Squamous cell carcinoma is the most common tumor of the esophagus, accounting for approximately 95% of esophageal cancers worldwide and 60% of esophageal cancers in the United States. Unless detected in its earliest stages, it is usually fatal in less than 5 years. Histologically, the tumor is composed of sheets of polygonal or polyhedral cells with varying degrees of differentiation. Well-differentiated tumors contain features such as keratin pearls and intercellular bridges, whereas poorly differentiated tumors have marked nuclear and cellular pleomorphism. The majority of tumors, however, are moderately differentiated. Macroscopically, 60% of these lesions are fungating intraluminal growths, 25% are ulcerative lesions associated with extensive infiltration of the adjacent esophageal wall, and 15% are infiltrating. Approximately 8% of tumors occur in the cervical esophagus, 55% in the upper and midthoracic segments, and 37% in the lower thoracic segment (Orringer, 1997).

Adenocarcinomas can arise at any level but are located most often at or near the gastroesophageal junction. Histologically, various degrees of glandular differentiation are noted, but well-differentiated tumors predominate. Esophageal adenocarcinoma is typically flat or ulcerated, although about one third of lesions are polypoid or fungating.

Several other rare types of esophageal malignant tumors occur, and all have a poor prognosis. Anaplastic small cell (oat cell) carcinoma accounts for fewer than 2% of esophageal cancers. Like their pulmonary counterparts, they arise from the APUD cell system and demonstrate neurosecretory granules on electron microscopy. Malignant melanoma is exceedingly rare and constitutes less than 0.1% of esophageal malignancies. The tumor is more common in men and is clinically indistinguishable from other esophageal neoplasms. Adenoid cystic carcinoma typically occurs as a middle-third esophageal tumor and is usually discovered late in its course. Carcinosarcoma of the esophagus (also known as pseudosarcoma, spindle cell carcinoma, or polypoid carcinoma) is a tumor with histologic features of both squamous cell carcinoma and malignant spindle
cell sarcoma. Found primarily in the distal two thirds of the esophagus, it can grow large (10 to 15 cm) (Xu et al, 1984, Orringer, 1997). Sarcomas of the esophagus are rare, but a number of variants have been described. These include leiomyosarcoma, fibrosarcoma, rhabdomyosarcoma, liposarcoma, and malignant mesenchymoma. Primary malignant lymphoma is also infrequent but is occasionally reported in patients with AIDS (Moses et al, 1995). Finally, involvement of the esophagus by another primary tumor, either by direct extension or metastatic spread, has been reported with cancers of the breast, lung, liver, kidney, prostate, and stomach (Kadakia et al, 1992; Vansant & Davis, 1971; Nussbaum & Grossman, 1976).

Dysphagia and weight loss are the initial symptoms of carcinoma of the esophagus in 90% of patients (Table 24-3). Unfortunately, these are late symptoms in the natural history of the disease. Because of its distensibility, difficulty in swallowing does not occur until at least half the circumference of the esophagus has been infiltrated by cancer (Skinner, 1976). By this time, the tumor may have grown to a significant size, with local invasion or metastases. Occasionally, the onset of dysphagia is sudden, but most patients complain of an ill-defined retrosternal discomfort or a vague difficulty in swallowing for the preceding 3 to 6 months. Although most patients can localize the site of obstruction, this does not always correlate with the actual location of the tumor. Odynophagia (painful swallowing) occurs in more than 20% of patients and may be the only presenting symptom. Weight loss is common, but severe weight loss and cachexia are infrequently seen and are usually indicative of locally advanced or widespread disease. Patients may also experience regurgitation of undigested food, epigastric pain, or aspiration pneumonia.

Advanced lesions may present with a variety of symptoms such as hematemesis, melena, superior vena cava syndrome, cough from a bronchoesophageal or tracheoesophageal fistula, hemoptysis, or problems related to nerve involvement (ie, Horner’s syndrome or paralysis of the recurrent laryngeal or phrenic nerve) (Akiyama, 1990; Roth et al, 1997). Aortoesophageal fistula is a rare but lethal complication. Other signs of unresectable malignant disease may be found with malignant pleural effusion or malignant ascites.

