Background: Most safety and efficacy trials of the SARS-CoV-2 vaccines excluded patients with cancer, yet these patients are more likely than healthy individuals to contract SARS-CoV-2 and more likely to become seriously ill after infection. Our objective was to record short-term adverse reactions to the COVID-19 vaccine in patients with cancer, to compare the magnitude and duration of these reactions with those of patients without cancer, and to determine whether adverse reactions are related to active cancer therapy. Patients and Methods: A prospective, single-institution observational study was performed at an NCI-designated Comprehensive Cancer Center. All study participants received 2 doses of the Pfizer BNT162b2 vaccine separated by approximately 3 weeks. A report of adverse reactions to dose 1 of the vaccine was completed upon return to the clinic for dose 2. Participants completed an identical survey either online or by telephone 2 weeks after the second vaccine dose. Results: The cohort of 1,753 patients included 67.5% who had a history of cancer and 12.0% who were receiving active cancer treatment. Local pain at the injection site was the most frequently reported symptom for all respondents and did not distinguish patients with cancer from those without cancer after either dose 1 (39.3% vs 43.9%; P=.07) or dose 2 (42.5% vs 40.3%; P=.45). Among patients with cancer, those receiving active treatment were less likely to report pain at the injection site after dose 1 compared with those not receiving active treatment (30.0% vs 41.4%; P=.002). The onset and duration of adverse events was otherwise unrelated to active cancer treatment. Conclusions: When patients with cancer were compared with those without cancer, few differences in reported adverse events were noted. Active cancer treatment had little impact on adverse event profiles.
CO(2) laser can create cochleostomies comparable in operative time and intracochlear temperature to drilling while decreasing intracochlear sound levels. Further investigation is warranted to minimize trauma and maximize auditory function during cochleostomy.
Gastric cancer (GC) is the fifth most common malignancy with over 1,000,000 cases diagnosed annually and is the third leading cause of cancer death globally (1). The incidence is highest in Asia (with over half of all GC cases globally diagnosed in East Asia), Eastern Europe, and South America with comparatively lower rates in Africa, North America, and Europe. Approximately 95% of gastric tumors are gastric adenocarcinomas (GAC) which can be further divided into intestinal type gastric cancer (IGC), diffuse type gastric cancer (DGC), and mixed histology based on the 1965 Lauren classification (2-4). Approximately 50% of GAC are IGC, 30% are DGC, and 15-20% are mixed or indeterminate. DGC tends to occur in younger patients and in females, while IGC typically presents in older patients and in men (5-7). In the United States, the incidence of DGC also appears to be higher in the Hispanic population compared to non-Hispanic whites (8). The overall incidence of GAC has been declining since 1973 which may be due to a decrease in chronic H. Pylori infection, decreased tobacco use, and changes in diet (9). However, during the same period of time the incidence of DGC and signet-ring cell carcinoma (SRCC) had been increasing in both Asian and Western cohorts before decreasing in recent years (10-12). Reasons for this trend, as well as differences in ethnic and racial subgroups require additional research.The etiology of DGC is diverse. While intestinal metaplasia from chronic infectious etiologies (i.e., H. Pylori) is more commonly associated with IGC rather than DGC (13), Epstein-Barr virus (EBV) appears to be associated with DGC, though the strength of this association is not as clear (4,14). Tobacco use also appears to be related to the development of DGC (15,16). However, the role of other lifestyle factors such as diet and alcohol, along with the strength of these associations, merit further research (17)(18)(19). In addition to environmental etiologies, somatic and germline mutations in a number of genes can contribute to the development of DGC. These genes include CDH1, TP53, RHOA, CTNN1A, and CMTM2 (4,[20][21][22]. Approximately 1-3% of all GCs are due to hereditary diffuse gastric cancer (HDGC), with 40% of those associated with germline mutations in CDH1 (23,24). The risk of developing DGC in patients with germline
