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Belqis El Ferjani, Sheenu Chandwani, Meita Hirschmann, Seydeh Dibaj, Emily Roarty, Jianjun Zhang, Waree Rinsurnogkawong, Jeff Lewis, Jack Lee, Jack A. Roth, Stephen Swisher, John V. Heymach, Thomas Burke and George R. Simon

Background: NSCLC is the leading cause of cancer-related mortality worldwide. Recently reported clinical trials have firmly established the role of PD-1 and PD-L1 inhibitors in the treatment of patients (pts) with metastatic NSCLC (mNSCLC). We have established the prospective, observational, real-world Advanced Non-Small Cell Lung Holistic Registry (ANCHoR) to understand how the advent of immunotherapy impacts treatment choices and clinical outcomes. Objectives: The aim of this analysis is to measure the impact of immunotherapy on the treatment choice for the first-line treatment of mNSCLC and to determine the link between PD-L1 expression and the treatment choices made in routine clinical practice at the MD Anderson Cancer Center (MDA). Methods: From May 1, 2017, to June 30, 2018, English-speaking pts with mNSCLC at MDA who provided written informed consent were enrolled in ANCHoR and longitudinally followed. The PD-L1 testing rates were captured and the treatment decisions made were also captured and tabulated. The time of data cutoff for this study is June 30, 2018. Results: Of the 296 pts enrolled in the registry at the time of data cutoff, there were 49.7% males, 82.1% white, 45.9% ≥65 years old, 69.3% smokers, 83.1% with an initial stage IV diagnosis, 87.2% with nonsquamous histology, 36.1% with bone metastasis, 29.4% with brain metastasis, 43.2% with 0–1 performance status, and 21.6% with a known EGFR or ALK mutation. A total of 233 pts had been tested for PD-L1 (78.7%). Predominant reasons for not testing (63 pts) include not having available tissue (26 pts) or the test was not requested by the physician (31 pts). As of June 30, 2018, 38.5% of patients received immunotherapy as first-line therapy either as a single agent (18.9%, 56 pts) or in combination with chemotherapy (19.6%, 58 pts). Only 35.8% of the patients received platinum doublet chemotherapy alone. Two pts received chemotherapy combined with an anti-angiogenesis agent (0.68%). Targeted therapy was utilized either as a single agent (20.6%) or in combination with immunotherapy (2.4%). Conclusion: Immunotherapy is now utilized as a single agent or in combination in more than one-third of patients with mNSCLC. These numbers are expected to increase as data from recently reported studies get incorporated into common clinical practice. Compared to historic experience, there has been a dramatic decline in the use of chemotherapy with an anti-angiogenesis agent.

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Takashi Taketa, Kazuki Sudo, Arlene M. Correa, Roopma Wadhwa, Hironori Shiozaki, Elena Elimova, Maria-Claudia Campagna, Mariela A. Blum, Heath D. Skinner, Ritsuko U. Komaki, Jeffrey H. Lee, Manoop S. Bhutani, Brian R. Weston, David C. Rice, Stephen G. Swisher, Dipen M. Maru, Wayne L. Hofstetter and Jaffer A. Ajani

Current algorithms for surveillance of patients with esophageal adenocarcinoma (EAC) after chemoradiation and surgery (trimodality therapy [TMT]) remain empiric. The authors hypothesized that the frequency, type, and timing of relapses after TMT would be highly associated with surgical pathology stage (SPS), and therefore SPS could be used to individualize the surveillance strategy. Between 2000 and 2010, 518 patients with EAC were identified who underwent TMT at The University of Texas MD Anderson Cancer Center and were frequently surveyed. Frequency, type, and timing of the first relapse (locoregional and/or distant) were tabulated according to SPS. Standard statistical approaches were used. The median follow-up time after esophageal surgery was 55.4 months (range, 1.0-149.2 months). Disease relapse occurred in 215 patients (41.5%). Higher SPS was associated with a higher rate of relapse (0/I vs II/III, P≤.001; 0/I vs II, P=.002; SPS 0/I vs III, P≤.001; and SPS II vs III, P=.005) and with shorter time to relapse (P<.001). Irrespective of the SPS, approximately 95% of all relapses occurred within 36 months of surgery. The 3- and 5-year overall survival rates were shorter for patients with a higher SPS than those with a lower SPS (0/I vs II/III, P≤.001; 0/I vs II, P≤.001; 0/I vs III, P≤.001; and II vs III, P=.014). The compelling data show an excellent association between SPS and frequency/type/timing of relapses after TMT in patients with EAC. Thus, the surveillance strategy can potentially be customized based on SPS. These data can inform a future evidence-based surveillance strategy that can be efficient and cost-effective.

