Health Questions and Answers


October 7th, 2017

Who gets esophageal cancer?
Squamous cell cancer of the esophagus occurs in the 40- to 60-year-old age group and is seen mainly in men. The incidence is increased in Africa, China, Russia, Japan, Scotland, and the Caspian region of Iran. In the U.S. the nonwhite male population is at increased risk. Adenocarcinoma of the esophagus tends to occur in obese white men.

List of risk factors for esophageal cancer.

  • Excessive alcohol and/or tobacco use
  • Native Bantu beer (southern Africa)
  • Chronic hot beverage ingestion
  • Lye ingestion: > 30% of cases develop esophageal cancer
  • Tylosis: > 40% of cases develop esophageal cancer
  • Achalasia
  • Plummer-Vinson syndrome
  • Nontropical sprue
  • Prior oral and pharyngeal cancer
  • Occupational exposure to asbestos, combustion products, ionizing radiation
  • Other occupational exposure: waiters, bartenders, metal workers, and construction workers
  • Decreased dietary intake of fruits and vegetables throughout adulthood

Discuss the incidence of adenocarcinoma of the esophagus.
The incidence of esophageal adenocarcinoma has greatly increased over the past two decades. Adenocarcinoma of the esophagus is now more prevalent than squamous cell carcinoma in the United States and Western Europe, with most tumors located in the distal esophagus and esophagogastric junction.

What are the risk factors for adenocarcinoma of the esophagus?
Adenocarcinoma of the esophagus in a younger population without the traditional risk factors has been associated with chronic esophagitis, reflux disease, and Barrett’s esophagus.

How does esophageal cancer present?

  • Dysphagia: first with solids, then with liquids
  • Weight loss
  • Regurgitation
  • Occult GI bleeding
  • Aspiration pneumonia
  • Cough
  • Fever
  • Choking
  • Hoarseness
  • Chest pain on swallowing
  • Gastroesophageal reflux disease (GERD)

How should esophageal cancer be treated?
The only curative procedure is surgery. However, fewer than half of patients are operable at the time of presentation, and of these, only one half to two thirds have tumors that are resectable. Nonsurgical patients are treated with combined chemoradiotherapy or palliative measures alone if their performance status is too poor for active therapy. Some evidence indicates that survival in patients with adenocarcinoma of the esophagus is improved with preoperative combined chemotherapy and radiotherapy. Ongoing trials are investigating whether the outcome with chemoradiotherapy is equivalent to that of surgery.

List of risk factors for gastric cancer.

  • Precursor conditions
  • Chronic atrophic gastritis and intestinal metaplasia
  • Pernicious anemia
  • Partial gastrectomy for benign disease
  • H. pylori infection
  • Ménétrier’s disease
  • Gastric adenomatous polyps
  • Barrett’s esophagus
  • Genetic and environmental factors
  • Family history of gastric cancer
  • Blood type A
  • Hereditary nonpolyposis colon cancer syndrome
  • Low socioeconomic status
  • Low consumption of fruits and vegetables
  • Consumption of salted, smoked, or poorly preserved foods
  • Cigarette smoking (?)

Discuss the role of oncogenes and tumor-suppressor genes in gastric cancer.
The role of oncogenes and tumor suppressor genes is currently being elucidated. Allelic deletions of the MCC, APC, and p53 tumor-suppressor genes have been reported in 33, 34, and 64% of gastric cancers, respectively. Disparities between mutations associated with the intestinal and diffuse types of gastric cancers may account for their different natural histories.

List of the symptoms of gastric cancer at the time of diagnosis

Symptoms Frequency %
Weight loss 61.6
Abdominal pain 51.6
Nausea 34.3
Anorexia 32.0
Dysphagia 26.1
Melena 20.2
Early satiety 17.5
Ulcer- type pain 17.1
Lower-extremity edema 5.9

List the risk factors for pancreatic cancer.

  • Smoking (2-3 times increased risk)
  • Diet high in calories, fat, and protein, low in fruits and vegetables
  • Diabetes mellitus
  • Chronic pancreatitis
  • Surgery for peptic ulcer disease
  • Occupational exposure to 2-naphthylamine and petroleum products (> 10 yr increases risk to 5:1), dichlorodiphenyltrichloroethane (DDT)

What hereditary syndromes increase the risk for pancreatic cancer?
Familial pancreatic cancer, hereditary pancreatitis, familial adenomatous polyposis syndrome, familial atypical multiple mole melanoma syndromes (hereditary dysplastic nevus syndrome), BRCA2, and Peutz-Jeghers syndrome.

Do gender and ethnicity affect the risk for pancreatic cancer?

