Objectives: Non-melanoma skin cancer is the most common malignancy in US, with an annual incidence of in excess of 1.5 million cases. In the majority of cases, locoregional treatment is curative and systemic therapy is not indicated. Platinum-based chemotherapy regimens have been used most commonly in refractory cases. The use of cetuximab, a monoclonal antibody targeting epidermal growth factor receptor [EGFR], has been reported for skin cancer treatment. This current study evaluated eight cases of locally advanced and refractory basal cell or squamous cell cancers which were treated with cetuximab.Methods: This is a retrospective study on eight patients who had received cetuximab for treatment of cutaneous carcinoma since 2007 at Southern Illinois University School of Medicine (SIU-SOM) Medical Oncology clinic.Results: Three of the four patients with basal cell carcinoma and two of the four patients with squamous cell carcinoma maintained remission on treatment.. The main side effect was acneiform rash which required termination of treatment for one patient and dose reduction in another.Conclusion: The study indicates that cetuximab may have a beneficial role for patients with non-melanoma cutaneous carcinomas that are refractory to standard therapy.

Our study and several others now demonstrate the feasibility of combining anti-epidermal growth factor receptor (EGFR) therapy with chemoradiation, hint at improved survival outcomes with reduced distant metastatic rates, and suggest that maintenance therapy with anti-EGFR agent may be beneficial.

1534 Background: FPs, including 5-fluorouracil and capecitabine, are widely used to treat solid tumor malignancies like gastrointestinal (GI) cancers. One-third of patients (pts) develop severe toxicities which may lead to treatment delays or hospitalization. Toxicities can be partly due to genetic variations in DPYD. Herein, we describe the implementation of an in-house DPYD test and its impact on FP dosing at a multisite cancer hospital. Methods: This is an observational study of pts starting or continuing FP-based chemotherapy who received DPYD testing as part of routine care. Buccal swabs were collected in clinic and sent to an in-house lab for genotyping using a polymerase chain reaction-based Drug Metabolizing Enzyme assay that interrogates all 5 variants with moderate-to-strong evidence according to the Clinical Pharmacogenetics Implementation Consortium (CPIC) (c.1905+1G>A, c.2846A>T, c.1679T>G, c.1236G>A and c.557A>G). Phenotype translations and dosing were based on CPIC guidelines. Test results and dose recommendations were uploaded to the electronic medical record (EMR) and emailed to the care team. In April 2022, pre- and post-test EMR alerts were built to prompt test ordering and dose modifications. The primary objective was to evaluate the proportion of DPYD variant carriers in tested pts receiving FP. Secondarily, we evaluated turnaround time and impact on FP dosing. Results: From March 2020-December 2022, 491 pts across 14 clinics received DPYD genotyping (54% male, 74% White, 20% Black, median age 53 years). GI cancers (~50% colorectal) represented 90% of the diagnoses. The median lab turnaround time was 3 (IQR 2-6) days. Pretreatment testing was ordered in 389 (79%) pts, of which 360 (93%) had results before cycle 1. Overall, 30 pts (6.1%) were heterozygous carriers (4.9% in pretreatment and 10.8% in reactive testing groups). Variants observed were c.1236G>A (n=13), c.2846A>T (n=8), c.1905+1G>A (*2A) (n=4), c.557A>G (n=4), and c.1679T>G (*13) (n=1). FP dose was modified in 27 (90%) pts (reduced in 25, avoided in 1, discontinued in 1). Of 19 carriers with pretreatment testing, 17 (90%) received an upfront dose reduction (mean reduction 42%; 3 had subsequent dose escalations); 1 avoided FP and 1 declined chemotherapy. Of 11 carriers with reactive testing, 9 had dose reductions (mean reduction 39%) and 2 discontinued FP due to toxicity. The mean FP dose intensity at cycle 1 was 56% in pretreatment carriers, 97% in reactive carriers, and 94% in wild type pts. Conclusions: DPYD genotype-guided FP dosing is feasible at a multisite cancer hospital. In-house rapid turnaround DPYD testing identified variant carriers and resulted in treatment/dose modifications for most carriers, potentially avoiding or mitigating severe toxicities and/or hospitalization, particularly with pretreatment testing. Toxicity evaluation is ongoing.

Background: Fatigue, sleep dysfunction, and joint symptoms may negatively impact quality of life in breast cancer survivors (BCS). Prior studies examining associated factors have yielded inconsistent results. Objective: Determine demographic, medical, exercise-related, body composition and serum inflammatory factors associated with fatigue, sleep dysfunction, and/or joint symptoms in BCS. Methods: Post-hoc analysis of baseline data completed by 37 BCS enrolled in a pre/post intervention study or randomized trial. Self administered survey assessed demographics, medical variables, self-efficacy (i.e., confidence in ability to exercise), fatigue (FSI), sleep dysfunction (PSQI), and joint symptoms (WOMAC). Sleep was also objectively assessed with an accelerometer. Body composition was assessed by body mass index (BMI), waist-to-hip ratio (WHR), and percent body fat (bioelectrical impedance). Cardio respiratory fitness was assessed with sub maximal treadmill test and muscle strength with back/leg extensor dynamometer. Multiplex high sensitivity assay or ELISA was performed on fasting serum samples to determine levels of cytokines or other markers related to body composition. Due to the skewed nature of several variables, Spearman correlations (r) were performed. A significant p value was set at <.05. Results: Participant mean age and education were 55 ± 10.1 and 15 ± 2.8 years, respectively. The majority (87%) were of European heritage with breast cancer stage distribution being I (51%), II (38%) or III (11%). Daily amount of fatigue was significantly associated with months since chemotherapy (r=.43, p = .027), number of comorbidities (r = .33, p = .0497), and fitness (r = -.35, p = .033). Depending on the subscale, self reported sleep dysfunction was associated with income (r = -.36, p = .029), number of comorbidities (r = .37, p = .028), WHR (r = .45, p = .005), tumor necrosis factor (TNF) α (r = .36, p = .029), interleukin (IL)-8 (r = -.45, p = .006), IL-10 (r = -.42, p = .011), TNF α /IL-10 ratio (r = .54, p = <.001), insulin (r = .48, p = .003), and adiponectin (r = -.36, p = .031). Time awake while in bed (accelerometer) was significantly associated with race (r = -.39, p = .019), muscle strength (r = -.35, p = .034), fitness (r = -.48, p = .003), adiponectin (r = -.39, p = .020), and monocytic chemotactic protein (MCP)-1 (r = -.33, p = .047). Time asleep was associated with race (r = .36, p = .031) and leptin (r = -.36, p = .031). Joint symptoms were significantly associated with age (r = .43, p = .008), education (r = -.34, p = .041), number of comorbidities (r = .60, p = <.001), self-efficacy (r = -.55, p = .003) and BMI (r = .33, p = .048). Conclusion: Fatigue and sleep dysfunction were significantly associated with medical factors and fitness. Sleep dysfunction was also associated with demographics, inflammation, strength, and body composition. Joint symptoms were associated with demographics, medical factors, self-efficacy and BMI. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1830. doi:10.1158/1538-7445.AM2011-1830

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