2587 Pre-orchiectomy Leydig Cell function in testicular germ cell cancer (TGCC) patients

2587 Pre-orchiectomy Leydig Cell function in testicular germ cell cancer (TGCC) patients

Abstracts S507 Table 1 (abstract 2586). Treatment and survival of mRCC pts with BM by subgroup of BM presentation TKI exposure (%) mTOR exposure (%...

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Abstracts

S507

Table 1 (abstract 2586). Treatment and survival of mRCC pts with BM by subgroup of BM presentation

TKI exposure (%) mTOR exposure (%) Whole brain radiotherapy (%)§ Neurosurgery (%)§ Stereotactic radiotherapy (%)§ Combination Nsurg + WBRT Stage IV to systemic treatment (median, mths) Stage IV to BM (median, mths) Start of TT to BM (median, mths) mRCC-OS (mths) (95% CI) BM-OS (mths) (95% CI) §

BM-TT N = 51

Observation prior to BM N = 14

BM at Dx N = 13

TT prior to BM N = 24

50 (98) 15 (29) 37 (73) 10 (20) 28 (55) 19 (37) 5.0 11.2 11.2 27.6 (18.2–42.6) 8.6 (5.3–15.6)

13 (93) 3 (21) 10 (71) 7 (50) 5 (36) 3 (21) 12.8 8.7 NA 54.2 (19.2–80.1) 18.2 (12.6–33.9)

13 (100) 2 (15) 8 (62) 3 (23) 10 (77) 7 (54) 6.2 NA NA 15.6 (5.3–32.0) 15.6 (5.3–32.0)

22 (92) 6 (25) 20 (83) 1 (4) 11 (46) 9 (38) 2.3 19.9 11.2 27.6 (12.5–44.0) 5.1 (3.0−7.7)

Not mutually exclusive groups.

2586 POSTER Pattern of presentation of brain metastases (BM) in metastatic renal cell cancer (mRCC) patients (pts) treated with targeted therapies (TT): Implications for screening practice L. Spain1 , A. Dowling2 , E. Kwan3 , C. Pezaro4 , D. Dai5 , P. Chia6 , B. Tran5 , D. Pook3 , A. Weickhardt7 . 1 Austin Hospital, Medical Oncology Unit, Melbourne, Australia; 2 St Vincent’s Hospital, Medical Oncology, Melbourne, Australia; 3 Monash Health, Medical Oncology, Melbourne, Australia; 4 Monash University Eastern Health Clinical School, Medical Oncology, Melbourne, Australia; 5 Royal Melbourne Hospital, Medical Oncology, Melbourne, Australia; 6 Austin Hospital, Medical Oncology, Melbourne, Australia; 7 Austin Hospital & Olivia Newton John Cancer Research Institute, Medical Oncology, Melbourne, Australia Background: BM develop in 7−15% of patients with mRCC. The utility of screening for BM in mRCC is unknown and clinical practice varies. Identification of the timing of presentation of BM may optimise screening strategies for early BM detection. Methods: Pts with mRCC from 5 Australian institutions treated with antiVEGF or mTOR inhibitor targeted therapy (TT) and a diagnosis (dx) of BM were evaluated. The timing of dx of BM, clinicopathologic features, systemic and central nervous system (CNS) treatment were assessed. Prevalence data of BM in pts with mRCC treated with TT was evaluable from 2 institutions. A survey of Australian genito-urinary oncologists was conducted to evaluate current CNS screening practice. Results: From 2005 to 2014, 51 pts with mRCC had received TT prior/ subsequently to dx of BM (BM-TT). Median age was 57 yrs, 80% had clear cell histology and 82% had symptoms at dx of BM. 27% were dx with mRCC, observed, then dx with BM prior to TT, while 25% were dx with BM at initial dx of mRCC. After initiation of TT, 47% (24/51) developed BM. This occurred at a median of 19.9 months following mRCC dx and 11.2 months after commencing TT. BM were dx during 1st line TT in 71% (17/24). For the BM-TT group, median survival from diagnosis of stage IV disease (mRCC-OS) was 27.6 months (95% Confidence Interval (CI) 18.2 to 42.6) and from dx BM (BM-OS) was 8.6 months (95% CI 5.3 to 15.6) respectively. In two of the five institutions a total of 201 patients with mRCC were treated with TT and the prevalence of BM was 33/201 (17%). mRCC-OS for the pts without BM who were treated with TT was similar to the BM-TT group at 28.8 months (95% CI 21.4 to 45.5; p = 0.53). When surveyed, 18/40 practicing oncologists (45%) responded, with only 5 (28%) routinely using CNS surveillance. Conclusions: 47% of mRCC-BM pts present after commencing TT, with the majority diagnosed during first line TT. Interestingly, mRCC pts with BM treated with TT had similar OS to those without BM. CNS surveillance imaging is not routinely performed in clinical practice in Australia and may not impact OS. No conflict of interest. 2587 POSTER Pre-orchiectomy Leydig Cell function in testicular germ cell cancer (TGCC) patients M. Bandak1 , N. Jørgensen2 , A. Juul2 , M.G.G. Kier1 , J. Lauritsen1 , G. Daugaard1 . 1 Rigshospitalet, Department of Oncology, Copenhagen, Denmark; 2 Rigshospitalet, Department of Growth and Reproduction, Copenhagen, Denmark Background: Impaired Leydig Cell function and testosterone deficiency can be observed in 5%-20% of TGCC patients following treatment. The purpose of the present study was to clarify any possible influence of

