Thompson, R. Houston

617 Background: Anxiety and depression are psychosocial factors which have been demonstrated to have mixed interactions with mortality across various malignancies. While these variables have been associated with poor overall survival for patients with metastatic RCC, the influence on outcomes for localized RCC has been poorly studied. We evaluated the association of anxiety or depression with survival in patients with surgically treated localized clear cell RCC (ccRCC). Methods: We performed retrospective review of our institutional nephrectomy registry to identify 1,990 patients who underwent radical or partial nephrectomy for unilateral, sporadic, non-metastatic ccRCC between 1995- 2011. Baseline anxiety and depression were identified using ICD-9 codes. Associations of anxiety or depression with outcomes of interest were evaluated using Cox proportional hazards models. Two propensity score (PS) techniques were used: adjusting for PS quintile and re-weighting by stabilized inverse probability weights. Results: A total of 197 (10%) patients had diagnoses of anxiety or depression (57 had anxiety alone, 107 had depression alone, and 33 had both anxiety and depression). Median follow-up among survivors was 10.0 (IQR 7.3-13.6) years, during which time 864 died, including 363 from RCC. Patients with anxiety or depression were younger (mean age 59 vs 62 years, p < 0.001) and had more recent operations (75% vs 47% in 2005-2011, p < 0.001) compared to those with neither diagnosis. After PS adjustment, all clinical and pathologic features were well balanced between groups. After PS adjustment, there were no significant differences in time to local ipsilateral recurrence, distant metastases, and death from RCC between groups. We did note a trend to poorer overall survival in patients with anxiety or depression (HR 1.29, 95%CI = 0.98-1.69, p = 0.065). Conclusions: Our results suggest that neither anxiety nor depression is significantly associated with oncologic outcomes among patients with localized surgically treated ccRCC. The trend toward worse overall survival among patients with anxiety or depression warrants further investigation.

Objective To investigate the association between smoking status and pathological response to cisplatin‐based neoadjuvant chemotherapy ( NAC ) and survival outcomes in patients with muscle‐invasive bladder cancer ( MIBC ) treated with radical cystectomy ( RC ). Patients and Methods We reviewed 201 patients treated with NAC and RC for cT 2– cT 4N0M0 BC between 01/1999 and 01/2015. Smoking status was categorised as: ‘never', ‘former', and ‘current' smoker. Pathological response to NAC was defined as: complete (ypT0N0), partial (ypTis/Ta/T1, N0), and no response (ypT2–4 or ypN+). Clinicopathological characteristics were analysed according to smoking status. Logistic regression analyses tested the association between smoking status and pathological response to NAC . Cox regression analyses tested risk factors associated with recurrence, overall ( OM ) and cancer‐specific mortality ( CSM ). Results Overall, there were 58 (28.9%) never smokers, 87 (43.3%) former smokers, and 56 (27.9%) current smokers. No response to NAC was more frequently noted in current smokers (73.2%; P = 0.007). Former smoker ( odds ratio [OR] 2.28; P = 0.024) and current smoker statuses ( OR 4.52; P < 0.001) were significantly associated with no response to NAC , after adjusting for age, gender, Charlson Comorbidity Index, and clinical stage. Similarly, current smoking status ( hazard ratio [HR] 2.14; P = 0.03) and extravesical pathological tumour stage ( HR 3.31; P < 0.001) were independently associated with an increased risk of recurrence after RC . Conclusion Cigarette smoking was significantly associated with adverse pathological response to cisplatin‐based NAC in patients with MIBC treated with RC . Current smokers were at significantly higher risk of disease recurrence as compared to former and never smokers.

e13073 Background: We observed several patients with a personal history of both RCC and myeloid malignancy, and aimed to explore a possible association, especially given the similarity in their epigenetic landscape, with both being characterized by widespread aberrant hypermethylation (Hu C et al, CCR 2014; Jiang Y et al, Blood 2009). Methods: Mayo Clinic’s ‘Advanced Cohort Explorer’ database was used to identify patients with a history of both RCC and a myeloid malignancy - Acute Myelogenous Leukemia (AML), Myeloproliferative Neoplasms (MPN), Myelodysplastic syndromes (MDS) - and to determine the clinical characteristics. The incidence of MDS in patients ≥65 years with a history of RCC was compared to that in the general population ≥65 years (SEER- Medicare database) as well as the general patient population at Mayo Clinic, using one sample test of proportions. Results: A total of 59 patients were identified, with both biopsy proven RCC and a myeloid malignancy during their life time (12 AML, 9 MPN, 9 low risk MDS and 29 intermediate- high risk MDS). The cohort was characterized by marked male predominance (4.4: 1). Median age at RCC diagnosis was 64 years (range 37-87) and myeloid malignancy was 75 years (range 44-90). 46/59 patients had the RCC antecedent, 10/59 concurrent and 3/59 subsequent to the myeloid malignancy with a median time of myeloid malignancy diagnosis after RCC diagnosis of 7.7 years. For patients ≥65 years, the risk of developing MDS with a history of stage I/II RCC and nephrectomy was 5.26 times that of the general population based on the SEER-Medicare database (Cogle, Blood 2011)(395/100,000 vs 75/100,000; p value < 0.001), and 3.07 times that of the general population at Mayo Clinic (395/100,000 vs 128.4/100,000; p value < 0. 001). Conclusions: We observed an association between RCC and myeloid malignancies, particularly MDS; with a history of RCC conferring a substantially increased risk of developing MDS. We hypothesize that the perturbation of epigenetic landscape in the form of widespread hypermethylation may explain, in part, the association between the two malignancies; and aim to explore the potential aberrancy of epigenetic regulators in our patient cohort with a genomic, epigenomic and transcriptomic analysis.