630 Background: Although overall incidence of colorectal cancer is declining, the incidence for young patients (age < 50) with colon cancer is increasing. Reasons for this rise are unclear. Understanding clinical and molecular differences between younger and older cohorts can help guide both patient education strategies and future research into the mechanisms of this phenomenon. Methods: A retrospective analysis of patients diagnosed with colon cancer between 2008 and 2015 who underwent molecular tumor profiling via next-gen sequencing of 26 commonly mutated genes at the University of Colorado. Data collected by chart review includes demographic, pathologic, treatment course, and outcomes. Age group cutoffs for data analysis were set at < 50, 50-65, and > 65 based on screening guidelines and average age of diagnosis Results: We evaluated a total of 242 patients, stage I (n = 1), stage II (n = 65), stage III (n = 68), stage IV (n = 105). Mean age was 59.5 (range 27 to 89). A higher percentage of younger patients were non-smokers (77% of youngest cohort vs 46% of oldest cohort, p < 0.001) and had a non-significant trend towards male gender (youngest cohort 63.8% male, oldest cohort 43.4% male, p = 0.065). Younger patients had similar body mass index (BMI) compared to older patients (BMI 27 vs 25.7, p = 0.35). Younger patients had higher rates of rectal cancer (42% vs 21%, p = 0.01) and lower rates of proximal/right sided colon cancer (20% vs 46.5%, p = 0.014). Younger patients also had lower rates of MSI-H tumors (8% vs 14%, p = 0.01). Finally, younger patients had significantly lower rates of APC (43.1% vs 69.3%, p = 0.009) and BRAF (3.5% vs 19.7%, p = 0.004) mutations. Conclusions: Younger patients ( < 50 years old) with colorectal cancer had lower rates of tobacco use and no difference in obesity rates compared to older patients. In addition, although APC and BRAF mutations were lower in younger patients, there were no mutations that were more prevalent in the young cohort. Therefore, further research into lifestyle factors (specific diet/exercise patterns) or alternative molecular mechanisms are needed.
209 Background: Despite national guideline recommendations for universal biomarker testing (KRAS, NRAS, BRAF, and mismatch repair/microsatellite instability [MMR/MSI]) in all patients with metastatic colorectal cancer (mCRC), little is known regarding adherence to these recommendations in the community. Methods: We evaluated 20,333 patients aged >18 years with mCRC diagnosed between 1/1/2013-12/27/18 from the nationwide de-identified Flatiron Health electronic health record-derived database. Changes in rates of biomarker testing based upon chart abstraction according to date of mCRC diagnosis were assessed in patients with ≥ 6 months of follow-up using Cochran-Armitage trend tests. We also assessed whether testing differed by patient characteristics using chi-square tests. Results: Biomarker testing rates increased between 2013 and 2018 (15.3 to 65.7% for NRAS, 23.9 to 56.6% for BRAF, and 34 to 76.6% for MMR, all p < 0.0001). There was no change in rate of KRAS testing (63.8 to 68.3% p= 0.1695) over this period of time. Univariate analysis showed that patients with, worse performance status, and Medicare/Medicaid insurance were less likely to be tested (for all variables, p <0.0001). There were no meaningful differences in testing rates by tumor sidedness, race, gender, or initial stage. Conclusions: In mCRC, adoption of guideline-driven recommendations for NRAS, BRAF and MMR/MSI testing increased significantly between 2013-2018. Adoption of BRAF and NRAS testing has neared the rate of KRAS testing. Interpretation of overall testing rates must recognize potential for missing biomarker test information for care not captured within the Flatiron network. Further study is required to characterize the magnitude of and reasons for absent biomarker testing among patients with metastatic colorectal cancer.