  • Males > females
  • Blacks > whites

List the symptoms and signs of pancreatic cancer based on tumor location.

Symptoms/Signs Head Body/Tail
Weight loss 92% 100%
Jaundice 82% 7%
Pain 72% 87%
Anorexia 64% 33%
Nausea 45% 43%
Vomiting 37% 37%
Weakness 35% 43%
Palpable liver 83%
Palpable gallbladder 29%
Tenderness 26% 27%
Ascites 19% 20%

Adapted from Moossa AR, et al: Tumors of the pancreas. In Moossa AR, et al (eds): Comprehensive Textbook of Oncology, 2nd ed. Baltimore, Williams & Wilkins, 1991, p 964.

How is the diagnosis of pancreatic cancer confirmed?
If a lesion in the pancreas is seen, CT or EUS-guided fine-needle aspirate can confirm the diagnosis of malignancy. Additional staging includes routine laboratory studies, chest x-ray, and other tests as directed by the history and physical. If there is bone pain or elevated alkaline phosphatase, then bone scan should be done.

What is the most important risk factor for hepatocellular carcinoma?
Underlying cirrhosis appears to be the most important risk factor for the development of hepatocellular carcinoma. Macronodular cirrhosis is found in 85% of patients with hepatocellular carcinoma. In the United States, alcoholic cirrhosis is an important cause. Chronic infection with hepatitis B or C viruses is the major etiologic agent for human hepatocellular carcinoma around the world since it causes the development of cirrhosis.

What may other risk factors be involved?
Extensive studies of aflatoxins in human foods in Africa suggest a quantitative relationship between average human aflatoxin consumption and the incidence of hepatocellular carcinoma. In a small proportion of hepatocellular carcinomas, the cause appears to be related to other factors, including other hepatotropic viruses, chemicals, mycotoxins, and hepatic parasites. The relative importance of these factors seems to vary among populations.

List the common presenting features of primary tumors of the liver.

  • Asthenia (85-90%)
  • Hepatomegaly (50-100%)
  • Abdominal pain (50-70%)
  • Jaundice (45-80%)
  • Fever (9.5%)

List the unusual ways in which hepatomas may present.

  • Hemoptysis secondary to pulmonary metastases
  • Rib mass secondary to bony metastasis
  • Encephalitis-like picture secondary to brain metastasis
  • Heart failure secondary to cardiac metastasis and thrombosis of the inferior vena cava
  • Priapism secondary to soft-tissue metastasis
  • Bone pain and pathologic fractures secondary to bony metastases

What are the systemic manifestations of hepatocellular carcinoma?

  • Endocrine: erythrocytosis, hypercalcemia
  • Nonendocrine: hypoglycemia, porphyria cutanea tarda, cryofibrinogenemia, osteoporosis, hyperlipidemia, dysfibrinogenemia, alpha-fetoprotein synthesis

Which environmental factors are thought to be related to the development of colon cancer?
Abundant epidemiologic data support the link between environmental factors and colorectal cancer:

  • A diet high in fat and red meat increases the risk of developing colon cancer.
  • Consuming fresh fruits and vegetables decreases the risk.
  • Physical inactivity and central obesity increase the risk of developing colon cancer.
  • Regular use of NSAIDs, especially aspirin, may lessen the risk of developing colorectal cancer.

Nevertheless, as with all epidemiologic data, confounding factors not identified may be significant.

Other risk factors associated with the development of colon cancer besides environmental factors. 
Up to 15% of patients with colorectal cancer have a family history of the disease, suggesting the involvement of a genetic factor or factors. Among the genes identified for involvement in colorectal carcinogenesis are K-ras, APC, DCC, hMSH2, hMLH1, hPMS1, and p53. Patients who have had polyps or whose first-degree family members had polyps are at a moderately increased risk. Patients with inflammatory bowel disease, especially ulcerative colitis, are at very high risk of developing colorectal cancer.

What syndromes are associated with colon cancer?
Familial adenomatous polyposis, Gardner’s syndrome, and hereditary nonpolyposis colorectal cancer are autosomal dominant syndromes. The first two account for < 1% of all colorectal cancers, and the last for 6-15%. Hereditary nonpolyposis colorectal cancer is a familial cancer syndrome that differs in natural history and genetic characteristics from sporadic colorectal cancer.

What is familial polyposis coli?
Familial polyposis coli is characterized by thousands of adenomatous polyps throughout the large bowel. If left untreated, cancer will develop in all patients with this syndrome. Cancer will usually manifest before age 40. The more common nonpolyposis syndrome also involves the proximal large bowel. The median age at presentation is < 50 years, and patients with a strong family history should be intensively screened.