Apart from features of recent weight loss, the physical examination is often unremarkable, and the diagnosis of esophageal cancer will depend on radiographic or endoscopic data. However, the physical examination should encompass a thorough search for evidence of metastases. Supraclavicular or cervical lymph nodes should be sought and samples taken for biopsy if palpable. Enlargement of the left gastric, celiac, and retropancreatic nodes may be palpable in thin or cachectic patients, and there may be hepatomegaly in patients with liver metastases. Other evidence of intra-abdominal disease includes the presence of an epigastric mass, ascites, enlarged ovaries (Krukenberg tumors), or a Blumer’s shelf on rectal examination (Fok & Wong, 1996). Documentation of metastatic disease establishes the presence of a stage IV tumor.

Squamous cell carcinoma of the esophagus is an aggressive tumor. It tends to infiltrate locally, involving adjacent lymph nodes and metastasizing widely by lymphatic or hematogenous routes. Lack of an esophageal serosal layer tends to favor local tumor extension into such structures as the pericardium, aorta, tracheobronchial tree, diaphragm, and left recurrent laryngeal nerve. Lymph node metastases are present in at least 75% of patients at the time of diagnosis. Distant spread to the liver and lung is common. The overall prognosis of invasive squamous cell carcinoma is poor, with only 5% to 12% of patients surviving 5 years. Extraesophageal tumor extension is present in 70% of cases at the time of diagnosis, and the 5-year survival rate is only 3% when lymph node metastases are present, compared with 42% when there is no lymph node spread (Orringer, 1997).

As is the case with squamous cell carcinoma, adenocarcinoma of the esophagus exhibits aggressive behavior, with frequent transmural invasion and lymph node metastases. Distant spread is common, with the liver and lung most frequently involved. The 5-year survival rate for esophageal adenocarcinoma is only 0% to 7%, with the presence of lymph node metastases significantly decreasing survival (Orringer, 1997).

Once the diagnosis of esophageal carcinoma has been established histologically, staging of the tumor is the next critical step in determining which therapeutic option is appropriate.

Computed tomography (CT) of the chest and upper abdomen is now the standard noninvasive technique for staging esophageal carcinoma. It may be of value in determining surgical
resectability or planning for radiation therapy or endoscopic palliation. CT scanning permits evaluation of esophageal wall thickness, mediastinal invasion, and the presence of regional or distant metastases. It is particularly useful in assessing local extension of disease and its relation to adjacent structures, especially when oral contrast medium is used. It is less accurate in assessing the degree of periesophageal lymph node involvement and often underestimates the length of the esophageal lesion.

Experience with magnetic resonance imaging (MRI) seems to indicate that it does not have any particular advantage over CT and shares many of its limitations. A major problem with MRI is lack of a suitable intraluminal contrast agent. A direct comparison of CT and MRI found a comparable accuracy in predicting resectability, with both sensitivity and specificity of 85% (Takashima et al, 1991; Krevsky, 1995).

Endoscopic ultrasound (EUS) can define the depth of tumor wall invasion and associated paraesophageal lymph nodes. The use of EUS may be limited if there is an obstructing tumor that cannot be traversed by the ultrasound probe. In patients in whom the probe can be positioned within the esophageal lumen involved by tumor, however, this procedure has an 86% accuracy in defining involved mediastinal lymph nodes (Orringer, 1997).

Depending on the location of the tumor, some patients may require additional staging modalities such as mediastinoscopy, bronchoscopy, laparoscopy, thoracotomy, or thoracoscopy. Bronchoscopy may be useful in patients with carcinomas of the upper and middle third of the esophagus to evaluate for airway invasion. Endoscopic evidence of invasion to the tracheobronchial tree precludes a safe esophagectomy. Similarly, laparoscopic and thoracoscopic staging of esophageal cancer has been found to be advantageous. Preliminary results indicate that with its use, correct staging of esophageal tumors approaches 90%.

Surgical resection is the primary treatment modality for patients with carcinoma of the esophagus in the absence of known metastatic disease or medical contraindications to surgery. It is the only proven curative single-treatment modality for esophageal cancer and remains the gold standard by which all other therapeutic modalities are measured. Unfortunately, only half of patients have resectable disease at the time of presentation. The goal of surgical resection is the eradication of all disease, including regional lymph nodes, while relieving dysphagia and maintaining gastrointestinal continuity. Esophageal resection with lymphadenectomy offers the best chance for long-term survival in these patients, with many achieving 20% 5-year survival rates (Lee & Miller, 1997).

