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Lung Cancer

What is The Prognosis?

Lung cancer generally has a grim prognosis, which can be defined by means of the blood tests mentioned above as well as the following tests:

Tumor markers. Tumor markers are substances produced by cancer cells. They reflect the presence or absence of cancer, and indicate whether a cancer returns (recurs) after treatment. Measuring the following six tumor markers is essential to daily lung cancer management. They are measured either by blood testing or by testing the tumor biopsy sample:

  • Carcinoembryonic antigen: High carcinoembryonic antigen (CEA) levels in the blood (>10 ng/mL before and after surgery) are linked with poor survival (Tomita M et al 2005).
  • Neuron-specific enolase: Neuron-specific enolase (NSE) in the tumor biopsy sample is a significant predictor of survival (Komagata H et al 2004; Ferrigno D et al 2003).
  • Sialyl Lewis X-i antigen: Sialyl Lewis X-i antigen (SLX) identifies the presence of lung metastasis (Satoh H et al 1998).
  • Serum cytokeratin fragment 21.1: Serum cytokeratin fragment 21.1 (CYFRA) diagnoses NSCLC, especially squamous cell and adenocarcinoma (Chantapet P et al 2000).
  • Squamous cell carcinoma antigen: Some 85 percent of patients with squamous cell carcinoma antigen (SCC) levels higher than 2 ng/mL have squamous tumors (Molina R et al 2003).
  • Pro-gastrin-releasing peptide: High levels of pro-gastrin-releasing peptide (ProGRP) are found in SCLC patients, and this test is more specific than NSE for SCLC (Molina R et al 2004).

Cyclooxygenase-2. Cyclooxygenase-2 (COX-2) is associated with a worsening prognosis in lung cancer. Therefore, COX-2 inhibitors, taken as either prescription medication or nutritional supplements, may be beneficial in addition to standard treatments and in the prevention of lung cancer (Scagliotti GV et al 2003). COX-2 inhibitors enhance the cancer-killing effects of chemotherapy and radiation therapy in lung cancer cell lines with high levels of COX-2 (Saha, P et al 2005).

Advanced lung cancer patients who took Celebrex® (celecoxib; 200 mg twice daily), medroxyprogesterone (500 mg twice daily), and oral food supplementation for six weeks had stable weight (±1 percent) or gained weight and had significant appetite improvement and relief from nausea and fatigue (Cerchietti LC et al 2004). Consequently, clinical trials are currently assessing Celebrex® alone for preventing lung cancer in heavy smokers and Celebrex® in combination with chemotherapy or after radiation therapy in lung cancer treatment. More information on ongoing clinical trials may be found at www.clinicaltrials.gov.

The following may also inhibit the effects of COX-2:

  • Eicosapentaenoic acid (EPA) from fish oil (Yang P et al 2004), alpha-tocopheryl succinate (Lee E et al 2006); and a tea made from clove (Banerjee S et al 2006) hinder COX-2 in lung cancer cells.
  • Aspirin also slows down COX-2 activity in lung cancer cells and may prevent tobacco carcinogenesis (Harris RE et al 2005).

Gene abnormalities. Mutations in K-ras genes are associated with a poor prognosis in NSCLC (Mascaux C et al 2005; Slebos RJ et al 1990), while tumor amplification of c-myc is associated with a poor prognosis in SCLC (Zajac-Kaye M 2001) and shorter survival in NSCLC (Yakut T et al 2003). The p16/CDKN2 gene is abnormal in 10 percent of SCLCs and in more than 50 percent of NSCLCs, and its detection may improve early diagnosis (Su C et al 2002).

Detection of K-ras mutations may help predict treatment outcome. For example, tumors in patients with a mutant ras gene are more difficult to kill with radiation than are tumors in people without the mutation. K-ras mutations can be detected in blood, sputum, lavage fluids, stool sample (Minamoto T et al 2000), and the tumor itself. Testing may be available through the Harvard Medical School-Partners Healthcare Center for Genetics and Genomics Laboratory for Molecular Medicine (www.hpcgg.org) or LabCorp (www.labcorp.com). Several gene therapies are under investigation:

  • Perillyl alcohol, found in lavender, cherries, and mint, slowed down ras activity and prevented lung cancer in experimental studies. Because it stimulated lung cancer cell death, it is being tested in clinical trials as an anticancer agent (Xu M et al 2004; Lantry LE et al 1997).
  • Theaflavins and epigallocatechin gallate (EGCG), black tea components, alter c-myc levels, resulting in a decreased occurrence and delayed onset of preinvasive lung cancers (Saha P et al 2005; Lin JK 2002).
  • Grape seed proanthocyanidins alter c-myc activity and protect against tobacco-induced death of healthy cells (Bagchi D et al 2002).