What other non-environmental risk factors may be involved in colorectal cancer?

  • Age > 40 yrs in symptomatic patients
  • Associated diseases: ulcerative colitis, granulomatous colitis, Peutz-Jeghers syndrome
  • Past history: colon cancer or polyps, female genital or breast cancer

What are the presenting symptoms of colon cancer?
The presenting symptoms depend on the location of the lesion. Lesions in the ascending colon, where the stool is still quite liquid, do not present with mass effects. However, these tumors frequently ulcerate, leading to chronic blood loss. Patients present with symptoms of anemia or with guaiac-positive stools on screening tests. In the transverse bowel, the stool is more concentrated and formed, so that symptoms of obstruction such as abdominal cramping, abdominal pain, or perforation may occur. Cancers in the rectosigmoid present with tenesmus, decreased stool caliber, and hematochezia.

What are the uses and limitations for CEA level testing?
CEA is an antigen produced by many colon cancers. It should not be used for cancer screening because it is very nonspecific and not sensitive enough to pick up early cancers. It is usually (85% of cases) normal in patients with stage I disease, those who are most amenable to curative surgery. It has also been found to be elevated in cancers of the stomach, pancreas, breast, ovary, and lung and with various nonmalignant conditions such as alcoholic liver disease, inflammatory bowel disease, heavy cigarette smoking, chronic bronchitis, and pancreatitis.

When should CEA testing be done?
Testing should be done preoperatively in patients undergoing resection for colon cancer so that the data can be used to follow the course of the disease. The CEA level is only useful if it is high before treatment. CEA should return to normal in 30-45 days after complete resection of cancer. A preoperative elevated level that returns to normal after surgery, but then subsequently becomes elevated, is a very reliable indicator of tumor recurrence. CEA can also be used as a marker for response to chemotherapy.

List the two roles of chemotherapy in the treatment of colon cancer.

  1. Treatment of metastatic disease
  2. Adjuvant treatment

Which agents are commonly used for the treatment of metastatic disease?
5-Fluorouracil (5-FU), leucovorin, capecitabine, irinotecan (CPT-11), and oxaliplatin, alone or in combination, plus newer agents such as bevacizumab (Avastin). Response rates in metastatic disease are in the range of 20-40%.

How is chemotherapy used as an adjuvant treatment for colon cancer?
Patients who were treated with 5-FU and leucovorin after curative-intent resections of stage III colon cancer were found to have reduced recurrence rate and death rate compared to untreated controls. Chemotherapy is now considered standard postoperative therapy for stage III patients. In stage II disease, adjuvant treatment is sometimes given to patients at high risk for recurrence, as judged by pathologic features of the resected specimens.



  • Devesa SS, et al: Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 83:2049-2053, 1998.
  • Fuchs CS, et al: Gastric carcinoma. N Engl J Med 333:32-41, 1995.
  • Evans DB, et al: Cancer of the pancreas. In DeVita, et al (eds): Cancer: Principles and Practice of Oncology, 6th ed. Philadelphia, Lippincott Williams & Wilkins, 2001.
  • Forsmark CE, et al: Diagnosis of pancreatic cancer and prediction of unresectability using the tumor-associated antigen CA19-9. Pancreas 9:731-734, 1994.
  • Kahl S, et al: Endoscopic ultrasound in pancreatic diseases. Dig Dis 20:120-126, 2002.
  • Margolis S, et al: Systemic manifestations of hepatoma. Medicine 51:381-390, 1972.
  • Winawer S: Early diagnosis of colorectal cancer. Curr Conc Oncol March/April 1981, p 8.

Posted in Oncology | 3 Comments »


September 2nd, 2013

What are the causes of anemia in patients with cancer?
Anemia in cancer patients is often multifactorial. Anemia may result from blood loss due to bleeding from tumors or from gastritis due to the use of nonsteroidal anti-inflammatory agents (NSAIDs). It may also be caused by hemolysis (secondary to antibodies associated with the tumor), disseminated intravascular coagulation (DIC), sepsis, or a paraneoplastic syndrome. Anemia is frequently caused by bone marrow suppression by chemotherapy or by marrow involvement by the tumor.

Define anemia of chronic disease.
Anemia of chronic disease is common in cancer patients. The diagnosis is made when no other cause of anemia can be found and plasma iron is < 60 mg/dl, total iron-binding capacity is 100-250 mg/dl, and ferritin is > 60 ng/ml. The hematocrit is generally 25-30%. An inadequate erythropoietin response to anemia and a blunted response to treatment with recombinant human erythropoietin have been demonstrated in some patients.

