Oncology – Upper gastrointestinal cancers
Esophageal cancer
Esophageal cancer is a malignant tumor that originates in the wall of the muscular tube that connects the pharynx to the stomach. Around 25 centimetres long, the oesophagus passes through the neck, thorax and diaphragm before reaching the oesogastric junction. It can be the site of two major histological types of cancer: squamous cell carcinoma, which develops from the squamous cells lining the upper and middle thirds of the oesophagus, and adenocarcinoma, which originates in the glandular cells of the lower third, most often against a background of Barrett's oesophagus - an intestinal metaplasia induced by chronic gastro-oesophageal reflux disease. These two forms differ profoundly in their risk factors, epidemiology, location and prognosis. Unfortunately, esophageal cancer is distinguished by its late diagnosis in the majority of cases: symptoms - dominated by progressive dysphagia, i.e. increasing difficulty in swallowing - often only appear at a stage when the tumour is already obstructing a significant part of the esophageal lumen. This late presentation explains why most esophageal cancers are diagnosed at an advanced stage, with an overall five-year survival that remains below 20 % for all stages combined, but can exceed 50 % when the tumor is detected at a localized stage. In Quebec, as in Canada as a whole, the incidence of esophageal adenocarcinoma has been rising steadily for several decades, in parallel with the progression of obesity and chronic gastro-esophageal reflux disease in the population.
Main histological types
The distinction between the two major histological types of esophageal cancer is fundamental, as it conditions the risk factors, tumor location, management, and prognosis:
| Features | Squamous cell carcinoma (SCC) | Adenocarcinoma (AC) |
|---|---|---|
| Cell origin | Malpighian cells (squamous epithelium) of normal esophageal mucosa | Glandular cells of intestinal metaplasia (Barrett's esophagus), transformation of squamous epithelium into intestinal columnar epithelium due to chronic acid reflux |
| Preferred localization | Upper and middle thirds of the esophagus (cervical and mid-thoracic esophagus) | Lower esophagus and gastroesophageal junction |
| Key risk factors | Smoking, excessive alcohol consumption, a diet low in fruits and vegetables, very hot beverages (mate), achalasia, history of cervical radiotherapy | Chronic gastroesophageal reflux disease (GERD), Barrett's esophagus, abdominal obesity, smoking, male sex, advanced age |
| Epidemiological profile | Predominant in developing countries and Central Asia; slightly decreasing in Western countries with the decline in smoking | Strongly increasing in Western countries since the 1970s-1980s; parallel to the obesity and GERD epidemic; primarily affecting white men over 60 years old |
| Relative Prognosis | Globally bleak prognosis for advanced stages; better than adenocarcinoma for early stages treated surgically. | Prognosis comparable to EC for advanced stages; better response to neoadjuvant chemotherapy in resectable stages |
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Barrett's esophagus is a precancerous lesion defined by the replacement of the normal squamous epithelium of the lower third of the esophagus by intestinal-type columnar epithelium, in response to chronic acid aggression from gastroesophageal reflux disease. It is present in approximately 10-15 % of patients with symptomatic chronic GERD. The risk of progression to adenocarcinoma is estimated at 0.1-0.3 % per year, but this risk increases considerably in the presence of high-grade dysplasia. Regular endoscopic surveillance (every 3-5 years depending on the degree of dysplasia) is recommended in patients with confirmed Barrett's.