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Mary B. Daly, Jennifer E. Axilbund, Saundra Buys, Beth Crawford, Carolyn D. Farrell, Susan Friedman, Judy E. Garber, Salil Goorha, Stephen B. Gruber, Heather Hampel, Virginia Kaklamani, Wendy Kohlmann, Allison Kurian, Jennifer Litton, P. Kelly Marcom, Robert Nussbaum, Kenneth Offit, Tuya Pal, Boris Pasche, Robert Pilarski, Gwen Reiser, Kristen Mahoney Shannon, Jeffrey R. Smith, Elizabeth Swisher and Jeffrey N. Weitzel

OverviewAll cancers develop as a result of mutations in certain genes, such as those involved in the regulation of cell growth and/or DNA repair,1,2 but not all of these mutations are inherited from a parent. For example, sporadic mutations can occur in somatic/tumor cells only, and de novo mutations can occur for the first time in a germ cell (i.e., egg or sperm) or in the fertilized egg itself during early embryogenesis. However, family studies have long documented an increased risk for several forms of cancer among first-degree (i.e., parents, siblings, and children) and second-degree relatives (i.e., grandparents, aunts or uncles, grandchildren, and nieces or nephews) of affected individuals. These individuals may have an increased susceptibility to cancer as the result of 1 or more gene mutations present in parental germline cells; cancers developing in these individuals may be classified as hereditary or familial cancers.Hereditary cancers are often characterized by mutations associated with a high probability of cancer development (i.e., a high penetrance genotype), vertical transmission through either mother or father, and an association with other types of tumors.3,4 They often have an early age of onset and exhibit an autosomal dominant inheritance pattern (i.e., occur when the individual has a mutation in only 1 copy of a gene).Familial cancers share only some features of hereditary cancers. For example, although familial breast cancers occur in a given family more frequently than in the general population, they generally do not exhibit the inheritance patterns or onset age consistent...
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Kazuki Sudo, Xuemei Wang, Lianchun Xiao, Roopma Wadhwa, Hironori Shiozaki, Elena Elimova, David C. Rice, Jeffrey H. Lee, Brian Weston, Manoop S. Bhutani, Adarsh Hiremath, Nikolaos Charalampakis, Ritsuko Komaki, Mariela A. Blum, Stephen G. Swisher, Dipen M. Maru, Heath D. Skinner, Jeana L. Garris, Jane E. Rogers, Wayne L. Hofstetter and Jaffer A. Ajani

Background: Among patients with localized esophageal cancer (LEC), 35% or more develop distant metastases (DM) as first relapse, most in the first 24 months after local therapy. Implementation of novel strategies may be possible if DM can be predicted reliably. We hypothesized that clinical variables could help generate a DM nomogram. Patients and Methods: Patients with LEC who completed multimodality therapy were analyzed. Various statistical methods were used, including multivariate analysis to generate a nomogram. A concordance index (c-index) was established and validated using the bootstrap method. Results: Among 629 patients analyzed (356 trimodality/273 bimodality), 36% patients developed DM as first relapse. The median overall survival from DM was only 8.6 months (95% CI, 7.0–10.2). In a multivariate analysis, the variables associated with a higher risk for developing DM were poorly differentiated histology (hazard ratio [HR], 1.76; P<.0001), baseline T3/T4 primary (HR, 3.07; P=.0006), and baseline N+ LEC (HR, 2.01; P<.0001). Although variables associated with a lower risk for DM were age of 60 years or older (HR, 0.75; P=.04), squamous cell carcinoma (HR, 0.54; P=.013), and trimodality therapy (HR, 0.58; P=.0001), the bias-corrected c-index was 0.67 after 250 bootstrap resamples. Conclusions: Our nomogram identified patients with LEC who developed DM with a high probability. The model needs to be refined (tumor and blood biomarkers) and validated. This type of model will allow implementation of novel strategies in patients with LEC.