, smoked opiates, and fungal toxins in pickled vegetables, long-term exposure to extremely hot tea, the ingestion of lye, radiation-induced strictures, and chronic achalasia

An esophageal web in association with glossitis and iron deficiency (i An esophageal web in association with glossitis and iron deficiency (i.e., Plummer-Vinson or Paterson- Kelly syndrome) and congenital hyperkeratosis and pitting of the palms and soles (i.e., tylosis palmaris et plantaris) have each been linked with squamous cell esophageal cancer, as have dietary deficiencies of molybdenum, zinc, selenium, and vitamin A

Patients with head and neck cancer are at increased risk of squamous cell cancer of the esophagus For unclear reasons, the SCC decreased in both black and white populations over the past 40 years, whereas the rate of adenocarcinoma has risen sevenfold, particularly in white males (male-to female ratio of 6:1)

Several strong etiologic for the esophageal adenocarcinoma chronic gastric reflux, often in the presence of Barrett’s esophagus (replacement of the normal squamous epithelium of the distal esophagus by columnar mucosa) ,more commonly in obese individuals …. dysplastic columnar epithelium …. Adenocarcinomas

Before frank neoplasia :aneuploidy & p53 mutations in dysplastic epithelium 15% of esophageal adenocarcinomas overexpress the HER2/neu gene These adenocarcinomas behave clinically like gastric adenocarcinomas, although they are not associated with Helicobacter pylori infections

CLINICAL FEATURES Upper third of the esophagus (cervical esophagus) About 5% , 20% in the middle third, and 75% in the lower third. Squamous cell carcinomas and adenocarcinomas cannot be distinguished radiographically or endoscopically. Progressive dysphagia and weight loss of short duration are the initial symptoms in the vast majority of patients

Dysphagia initially occurs with solid foods and gradually progresses to include semisolids and liquids By the time these symptoms develop, the disease is already very advanced, because difficulty in swallowing does not occur until >60% of the esophageal circumference is infiltrated with cancer

Dysphagia may be associated with pain on swallowing (odynophagia), pain radiating to the chest and/or back, regurgitation or vomiting, and aspiration pneumonia The disease most commonly spreads to adjacent and supraclavicular lymph nodes, liver, lungs, pleura, and bone

Tracheoesophageal fistulas may develop, primarily in patients with upper and mid-esophageal tumors As with other squamous cell carcinomas, hypercalcemia may occur in the absence of osseous metastases, probably from parathormone-related peptide secreted by tumor cells

DIAGNOSIS Attempts at endoscopic and cytologic screening for carcinoma in patients with Barrett’s esophagus Esophagoscopy in all patients suspected of having an esophageal abnormality, to both visualize and identify a tumor and also to obtain histopathologic confirmation of the diagnosis

Because the population of persons at risk for squamous cell carcinoma of the esophagus (i.e., smokers and drinkers) also has a high rate of cancers of the lung and the head and neck region, endoscopic inspection of the larynx, trachea, and bronchi should also be carried out

s A thorough examination of the fundus of the stomach (by retroflexing the endoscope) is imperative as well The extent of tumor spread to the mediastinum and para-aortic lymph nodes should be assessed by CT scans of the chest and abdomen and by endoscopic ultrasound

Positron emission tomography scanning useful for distant metastatic disease, spread to mediastinal lymph nodes(radiation therapy fields)

TREATMENT Esophageal Cancer The prognosis is poor Approximately 10% of patients survive 5 years after the diagnosis; thus, management focuses on symptom control Surgical resection of all gross tumor (i.e., total resection) is feasible in only 45% of cases, with residual tumor cells frequently present at the resection marginspostoperative ,mortality rate 5% due to anastomotic fistulas, subphrenic abscesses, and cardiopulmonary complications

Endoscopic resections Chemotherapy Radiotherapy