Risk factors
The risk factors for esophageal cancer differ depending on the histological type, but some—notably smoking—are common to both forms:
| Risk factor | Type(s) concerned | Mechanism and risk level |
|---|---|---|
| Current or former smoker | CE and AC | Tobacco carcinogens directly damage the esophageal lining and potentiate the effects of acid reflux; the risk is multiplied by 2 to 5 depending on the duration and intensity of smoking; the risk gradually decreases after quitting but does not return to the level of non-smokers for 20 to 30 years. |
| Excessive alcohol consumption | Primarily CE | Alcohol is a potent esophageal carcinogen for EC; the risk is multiplied 5 to 10 times for heavy drinkers; the combination of alcohol and tobacco is synergistic with a risk multiplied up to 40 times compared to non-smokers and non-drinkers. |
| Chronic gastroesophageal reflux | AC primarily | Untreated or inadequately controlled chronic acid reflux causes repeated inflammation of the lower third of the esophagus, inducing Barrett's metaplasia and progressively increasing the risk of adenocarcinoma; weekly symptomatic GERD doubles the risk compared to the general population. |
| Abdominal obesity | AC | Abdominal obesity increases intra-abdominal pressure, promotes acid reflux and Barrett's esophagus; it is also associated with increased insulin and protumoral growth factor levels; the risk of adenocarcinoma is multiplied by 2 to 4 depending on BMI. |
| Barrett's esophagus | AC | Direct precancerous lesion; the risk of progression to adenocarcinoma is 0.1 to 0.3 % per year in the absence of dysplasia, but can exceed 6 % per year in cases of high-grade dysplasia; justifies regular endoscopic monitoring |
| Achalasia | CE | Esophageal motor dysfunction leading to chronic food stasis and mucosal inflammation; the risk of esophageal cancer is multiplied by 10 to 50 compared to the general population after 15 to 20 years of evolution. |
| Diet low in fruits, vegetables, and antioxidants | Primarily CE | Deficiency in vitamins A, C, E, and zinc, micronutrients that protect the esophageal lining; associated with a higher incidence in populations with low consumption of fresh vegetables |
| Consumption of very hot beverages (mate, hot tea) | CE | Classified as a probable carcinogen (Group 2A) by the IARC when consumed at temperatures above 65°C; repeated thermal injury to the mucous membranes promotes carcinogenic mutations. |
| Male sex and age | CE and AC | Men are 3 to 4 times more affected than women by adenocarcinoma and 2 to 3 times more by squamous cell carcinoma; peak incidence between 60 and 70 years old for both forms. |
Symptoms
Esophageal cancer is often asymptomatic in the very early stages. Symptoms usually appear when the tumor has grown large enough to narrow the esophageal lumen or invade adjacent structures:
- Progressive dysphagia—increasing difficulty swallowing—first solids, then semi-liquids, and finally liquids; it is the cardinal symptom of esophageal cancer, present in over 80 % of cases at diagnosis, but it only appears when the tumor obstructs at least 50 to 60 % of the esophageal lumen.
- Odynophagia — pain on swallowing — localized in the sternal or interscapular region, which may precede or accompany dysphagia
- Unintentional and significant weight loss, often severe at the time of diagnosis due to reduced food intake related to dysphagia; a sign of poor prognosis and a marker of advanced malnutrition
- Regurgitation — effortless return of undigested food into the mouth without vomiting — secondary to progressive mechanical obstruction of the esophagus
- Persistent chest pain, retrosternal or dorsal, which may radiate to the back or shoulder, indicating tumor extension to mediastinal structures
- Hoarseness or dysphonia due to damage to the left recurrent laryngeal nerve, whose anatomical path runs along the esophagus in the upper mediastinum; sign of advanced local extension
- Chronic cough or recurrent pneumonias due to tracheoesophageal or esophagobronchial fistula—an abnormal communication between the esophagus and the airways—a formidable complication of tumors invading the respiratory tract.
- Persistent hiccups, hematemesis (vomiting blood) or melena (black stools) due to tumor bleeding; upper gastrointestinal bleeding which can be inaugural in some cases
- General signs of metastatic evolution: profound fatigue, anemia, bone pain, palpable cervical lymphadenopathies (Virchow's node in the left supraclavicular area)
Diagnosis
The diagnosis of esophageal cancer is based on a structured clinical and paraclinical evaluation, with upper gastrointestinal endoscopy with biopsies as the cornerstone:
- Medical history and physical examination: dysphagia assessment (onset, progression, affected foods), risk factors, weight loss, and overall nutritional status; palpation of cervical and supraclavicular lymph node areas
- Upper digestive endoscopy (gastroscopy) with multiple biopsies: a reference examination that allows direct visualization of the tumor, precise localization and endoluminal extension, and obtaining tissue fragments for histopathological analysis to confirm the histological diagnosis and the tumor type.
- Endoscopic ultrasound (esophageal ultrasound-endoscopy): precise locoregional staging to assess the depth of esophageal wall infiltration (T stage) and the involvement of peri-esophageal lymph nodes (N stage); fundamental surgical information
- Thoraco-abdomino-pelvic scan with contrast injection: staging for distant spread, search for hepatic, pulmonary, adrenal, or bone metastases, and assessment of anatomical relationships with mediastinal structures
- PET Scan (18F-FDG Positron Emission Tomography): detection of distant metastases not visible on CT scan, evaluation of mediastinal lymph node extension; modifies therapeutic strategy in 10 to 20 % of cases compared to CT scan assessment alone
- Bronchoscopy with biopsies: indicated for tumors in the upper and middle third of the esophagus to rule out tracheobronchial invasion that would contraindicate surgical resection
- Nutritional assessment and general condition evaluation (WHO/ECOG score, albuminemia, prealbuminemia): determines the indication and feasibility of heavy oncological treatments (surgery, chemotherapy).