What are the predisposing factors for infection in patients with cancer?
Predisposing factors for infection include defects in cellular and humoral immunity, organ compromise due to tumor-related obstruction, chemotherapy-related granulocytopenia, disruption of mucosal (e.g., respiratory and alimentary tract) and integumental surfaces, iatrogenic procedures or placement of prosthetic devices, central nervous system dysfunction, and hyposplenic or postsplenectomy states.

Discuss the sources of infection in patients with cancer.
The vast majority of infections originate from the patients’ own endogenous flora. Sources of infection in neutropenic patients include the lungs, urinary tract, skin, upper aerodigestive tract (mouth, skin, teeth), central nervous system, rectum, perirectum, biopsy sites, and GI tract (appendicitis, cholecystitis, perforations). In investigating the cause of an infection, cultures should include blood, urine, sputum, and, if appropriate to the patient’s clinical status, stool, pleural fluid, or peritoneal fluid.

Which tumors spread to bone most commonly?
Cancers of the lung, breast, kidney, prostate, and thyroid as well as multiple myeloma and malignant melanoma spread to bone most commonly.

Are metastatic bone lesions osteoblastic or osteolytic?
Renal cell carcinoma and multiple myeloma tend to be purely lytic, prostate carcinoma tends to be mainly blastic, and the others are mixed. Tumors that are lytic are most often associated with hypercalcemia, whereas blastic metastases are not generally associated with this complication.

To which bones does cancer most often metastasize?
The most frequently involved bones are the spine, ribs, pelvis, and long bones.

Characterize the pain associated with bone metastases.
The pain of bone metastases is characterized by a dull, aching discomfort that is worse at night and may improve with physical activity.

Which tumors metastasize to the lungs?
Most types of tumors can metastasize to the lungs. Therefore, the more common the tumor, the more commonly it is found to have spread to the lung (e.g., breast cancers). Although they also can spread to the lungs, GI cancers tend to first metastasize locally and to the liver before pulmonary involvement is seen. Tumors that spread via the bloodstream, such as sarcomas, renal cell carcinoma, and colon cancer, tend to produce nodular lung lesions. Those that spread via lymphatic routes, such as cancers of the breast, pancreas, stomach, and liver, often manifest a pattern of lymphangitic spread.

Discuss the symptoms of intracranial metastases.
Headache occurs in up to 50% of patients with intracranial metastases. It is classically described as occurring early in the morning, disappearing or decreasing after arising, and may be associated with nausea and/or projectile vomiting. Other symptoms include focal signs such as unilateral weakness, numbness, seizures, or cranial nerve abnormalities. Nonfocal complaints such as mental status changes or ataxia may occur.

How are intracranial metastases diagnosed and treated?
The diagnosis is made by contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI) of the brain. Treatment consists of decreasing intracranial pressure with steroids, followed by radiotherapy. Surgery is recommended for patients with single intracranial lesions.

What are the signs and symptoms of malignant pericardial effusion?
The presentation of malignant pericardial effusion can resemble heart failure, with dyspnea, peripheral edema, and an enlarged heart on chest x-ray. However, the dyspnea is often out of proportion to the degree of pulmonary congestion seen on the x-ray. Kussmaul’s sign, or jugulovenous distention with inspiration, and pulsus paradoxus of > 10 mmHg with distant heart sounds are clues to the presence of a pericardial effusion.

How is the diagnosis of malignant pericardial effusion confirmed?
Confirmation of the clinical diagnosis is made by echocardiogram or CT scan. Malignant effusions are usually exudates and are often hemorrhagic. Cytology is helpful if positive but does not exclude cancer if negative.

Discuss the treatment of malignant pericardial effusion.
Treatment depends on the patient’s condition but should include drainage of the fluid for diagnostic as well as therapeutic reasons. A nonsurgical approach is preferred, with catheter drainage followed by sclerosis of the pericardium, sometimes with a sclerosing agent such as doxycycline. Other approaches include subxiphoid pericardiectomy, balloon pericardiectomy, pericardial window, and pericardial stripping for patients with prolonged life expectancy.

What are the presenting symptoms and signs of spinal cord compression?
Ninety-five percent of cancer patients with spinal cord compression present with back pain. Other symptoms include lower extremity weakness, bowel or bladder incontinence, or increased deep tendon reflexes in the lower extremities.

How is spinal cord compression diagnosed?
The diagnosis is made by MRI or by myelography with CT, which will demonstrate blockage of the spinal canal.

