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.

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

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.

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