There are a variety of operative procedures used for the resection of esophageal cancers and subsequent reconstruction of the alimentary tract. The choice of procedure depends on many factors, including the preference of the surgeon, the location of the tumor, the patient’s age and physiologic fitness, and the extent of disease on EUS and intraoperative staging. Of these, location of the tumor and the surgeon’s preference are probably the two most important.

The most radical procedure is the en bloc resection. If preoperative staging is favorable, this procedure is undertaken with curative intent. The objective of en bloc resection is complete removal of the tumor with wide margins, together with most of the esophagus, adjacent connective tissue, and lymph nodes. Reconstruction of the gastrointestinal tract is usually accomplished with a gastric pull-up, but small bowel or colon can be substituted if necessary.

Regardless of the procedure used, surgical resection can be a formidable undertaking. Morbidity and mortality rates can be significant and are mainly caused by cardiopulmonary complications. A well-rehearsed team of experienced surgeons, anesthesiologists, intensivists, and support staff is critical for a successful outcome.

Although squamous cell carcinoma is generally believed to be radiosensitive, radiation therapy as a single modality of treatment seldom achieves cure in patients with carcinoma of the esophagus. The 5-year survival rate is only 6% (Earlam & Cunha-Melo, 1980). Locoregional failure has been the main limitation and can be expected in 60% to 80% of patients (Axelrad & Fleischer, 1998). Despite these results, radiation is an important method of nonoperative palliation and provides relief of dysphagia in approximately 80% of patients, one half of whom will remain free of dysphagia until the time of death (DeMeester, 1997).

Endoluminal radiation therapy (brachytherapy) works by implanting a radioactive source directly at the tumor bed. Delivery of radiation by this means theoretically provides maximal effect to the tumor itself, with minimal risk to surrounding tissues. A complete or partial response has been seen in more than 90% of patients, and more than 90% experience significant relief of dysphagia (DeMeester, 1997). Unfortunately, nearly half of patients experience moderate to severe complications that require further therapy. Additional evaluation is therefore required to determine the ultimate role of this modality in the treatment of esophageal cancer.

Unlike surgery and radiation therapy, systemic chemotherapy has a theoretical advantage in treating esophageal cancer because most patients present with widespread systemic disease. Several drugs have been used against esophageal carcinoma, but when administered as single agents the responses are usually partial and short-lived. This has prompted an evaluation of combination chemotherapy; most protocols include cisplatin in combination with 5-fluorouracil, bleomycin, methotrexate, and vindesine. Unfortunately, with the exception of the potential to improve resectability, none of these regimens has proven effective in providing local control or improving survival.

Since the late 1970s, esophageal cancer trials have focused on adding chemotherapy to radiation therapy or surgical resection. The rationale is to control distant disease while dealing directly with the locoregional tumor. There is also the suggestion that certain chemotherapeutic agents may act as radiation sensitizers,
thereby enhancing the efficacy of radiation therapy. At present, several ongoing studies are evaluating this form of therapy. Although surgical resectability has been improved, a clear survival advantage has not been seen. Most authors also report significant morbidity and mortality rates. Hence, there is no role for this form of therapy outside of a formal protocol.

Because most patients with esophageal cancer present with advanced disease, curative treatment is generally not possible and palliation is the primary goal. Palliative options include surgery, radiation therapy, chemotherapy, endoscopic therapy, or supportive management only.

Mechanical dilatation is a simple and inexpensive modality that can afford relief of dysphagia in up to 70% of patients. Maloney (mercury-filled rubber) bougies or Eder-Puestow (metal olives) or Savary-Gilliard (tapered plastic) dilators have all been used successfully. Unfortunately, the procedure has a 15% failure rate and relief of dysphagia is short-lived. Complications, such as perforation and bleeding, occur in 2% to 10% of patients (DeMeester, 1997). Dilatation is useful, however, as the initial step in several alternative nonoperative palliative techniques.

Transoral intubation with a prosthesis is the most popular worldwide method for palliating advanced esophageal cancer. Advantages include simplicity, short hospitalization, and immediate improvement in dysphagia. The overall reported mortality rate ranges from 3% to 15%, and a 20% to 60% complication rate has been reported (DeMeester, 1997; Orringer, 1997). Although most patients have improved swallowing, only 10% to 50% can eat solid food. The average length of survival after palliative intubation for esophageal carcinoma is less than 6 months (Orringer, 1997). Recently, self-expanding metallic stents have been introduced in an effort to improve the ease of insertion and to lessen the complications of the standard prosthesis.