How is spinal cord compression treated?
Treatment is directed first at relieving spinal cord swelling and pain, using high-dose steroids and adequate pain medication. However, definitive treatment must be carried out emergently to prevent further neurologic deterioration, which may be irreversible. Radiotherapy and/or surgery should be initiated immediately. Preservation of neurologic function is generally better with surgery.

Which tumors most commonly cause spinal cord compression?
The most common tumors causing cord compression are lung cancer, breast cancer, prostate cancer, carcinoma of unknown primary, lymphoma, and multiple myeloma. The most common site of cord compression is the thoracic spine, followed by the lumbosacral spine and the cervical spine.

Which tumors are associated with nonbacterial thrombotic endocarditis?
Also known as marantic endocarditis, this paraneoplastic syndrome is associated with mucinous adenocarcinomas, most commonly of the lung, stomach, or ovary, but has been described in other types of cancers as well.

How does nonbacterial thrombotic endocarditis present?
It is manifested by the appearance of embolic peripheral or cerebral vascular events causing arterial insufficiency, encephalopathy, or focal neurologic defects. Heart murmurs are often not present.

How is nonbacterial thrombotic endocarditis diagnosed and treated?
Echocardiograms may be negative, and the diagnosis is usually made post mortem. Treatment with anticoagulants or antiplatelet drugs has been tried with little success.

What are the tumor-related causes of hypercalcemia?

  • Lytic bone metastases, which release calcium into the bloodstream. This is the most common cause in solid tumors with bony metastases.
  • Humoral hypercalcemia of malignancy (HHM) occurs in patients without bony metastases. Cancers associated with this syndrome secrete a non-PTH substance with activity similar to parathyroid hormone. HHM is associated most commonly with squamous cell cancers of the lung, esophagus, or head and neck but can also be found in renal cell carcinoma, transitional cell carcinoma of the bladder, and ovarian carcinoma.
  • Formerly known as osteoclast-activating factor, osteolytic substances such as interleukin 1 (IL-1), IL-6, and TNF-alpha (lymphotoxin) may cause hypercalcemia in plasma cell dyscrasias.
  • Vitamin D metabolites produced by some lymphomas may promote intestinal calcium absorption.

What is tumor lysis syndrome?
When rapidly growing tumors are effectively treated with chemotherapy, breakdown products of tumor lysis are released into the bloodstream in large amounts. This process may cause hyperkalemia, hyperuricemia, hyperphosphatemia, and hypocalcemia. Renal failure can result from the hyperuricemia. This complication is seen within hours to days after treatment of tumors such as acute leukemia, Burkitt’s lymphoma, and other rapidly proliferating lymphomas. It is rarely, if ever, seen with solid tumors, but has been described in small cell carcinoma of the lung.

How is tumor lysis syndrome treated?
Treatment is the same as for renal failure, with vigorous hydration, dialysis if necessary, and appropriate treatment of electrolyte disorders. Prophylactic treatment with aggressive hydration and allopurinol prior to administering chemotherapy in susceptible patients can prevent this serious complication.

Which medications are commonly used for cancer pain?
As elucidated in the World Health Organization guidelines, pain medications are to be administered in a three-step ladder according to the intensity and pathophysiology of symptoms and individual requirements. For mild pain, the recommended baseline drugs are NSAIDs. Patients with moderate-to-severe pain generally require an opioid agent such as codeine or oxycodone; severe pain requires a stronger opioid such as morphine.

What are the neuromuscular complications of cancer?


  1. National Cancer Database:
  2. National Guideline Clearinghouse:
  3. PDQ Cancer Information Summaries:
  4. SEER Cancer Statistics Review, 1975-2000:


  • American Joint Committee on Cancer: Cancer Staging Manual, 6th ed. New York, Springer-Verlag, 2002.
  • Calabresi P, Schein PS (eds): Basic Principles and Clinical Management of Cancer, 2nd ed. New York, Macmillan, 1993.
  • Casciato DA, Lowitz BB (eds): Manual of Clinical Oncology, 5th ed. Boston, Little, Brown, 2000.
  • DeVita T Jr, Hellman S, Rosenberg SA (eds): Cancer: Principles and Practice of Oncology, 6th ed. Philadelphia, Lippincott Williams & Wilkins, 2001.
  • Haskell CM: Cancer Treatment, 4th ed. Philadelphia, W.B. Saunders, 1995.
  • Holland JF, Frei E, et al (eds): Cancer Medicine, 6th ed. New York, BC Decker, 2003.
  • Tannock IF, Hill RP (eds): The Basic Science of Oncology, 3rd ed. New York, McGraw-Hill, 1998.

Posted in Oncology | 2 Comments »