Classification and staging
The TNM (Tumor-Node-Metastasis) classification of the International Union Against Cancer (UICC) is used to stage esophageal cancer and guide therapeutic decisions:
| Stadium | Description | 5-year survival |
|---|---|---|
| Stage I (T1 N0 M0) | Tumor limited to the mucosa or submucosa, with no lymph node involvement or distant metastasis | 60 to 80 % - stage accessible to curative endoscopic or surgical treatment with excellent results |
| Stage II (T1-3 N0-1 M0) | Tumor invading the muscularis propria or adventitia, with or without involvement of 1 to 2 regional lymph nodes, without distant metastasis | 30 to 50 % — multimodal treatment (preoperative chemoradiotherapy followed by surgery); resectability still often possible |
| Stage III (T3-4 N1-2 M0) | Tumor invading adjacent structures (pleura, pericardium, diaphragm) or involving 3 to 6 regional lymph nodes, without distant metastasis | 15 to 30 % — induction chemoradiotherapy followed by surgical re-evaluation; resectability varies depending on treatment response |
| Stage IV (any T, any N, M1) | Presence of distant metastases (liver, lungs, bones, distal lymph nodes) regardless of local tumor status | Less than 5 % — palliative treatment; systemic chemotherapy, immunotherapy, and/or symptomatic treatment of dysphagia (esophageal prosthesis, palliative radiotherapy) |
Treatment options
Esophageal cancer management is multidisciplinary and depends closely on the histological type, tumor stage, location, and the patient's general condition:
| Treatment | Terms and conditions | Main indications |
|---|---|---|
| Endoscopic mucosal resection (EMR) | Endoscopic ablation of the tumor limited to the mucosa or superficial submucosa, without lymphovascular invasion | Very early stage I (T1a); treatment of high-grade dysplasia on Barrett's esophagus; minimally invasive technique with esophageal preservation and excellent oncological results in eligible stages |
| Surgery (esophagectomy) | Esophagectomy with reconstruction by esophagogastrostomy (stomach pull-up) or interposition coloplasty (colon interposition); minimally invasive approach (laparoscopy/thoracoscopy) or open surgery depending on the center | Resectable stages I to III; preceded by neoadjuvant chemoradiotherapy for stages II and III to reduce the tumor and treat micrometastases; operative mortality of 2-5% in expert centers % |
| Concomitant chemoradiotherapy (CRT) | Concurrent chemoradiotherapy (cisplatin + 5-fluorouracil or carboplatin + paclitaxel) and external beam radiation therapy to the tumor volume and draining lymph nodes | Neoadjuvant treatment before surgery (CROSS protocol for resectable adenocarcinomas and squamous cell carcinomas); curative exclusive treatment for unresectable cervical esophageal squamous cell carcinomas or in inoperable patients |
| Palliative chemotherapy | Platinum-based doublet (cisplatin or oxaliplatin) combined with 5-FU or capecitabine, with the addition of trastuzumab if HER2 is overexpressed for adenocarcinomas. | Unresectable metastatic or locally advanced cancers; aims to prolong survival and control symptoms; median survival of 10 to 14 months in the first line |
| Immunotherapy (checkpoint inhibitors) | Nivolumab (anti-PD-1) in combination with chemotherapy in the first-line metastatic setting; pembrolizumab depending on tumor PD-L1 status | Unresectable metastatic or recurrent esophageal cancer, in the first or second line depending on tumor biomolecular test results (PD-L1, MSI status); significantly improves overall survival compared to chemotherapy alone |
| Palliative treatment of dysphagia | Placement of a self-expandable metallic esophageal prosthesis (stent) via endoscopy, palliative decongestive radiotherapy, endoscopic dilation, feeding gastrostomy or jejunostomy | Unresectable metastatic or locally advanced cancers with disabling dysphagia; objective: restore food transit to improve quality of life and maintain nutritional status |
| Nutritional support | Enteral nutrition via nasogastric tube or percutaneous endoscopic gastrostomy (PEG), high-protein oral nutritional supplements | Systematic approach from diagnosis in case of malnutrition; essential before and during heavy treatments to maintain general condition and reduce surgical morbidity and treatment toxicity |
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The CROSS (ChemoRadiotherapy for Oesophageal cancer followed by Surgery Study) protocol has become the standard of care for resectable stage II and III esophageal cancers. It combines neoadjuvant chemoradiotherapy (carboplatin + paclitaxel + 41.4 Gy radiotherapy) followed by esophagectomy, and has demonstrated a significant improvement in overall survival compared to surgery alone, with a complete pathological response rate of approximately 30 % for adenocarcinomas and 49 % for squamous cell carcinomas.