Endoscopic laser therapy is most commonly performed with a Nd-Yag (neodymium-yttrium-aluminum-garnet) laser because of its deep tissue penetration and reliable hemostatic property. Relief of dysphagia occurs in 70% to 85% of patients, but multiple treatments are usually required. The dysphagia-free period is only 6 to 8 weeks.

Photodynamic therapy has recently emerged as a more selective form of laser treatment. This involves injecting a hematoporphyrin derivative, which is selectively retained by neoplastic and reticuloendothelial tissues. Argon dye lasers or gold vapor lasers are typically used to activate the hematoporphyrin derivative, leading to release of free oxygen radicals and cell death. Limited experience with photodynamic therapy is available for esophageal cancer. Although potentially curative for early tumors, possible complications, such as stricture, hemorrhage, and perforation, have not been adequately assessed (Krevsky, 1995; Likier et al, 1991).

Injection therapy has been performed with a variety of agents, such as absolute alcohol and sodium morrhuate (Payne-James et al, 1990). The technique involves passing an endoscope beyond the tumor and injecting 0.5- or 1-mL aliquots of sclerosant directly into the tumor. Tumor necrosis and restoration of luminal patency have been achieved. The experience, however, has not been extensive, and long-term results are inconclusive.

The vast majority of gastric malignancies are carcinomas. The incidence of gastric carcinoma increases with age. The current view is that carcinomas of the stomach have a long latency period that is often associated with recognizable precancerous lesions. Gastric acid inhibits the growth of bacteria within the stomach. Bacteria have been demonstrated to generate carcinogenic nitrosamine compounds from salivary and dietary nitrates. Conditions that lead to gastric achlorhydria may therefore predispose to gastric cancer. Intestinal metaplasia and chronic atrophic gastritis are two conditions associated with achlorhydria that have been linked with gastric cancer in correlation studies. Both chronic atrophic gastritis and intestinal metaplasia are more prevalent in areas with high rates of gastric cancer (Dobrilla et al, 1994).

Helicobacter pylori is a recently discovered microaerophilic, gram-negative, spiral-shaped bacterium that commonly has been found in patients with acute and chronic inflammation of the gastric antrum. Because of the known association between gastritis and gastric cancer, there has been speculation about the role of H. pylori in the causation of gastric cancer, and several large cohort studies have confirmed this suspicion. However, H. pylori infection is common in the general population, and most persons with H. pylori will not develop cancer (Mera, 1995; Graham et al, 1995).

One reason for the lack of success in indicting a particular agent or sequence as the definitive cause of gastric carcinoma is the large number of strongly associated factors that have been studied. The sharp fall in gastric cancer in this country began in 1930, shortly after the passage and enforcement of the Pure Food and Drug Act of 1927. This realization contributed to a search for a nutritional cause of gastric cancer that began in the 1950s and continues today. In the course of that work, it has been found that diets rich in smoked or pickled foods containing preformed N-nitroso compounds or nitrites, respectively, (Neugut et al, 1996) or high consumption of salted foods or alcohol (Francheschi & LaVecchia, 1994) are closely correlated with an increased lifetime risk of developing gastric carcinoma. Conversely, diets high in raw fruits and vegetables and antioxidants such as vitamins C, E, and beta-carotene (Correa, 1995; Hwang et al, 1994) are strongly correlated with a reduction in the risk of gastric carcinoma (Correa, 1995).

Two histologically distinct types of gastric carcinoma have been described (Lauren, 1965). The distinction between intestinal and diffuse types of carcinoma continues to have relevance today, not only as a descriptive device but because the two types are thought to have different origins, risk factors, population distributions, and prognoses (see the section on epidemiology).

Intestinal-type gastric tumors are true adenocarcinomas. They are characterized by a proliferation of atypical glandular elements containing large numbers of mucin-containing goblet cells. There is commonly a loss of polarization with a varying amount of nuclear atypia in the cells lining these glandular formations. Histologically, the diffuse type of gastric carcinoma largely lacks recognizable glandular elements and consists predominately of stromal tissue. The hallmark of this type of tumor is the large number of signet-ring cells with deeply staining basophilic nuclei. Grossly, either of these tumors may be raised, flat, or ulcerated on endoscopic examination; in addition, intestinal-type tumors may be polypoid. The gross appearance of the lesion has little association with the true depth of invasion.

