Lung cancer is a leading cause of death for both men and women. The treatment of lung cancer has been stifled with pessimism for many years. However, molecularly targeted therapies directed at pathologic epidermal growth factor receptor tyrosine kinases have come to market and, with them, a new tone to an old diagnosis. Treatment of lung cancer is a complex science that requires not only anatomical knowledge of the patient but also an understanding of the patient's overall physiologic condition. When patients are treated appropriately, this drug can transform the natural progression of their disease and improve survival. Interestingly, the clinical solidarity of these first-generation tyrosine kinase inhibitors (TKIs) has become the prelude to a second wave of advances in molecular targeting that we can expect to further improve how we classify and treat lung cancers. Cancers that become resistant to epidermal growth factor receptor (EGFR)-specific TKIs through a secondary mutation are likely to be dependent on the activated kinase for their growth and survival. Therefore, discovering a secondary means of inhibiting EGFR T790M may be therapeutically necessary. This has prompted the preclinical and clinical development of second and third-generation kinase inhibitors. Tumor subtypes are also now being identified, potentially allowing patients to be treated with drugs that most benefit their tumor subtype. We used the TriNetX research platform to analyze the rate of patients being prescribed first, second, and third-generation EGFR TKIs and propose a rationale for the trends seen over time.

BackgroundThe landscape for patients with multiple myeloma has improved dramatically over the last 15 years. Immunomodulatory imide drugs (IMiDs) have shown great efficacy in both the setting of initial therapy and as maintenance after autologous stem cell transplant (ASCT). Concern has arisen, however, regarding the risk of second primary malignancies (SPMs) that appear to be associated with the use of IMiD agents. SPMs are a known sequela of multiple myeloma treatment, particularly as a consequence of maintenance lenalidomide status-post stem cell transplant (SCT). The benefit of SCT has become less clear with the utilization of newer, more effective initial therapies. ObjectivesTo determine the effect of SCT on SPM risk and overall survival in multiple myeloma patients at 5 and 10 years after treatment initiation. MethodsWe used TriNetX, a global federated health research network providing access to electronic medical records (diagnoses, procedures, medications, laboratory values, genomic information) from approximately 58 million patients in 49 large healthcare organizations. We created two patient cohorts who had all received treatment with thalidomide, lenalidomide, or pomalidomide. One cohort had received SCT while the other had not. Both cohorts were then analyzed for the development of all non-myeloma malignancies which occurred at least one year after initiation of treatment. ResultsAt 5 years, SPMs were 5.8% more likely in patients who received stem cell transplant (22.4% vs 16.6%, RR 0.741, p value <0.0001) but 5-year survival favored transplanted patients by 2.38% (64.85% vs 62.474%, p value 0.0044). 10-year survival favored patients who did not receive transplant by 1.44% (42.279% vs 40.838%, p value 0.0279). The Kaplan-Meier curves cross at year 6. ConclusionsIt has previously been shown that the use of alkylating agents in myeloma patients significantly increases the risk of SPM, but that difference had curiously not been shown to have a negative impact on survival. Our analysis shows that this negative survival impact does exist but requires six or more years of follow up to become evident. Recent analyses from studies using older regimens show no overall survival benefit from the use of stem cell transplant. As non-transplant regimens become more effective at producing minimal residual disease (MRD) negativity, it seems that transplantation for myeloma patients will soon be regarded as unnecessary or even detrimental.

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10578 Background: The lung cancer obesity paradox is the unexpected inverse relationship between body mass index (BMI) and lung cancer mortality. While there is a growing body of evidence to support the existence of the obesity paradox in lung cancer, little is known about its magnitude and relationship to cancer incidence and its impact on outcomes from surgery, chemotherapy, immunotherapy, and radiation treatment. Methods: To evaluate the impact of obesity on lung cancer incidence, we used TriNetX, a global federated health research network providing access to electronic medical records (diagnoses, procedures, medications, laboratory values, genomic information) from approximately 69 Million patients in 49 large Healthcare Organizations. We evaluated 2 patient cohorts of 216,462 adult smokers aged 18 to 75 that were matched for age, race, gender, and ethnicity. One cohort of patients carried a diagnosis of overweight and obesity (ICD-10 code E66), while the other cohort required exclusion of those diagnoses. Results: We found a statistically significant decrease in lung cancer incidence for patients with obesity (1.407% vs 2.039%, p < 0.0001), in addition to superior overall survival (95.344% vs 92.039%, p < 0.0001). A subset analysis of patients who contracted lung cancer showed a statistically significant benefit in median survival in favor of patients with overweight and obesity (851 vs 602 days, p value 0.0009). Conclusions: These findings support the existence of the obesity paradox in lung cancer, and its positive impact on both lung cancer incidence and outcome.