scout

Lung Cancer

Latest News


CME Content


In the conclusion to the article “Proton Radiation Therapy for Lung Cancer: Is There Enough Evidence?” Dr. David Bush puts his finger on the critical issue underlying most debates about the value of new medical technologies. He notes that “The evidence required to bring new technology into clinical practice is poorly defined.”[1] In the specific context of this article, the answer to the question of whether or not there is enough evidence depends entirely on how one chooses to define “enough.” Some experts believe that biological modeling based on dose distributions is sufficient to conclude that proton therapy improves health outcomes. Others have argued that the evidence is only adequate once randomized clinical trials have been completed to directly compare alternative interventions. Whatever one’s position on this issue, the lack of clarity on the question of adequacy of evidence is a major contributor to the gaps in knowledge about the comparative effectiveness of many widely used clinical interventions. Accelerating the rate at which this knowledge is generated will require a serious and sustained effort to define these evidence thresholds. This would allow more energy to be channeled into generating the needed evidence and less energy to be devoted to debating whether or not the evidence we have today is good enough.

Just as in recent years attitudes and treatment therapies have changed regarding non–small-cell lung cancer (NSCLC), it is time that the same occur for its small-cell counterpart. Although treatment for advanced-stage small-cell lung cancer (SCLC) is fairly standardized, there remain a number of controversies that have yet to be clarified by evidence-based data.

Proton radiation for cancer offers the ability to conform the high-dose region of radiation therapy to the tumor while reducing the dose of radiation to adjacent normal tissues. In lung cancer, this equates to greater sparing of uninvolved lung, heart, esophagus, and spinal cord. Sparing these normal tissues permits the delivery of higher-radiation doses to the tumor. Studies that compare the distribution of radiation doses for lung cancer show that proton radiation is superior, even when factors such as respiratory motion are considered. Clinical experience confirms the feasibility of proton radiation for early-stage non-small-cell lung cancers, and clinical trials are being conducted in locally advanced tumors: To date, evidence indicates that proton radiation should be further explored.

Despite a decreasing incidence in the United States, small-cell lung cancer (SCLC) remains a major clinical problem, with approximately 30,000 new cases each year. The diagnosis of SCLC is usually not difficult. The Veterans Administration Lung Study Group (VALSG) staging system is less accurate than the American Joint Committee of Cancer tumor-node-metastasis (TNM) system (7th edition) at predicting survival in SCLC, especially in lower stage disease. Surgery has not played a major part in the management of SCLC, but emerging data suggest that resection may have a role in earlier stage disease. While the frontline treatment of SCLC has not changed significantly in the past decade, newer agents that are currently being investigated provide hope for better treatment of relapsed/refractory disease for the future.

In this issue of Oncology, Levy and colleagues provide a comprehensive review of bronchioloalveolar carcinoma [BAC], with a focus on the management of this rare disease, which represents 4% of all lung cancers.[1] The definition of BAC was revised by the World Health Organization (WHO) in 2004, with changes made to the diagnostic criteria and classification.[2] BAC was defined as an adenocarcinoma of the lung that grows in a lepidic fashion along the alveolar septa without invasion of stroma, blood vessels, or pleura. BAC has been sub-classified into three types: nonmucinous, mucinous, and mixed.

Bronchioloalveolar carcinoma (BAC) is a subset of pulmonary adenocarcinoma characterized by distinct and unique pathological, molecular, radiographic, and clinical features. While the incidence of pure BAC is rare, comprising only 1% to 4% of non–small-cell lung cancer (NSCLC), mixed subtypes (including BAC with focal invasion and adenocarcinoma with BAC features) represent as much as 20% of adenocarcinomas-and that figure may be increasing. Despite the longstanding recognition of this entity, there is no established treatment paradigm for patients with multifocal BAC, resulting in competing approaches and treatment controversies. Current options for multifocal BAC include both surgery and systemic therapies. Unfortunately, prospective data on systemic approaches are limited by study design and small patient numbers; there are only seven phase II studies involving four therapies. This article evaluates key characteristics of BAC, including the current understanding of histopathology and tumor biology. In addition, it comprehensively reviews the systemic phase II studies in an attempt to clarify the therapeutic challenges in this disease. It also includes the first proposed treatment paradigm that integrates both EGFR mutational status and the sub-histologies, mucinous and nonmucinous BAC.

Metformin, a biguanide antidiabetic drug administered orally, could play a critical role in controlling, and possibly preventing, lung cancer in at-risk patients. Animal studies conducted at NCI demonstrated that treating mice with metformin reduced lung tumor volume by about 50%.

Lung cancer is not a discriminate disease, but the disease burden is especially high on African Americans in the U.S. The statistics are stark: African-American men are 37% more likely to develop lung cancer than white men and are 22% more likely to die of it. In addition, only 12% of African Americans live longer than five years after a diagnosis of lung cancer, compared with 16% of whites, according to a recent report by the American Lung Association.

Results of a new study published in the Annals of Internal Medicine [Ann Intern Med 152:505-512, 2010] indicate that the risk for false-positive results of CT lung cancer screening tests is substantial. Led by Jennifer M. Croswell, MD, researchers from NCI sought to quantify the cumulative risk in a 1- or 2-year lung cancer screening exam, based on at least one false-positive finding.

The review by Oxnard and Miller provides a thoughtful update on the use of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) gefitinib (Iressa) and erlotinib (Tarceva) as front-line therapy in patients with non–small-cell lung cancer (NSCLC).

African Americans have a higher mortality rate from lung cancer than Caucasians, a fact first discovered in the early 1980s. For decades, researchers have looked for differences in access to care, rates of surgery, and patient preferences to explain the disparity. Now it seems the answer may relate at least partly to the way African Americans think about lung cancer.

The first issue deserving comment is the heterogeneity of stage III disease. Stage IIIA N2 non–small-cell lung cancer (NSCLC) includes patients with at least one “incidental” N2 node detected at the time of surgical resection in patients who had a negative mediastinal evaluation (including mediastinoscopy) preoperatively. It also includes patients whose initial computed tomography (CT) and positron-emission tomography (PET) scans show multiple bulky (> 2 cm) nodes that are confirmed by either mediastinoscopy or endobronchial ultrasound-guided bronchoscopy.

Probably no other topic in thoracic oncology has resulted in more controversy than that of the management of locally advanced non–small-cell lung cancer (NSCLC). Although recent large randomized studies have yielded more reliable and objective data on which to base treatment decisions than were available a decade ago, management of these patients is still influenced by specialty bias and philosophical beliefs.

Malignant pleural effusion complicates the care of approximately 150,000 people in the United States each year. The pleural effusion is usually caused by a disturbance of the normal Starling forces regulating reabsorption of fluid in the pleural space, secondary to obstruction of mediastinal lymph nodes draining the parietal pleura.