Although 92% to 98% of all gastric malignancies are adenocarcinomas, there are also three relatively uncommon tumors. The first of these is the primary gastric lymphoma. This represents 3% to 4% of all gastric malignancies and is predominately of the non-Hodgkin’s type. Gastric lymphomas arise from the mucosal-associated lymphoid tissue. The majority of these tumors are composed of B-lymphocytes and have long growth cycles, tending to remain within the stomach (Isaacson & Spencer, 1996). Primary T-cell lymphomas are much less common and tend to be more aggressive in their growth and spread. Finally, although histiocytic lymphomas and true Hodgkin’s disease of the stomach have been reported in the literature, the incidence of these tumors is vanishingly small. Like lymphoma at most other sites in the body, gastric lymphomas tend to be highly responsive to radiation and chemotherapy. Nonetheless, surgical excision, where possible, remains an important part of the therapeutic regimen.

Prognosis for all of these tumors is related to the stage of the disease at diagnosis and the histologic type of tumor. Early B-cell lymphomas are reported to have a 75% 5-year survival rate and late-stage T-cell lymphomas as low as a 32% 5-year survival rate (Aozasa et al, 1988).

Gastric leiomyosarcomas constitute approximately 1% to 2% of all gastric malignancies. These smooth muscle tumors can grow to large size, protruding primarily into the peritoneal cavity rather than into the lumen of the stomach. They are usually slow-growing tumors and it can be challenging to distinguish them from benign leiomyomas. Often the definitive diagnosis of malignancy can be made only after surgical resection, when the entire specimen is available for examination. In most cases, though, size is a good indicator of malignancy: tumors less than 4 cm are likely to be benign, those exceeding 6 cm malignant. Five-year survival rates after surgical excision have been reported to be as high as 55% for patients with smaller tumors but 30% for those with tumors greater than 8 cm.

The third major noncarcinoma tumor is the gastric carcinoid tumor. These endocrine tumors have been estimated to represent 3% of all gastric tumors. Although histologically similar, the gastric carcinoids are divided into two classes based on the prevailing gastric mucosa (Bordi, 1995). The first class is the classic carcinoid tumor, which is strongly associated with chronic atrophic gastritis and Zollinger-Ellison syndrome. The hypersecretion of gastrin seen in these patients is thought to cause hyperplasia of enterochromaffin cells, resulting in carcinoid tumors. The second class of carcinoid-type tumors arises in histologically normal gastric mucosa without detectable antecedent endocrine abnormalities. These spontaneous or sporadic carcinoids are, in fact, true neuroendocrine carcinomas.

The gastritis-associated class of gastric carcinoid tumors is usually confined to the mucosa. Small tumors of this class are amenable to repeated endoscopic fulguration and treatment of the underlying gastric pathology, whereas larger tumors require surgical excision. The sporadic class is often poorly differentiated and more likely to metastasize to regional lymph nodes and distant sites. These tumors are rarely suitable for surgical intervention and have a markedly poor prognosis (Akerstrom, 1996).

Gastric cancer is characteristically silent in its early stages. This contributes to the late stage at which most gastric cancers are diagnosed. Characteristic symptoms of gastric tumors such as early satiety, pain, and obstruction appear late in the course of the disease. These symptoms herald extensive involvement of the gastric body or pylorus. Occasionally, large extraluminal tumors may be palpable through the abdominal wall. Linitis plastica (leather-bottle stomach) is a classic sign associated with tumor infiltration throughout the stomach. It manifests as extremely early satiety resulting from a dramatic decrease in gastric distensibility and can often be palpated through the abdominal wall in the right upper quadrant.

Although advanced gastric cancer continues to have a uniformly poor prognosis, when gastric cancer is found and treated early, survival rates can be quite high. In 1993, Wanebo et al reviewed the American experience with gastric cancer from 1982 to 1992. The results of this study found that 5-year survival rates after surgical resection with curative intent depended on stage. Patients with stage I tumors had a 50% 5-year survival, with stages II, III, and IV carrying survival rates of 29%, 13%, and 3%, respectively. An important point revealed by this study was that more than two thirds of these patients had advanced disease (stage III or IV) at the time of diagnosis. Further, most of these patients did not receive radical lymph node dissection. Local recurrence occurred in 40% of patients and distant disease in 60%.

