I had previously written about a spectrum from pure bronchioloalveolar carcinoma (BAC) to invasive adenocarcinoma in one of my first posts here, but the real credit for this concept goes back to Dr.

Radon is a product of the decay of naturally occuring uranium in the earth, and it's estimated to be responsible for perhaps 2-3% of lung cancers overall. In one reference (here) doesn't offer any details of where the numbers come from, an estimated 26% of lung cancer in never-smokers is caused by radon:

It has been noted for many years that Asian women appear to be particularly predisposed to lung cancer despite a low frequency of smoking. Many of the series from resected NSCLC series have never-smoker rates of 30-50%, with the majority of these never-smokers as women. As we've struggled to understand and explain risks, hormonal differences between men and women have emerged as a possibility, as has genetic differences.

A cancer has to grow faster than the tissue around it to become a tumor. Progressive growth is therefore a central feature of a cancer and a critical factor in distinguishing cancerous nodules from benign ones. There is a characteristic "volume doubling time" (VDT), the interval it takes for a nodule to double in volume. It's worth keeping in mind that because a nodule is generally spherical, an increase in the diameter by just 28% (such as a 2 mm increase from 7 to 9 mm) actually represents a doubling of the volume of a nodule.

As you might suspect, there are features of different spolitary pulmonary nodules (SPNs) that makes us more or less suspicious for cancer. The first is the size of the nodule. Looking at multiple series of SPNs, the likelihood of cancer among nodules that measured under 5 mm is generally in the 0-1% range. Nodules in the 5-10 mm range have been found to be cancer in up to about about 28% of cases, with most studies showing the risk of cancer in this range to be one in four or five.

We know PET scans can provide additional metabolic information that can be more sensitive and specific for cancer than chest x-rays and even CT scans in the initial staging of lung cancer (see prior post on introduction to PET scans). PET scans are now nearly universally employed in the initial workup, at least of patients who have NSCLC and aren’t already known to have stage IV disease.

Among the key issues in following patients with a history of treated lung cancer is the pattern of recurrence. We need to have a sense of when the risk is highest and where people are more likely to demonstrate new evidence of disease. Fortunately, there are several studies that can help us with these questions.

A substantial revision of the staging system was presented at the World Conference on Lung Cancer in Korea this week. This project involved multiple lung cancer experts from all over the world and from a variety of specialties over the last several years, who reviewed the data on approximately 100,000 lung cancer cases, both NSCLC and SCLC. They looked at various ways to break down this large database of cases in order to provide a more accurate prognosis for patients.

Many members have asked questions about increased risk of lung cancer among family members of people who have developed lung cancer. Overall, I have not highlighted this, partly because we don't tend to highlight genetics as a major contributor of lung cancer risk. But the fact is that 10-15% of people who develop lung cancer never smoked, and the vast majority of smokers never develop lung cancer.

I've been meaning to write on tumor markers detectable in the blood for the management of lung cancer. These are proteins that are produced by some tumors, and the idea is that the levels of the tumor markers in the blood can potentially be used to monitor the status of the disease.