Background Despite national guideline recommendations for universal biomarker testing (KRAS, NRAS, BRAF, and mismatch repair/microsatellite instability [MMR/MSI]) in all patients with metastatic colorectal cancer (mCRC), little is known regarding adherence to these recommendations in routine practice. Methods We retrospectively reviewed patients with mCRC diagnosed between 1/1/2013-12/27/18 from a de-identified electronic health record (EHR)-derived database. We analyzed disparities in KRAS, NRAS, BRAF, and MMR/MSI testing by race, age, gender, and insurance status using Chi-Square tests and T-tests. We evaluated changes in biomarker testing over time with attention to changes around dates of landmark publications and guideline updates using Chi-square tests and Cochran-Armitage tests. Results A total of 20,333 patients were identified of which 66.6% had test results for any biomarker. Rates of test results for all four biomarkers significantly increased over time (p < 0.001). However, as of 6/30/2018 the rate of test results was only 46% for NRAS, 56% for KRAS, and 46% for BRAF. As of 12/31/2017 rate of MMR/MSI testing was 59%. Higher documented testing rates were associated with younger age, lower ECOG performance status, and commercial insurance. There were no clinically meaningful and/or statistically significant differences in documented testing rates by tumor sidedness, race, gender, or initial stage. Conclusions Increased rates of documented testing for NRAS, BRAF and MMR/MSI in mCRC was seen between 2013-2018 reflecting adoption of guideline recommendations. However, the rate of documented testing remains lower than expected, and warrants additional research to understand the extent to which this may represent a clinical practice quality concern.
e18648 Background: Cancer-related malnutrition and cachexia can lead to body composition changes. BCM can be assessed at the third lumbar (L3) vertebra by CT, which is available as part of pre-trial evaluation. We previously found that malnutrition and low psoas muscle area (PMA) are associated with adverse P1 outcomes including higher rates of ≥ Grade 3 toxicity (G3T). Here we evaluate the relationships between comprehensive cross-sectional muscle and adipose tissue BCM at L3 on P1 outcomes. Methods: Baseline CT scans for 82 patients (pts) were reviewed and images at the level of L3 were identified by 3 independent reviewers. A CT L3 image selected by at least 2 reviewers underwent analysis by Slice-O-Matic software (Tomovision, Canada) to generate BCM including: skeletal muscle area (SMA), skeletal muscle radiodensity (SMD), and adipose tissue area [intermuscular (IMAT), visceral (VAT), subcutaneous (SAT), and total adipose (TAT)] in cm2. SMA was normalized by height (m2), yielding cross-sectional skeletal muscle index (SMI). We stratified pts by having a SMI, SMD, IMAT, VAT, SAT, and TAT above or below the median value. We evaluated for associations between BCM and the following outcomes: rates of ≥ G3T, frequency of dose reductions/interruptions, hospitalizations, tumor response, disease control, duration on study (DOS), and overall survival (OS). Chi-square analysis was used to determine statistical significance between groups. Kaplan-Meier curves were used to compare DOS and OS. A multivariable analysis (MVA) was conducted via logistic regression to evaluate the association between SMI, VAT, PMA and ≥ G3T controlling for age and gender. Results: 82 P1 pts were included (38 M, 45 F), with a median age of 60 (range 28-85). The most common disease site was gastrointestinal (33%). Mean SMI was 44.78 cm2/m2 (range 25.70-79.89). Higher SMI was associated with a reduced risk of ≥ G3T (36.6% vs 58.5%; p = 0.047) and a trend towards improved OS (p = 0.07). There was no association between SMD, IMAT, SAT, or TAT and toxicity, however, higher VAT was associated with reduced risk of ≥ G3T (31.7% vs 63.4%, p = 0.004), and improved response to therapy (p = 0.001). A MVA controlling for age and gender showed that reduced SMI (AUC 0.7072), increased VAT (AUC 0.7597), and reduced PMA (AUC 0.757) were similar in their ability to predict ≥ G3T. Conclusions: P1 trials are designed to determine the safety and tolerability of investigational agents. In this population of P1 pts, BCM including higher baseline CT L3 SMI and VAT were associated with a reduced risk of ≥ G3T. BCM were also tied to efficacy as high VAT was associated with improved tumor response while a trend towards improved OS was noted for pts with higher baseline SMI. Future research should examine the value of integrating CT-based BCM into dose-selection algorithms when evaluating safety in P1 trials to minimize treatment-related toxicity and optimize therapeutic benefit.
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