Reports on the long-term survival of patients undergoing resection for cure and intraoperative radiotherapy are becoming available for review from many centers. The 5-year survival rate was improved in patients with stage II, III, and IV disease from 62%, 37%, and 0%, respectively, to 83%, 62%, and 14%, respectively, using mid- to high-dose radiation (28 to 36 Gy) in selected patients (Abe et al, 1987).

The first-line treatment of newly diagnosed gastric cancer continues to be surgical excision. In most cases, total gastrectomy with attempts to remove all involved tissues back to microscopically clean margins is the ultimate goal. Such an operation is currently not possible for the majority of patients presenting with locally advanced or metastatic cancers (Dalton & Eisenberg, 1994). The standard surgical treatment in Japan has differed from that in Western countries. Japanese surgeons are generally more aggressive, making use of systemic or radical lymph node dissection. The results of such surgery have yielded significant improvements in long-term survival rates in Japanese populations. Attempts to reproduce these results in Europe and the United States have not been as successful. At first, this was attributed to lack of familiarity with the surgical technique, but with increasing Western experience with radical gastrectomy, it seems that at least a portion of the Japanese success may be related to differences in the pathophysiologic variants of gastric cancer between Japan and Western countries (Maruyama et al, 1996). These differences may render the Japanese variant more susceptible to surgical excision.

The radical nature of surgical gastrectomy for gastric cancer (whether Japanese or Western) is fraught with intra- and postoperative dangers. These are often long procedures associated with massive intra- and extracellular fluid shifts. Patients are frequently malnourished and compromised by pulmonary or cardiac abnormalities. In addition, many of these operations involve removal of the pylorus or pancreas, leaving the patient prone to dumping syndrome or postoperative diabetes (Averbach & Jacquet, 1996). Clearly, such treatment requires detailed preoperative discussion to ensure that the patient understands both the nature of the disease process and the risks of the surgical resection.

To date, no chemotherapeutic agent, either alone or in combination, has proven effective as the sole treatment for gastric cancer. As a consequence, recent research has turned toward the use of chemotherapy in conjunction with surgery. Adjuvant combination chemotherapy has shown some efficacy after curative resection, but an overall survival advantage has yet to be demonstrated (Schipper & Wagener, 1996), and toxicity can be significant. These agents affect all rapidly proliferating cell populations. This includes bone marrow suppression, with its immunocompromising effect; gastrointestinal mucosal sloughing, with concomitant malabsorption; and impairments in wound healing and regeneration of skin appendages, resulting in, among other things, hair loss.

Another strategy under study is the use of neoadjuvant therapy before surgical resection (Fink et al, 1995). Downstaging of tumor preoperatively may make curative resection more feasible. Initial studies have indicated improved tumor-free survival after neoadjuvant chemotherapy and primary resection with lymphadenectomy versus resection and lymphadenectomy alone (Nakajima, 1995). Further studies in this area are required to define which patients will benefit from this technique.

Finally, true multimodal therapy for gastric cancer is under study at various centers (Jessup et al, 1993). This approach makes use of neoadjuvant chemotherapy to shrink the tumor, followed by resection and lymphadenectomy with intraoperative radiotherapy. Although this therapy is promising, long-term survival data are not yet available and are eagerly awaited.

Early in the history of gastric cancer research, a link was identified between certain dietary components (eg, smoked meats, salted foods, alcohol) and an increased incidence of gastric carcinoma. More recently, an association between common dietary antioxidants and a decreased risk of gastric cancer has been studied. Experimental and epidemiologic data to this effect suggest that vitamin C and carotenoids may be of value in preventing gastric cancer when taken consistently in adequate amounts. The evidence in favor of vitamin E and selenium is not as strong (Kono & Hirohata, 1996). These data support the recommendation of a diet high in fresh fruits and vegetables, consistent with current FDA recommendations. There is littlecredible
support for megadosage or specific supplementation of these nutrients beyond that provided naturally (Buiatti & Munoz, 1996).

Benefits in prevention of cancer have also been ascribed to various teas and native foods. The current literature indicates that these benefits are probably a result of the combined effect of lifestyle, balanced diets, and varying population risks rather than any single dietary substance.