Complications and sequelae of treatment
The treatment of esophageal cancer, particularly surgery and chemoradiotherapy, can lead to significant complications and functional sequelae that you should be aware of:
- Anastomotic esophageal fistula after esophagectomy — a connection between the esophagogastric anastomosis and the surrounding spaces — the most feared surgical complication, occurring in 10 to 20 % of cases depending on the series, sometimes requiring reoperation or radiological drainage
- Aspiration pneumonia and postoperative respiratory complications, favored by partial diaphragm paralysis and stomach herniation into the chest
- Dumping syndrome - accelerated gastric emptying causing malaise, sweating, and diarrhea after meals - secondary to pyloroplasty performed during gastric reconstruction
- Severe gastroesophageal reflux after esophagectomy due to the absence of the lower esophageal sphincter; requires strict dietary and lifestyle measures (fractionated meals, semi-sitting position, avoidance of acidic foods).
- Late anastomotic stenosis requiring repeated endoscopic dilatations to maintain satisfactory food transit
- Toxicities of chemoradiotherapy: painful acute radiation esophagitis, myelosuppression, platinum-related peripheral neuropathy, nausea, and persistent fatigue
- Chronic malnutrition and nutritional deficiencies (vitamin B12, iron, calcium, fat-soluble vitamins) requiring long-term supplementation and specialized dietary monitoring
Prevention and screening
In the absence of a systematic screening program for the general population in Quebec, primary prevention and surveillance of at-risk groups are the main strategies to reduce mortality related to esophageal cancer:
- Smoking cessation: most effective primary prevention measure for both histological types; risk gradually decreases after cessation but remains higher than in non-smokers for 20 to 30 years.
- Reduced alcohol consumption, particularly in combination with tobacco, whose carcinogenic effect is strongly synergistic on the esophageal mucosa
- Active management of chronic gastroesophageal reflux disease with dietary and lifestyle measures, proton pump inhibitors, and regular monitoring in persistently symptomatic patients
- Body weight control and treatment of abdominal obesity, an independent risk factor for esophageal adenocarcinoma
- Regular endoscopic surveillance of patients with confirmed Barrett's esophagus, according to the recommendations of gastroenterology societies (intervals varying from 3 to 5 years depending on the presence and degree of dysplasia)
- Preemptive treatment of high-grade dysplasia in Barrett's esophagus by radiofrequency ablation (RFA) or endoscopic resection, before transformation into invasive adenocarcinoma
- Diet rich in fresh fruits and vegetables, providing antioxidants (vitamins C, E, beta-carotene) that protect the esophageal lining
- Avoid drinking very hot beverages (maté, tea) at temperatures above 65°C, classified as probable carcinogens by the IARC.
Signs requiring immediate medical attention
Any progressive dysphagia—increasing difficulty swallowing solids, then semi-liquids—appearing in an adult over 50 years of age, with or without unintentional weight loss, must be promptly evaluated by a physician. This symptom is a major red flag that requires an urgent diagnostic gastroscopy to rule out esophageal cancer or other severe organic pathology of the upper digestive tract. Persistent odynophagia, unexplained chest pain, food regurgitation, and recent onset hoarseness are other warning signs that warrant a rapid consultation, particularly in patients with risk factors (smoking, alcohol consumption, chronic GERD, history of Barrett's esophagus).
In the presence of upper gastrointestinal bleeding (vomiting blood or black stools), complete dysphagia to liquids, or respiratory distress associated with swallowing disorders, immediately call 911 or go to the nearest emergency room. For any persistent dysphagia or upper gastrointestinal symptoms without signs of immediate emergency, a consultation at Clinique Omicron allows for a rapid medical evaluation and referral to appropriate gastroenterological or oncological resources.
Consult at Clinique Omicron
Clinique Omicron provides initial assessment of upper digestive symptoms, prescription of biological assessments, and referrals to specialized gastroenterology and digestive oncology resources across its multiple service points in Quebec and via telemedicine. A physician or nurse practitioner (NP) can assess your symptoms, prescribe appropriate investigations, and coordinate an urgent referral to a gastroenterologist for gastroscopy if a red flag symptom is identified. To book an appointment at one of our service points or via telemedicine, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not substitute for professional medical advice. Consult a doctor for any persistent digestive symptoms, abnormal results, or health decisions.
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