pre-treatment Leydig Cell dysfunction on this development. A combined evaluation of luteinizing hormone (LH) and testosterone (T) has been shown to be superior for evaluation of Leydig Cell function than the evaluation of either of the hormones independently and therefore this method was applied. Methods: All TGCC patients treated in the period 1993–2012 with preorchiectomy analysis of T, LH, estradiol (E) and sex hormone binding globulin (SHBG) (n = 454) were assessed for inclusion in the study. Patients with unknown pre-orchiectomy levels of human chorionic gonadotropin (hCG) (n = 22) were excluded, leaving 432 patients eligible. As hCG alters the pituitary-gonadal axis, patients with pre-orchiectomy hCG elevation (n = 117) were analyzed separately. A cohort of 564 healthy, age-matched men served as controls. Reproductive hormones in hCG-negative patients (n = 315) and hCG positive patients (n = 117) were compared with controls using parametric tests when normally distributed, otherwise Mann–Whitney U test was applied. Bivariate reference charts of LH and T were created based on the control-group in order to perform combined evaluation of LH and T. Free T was calculated from total T and SHBG concentrations using the method of Vermeulen et al. Results: In the hCG-negative patients, pre-orchiectomy free T and E were significantly lower than in controls (p < 0.05) while there were no significant differences in LH and total T between hCG-negative patients and controls. When using combined evaluation of T and LH, 66 of the hCGnegative patients (21%) were outside the reference level as a sign of Leydig Cell dysfunction. In the hCG-positive patients, all evaluated reproductive hormones were significantly different from controls (p < 0.05) Conclusions: In total, 21% of hCG-negative TGCC patients had an LH/Trelation outside the limits of normality as a sign of pre-orchiectomy Leydig Cell dysfunction. We hypothesize that TGCC patients with pre-existing Leydig Cell dysfunction may carry an increased risk of a decreased Leydig Cell function and testosterone deficiency during follow-up or after systemic treatment. Data clarifying this issue will be presented. No conflict of interest. 2588 POSTER Predicting the risk factors for regional lymph node metastasis in indian patients with penile squamous cell carcinoma K. Shankar1 , M.V. Kumar1 , V.M. Kumar1 , S. Bharatnur2 . 1 Kidwai memorial institute of Oncology, Department of Surgical Oncology, Bangalore, India; 2 Kidwai memorial institute of Oncology, Department of Pathology, Bangalore, India. Background: Our data represents the largest single institution experience in Indian patients with Penile Cancer. Penile Cancer is a common genitourinary malignancy in developing countries like India. The presence and the extent of lymph node metastasis is the most significant predictor of survival in patients with Penile invasive squamous cell Carcinoma. We performed the study to determine if histopathological factors of the primary penile tumour can predict the risk of development of inguinal node metastasis. Materials and Methods: This is a single institution prospective study of 117 Indian patients with penile carcinoma between January 2012 to March 2015. All the patients who presented to us during the study period underwent treatment of the primary malignancy. Fiftytwo patients underwent inguinal block dissection (clinically/pathologically positive inguinal lymph nodes), no patients underwent a pelvic lymph node dissection. The parameters evaluated in the primary lesion included histopathological classification, histopathological grade, pathological stage, invasion depth, vascular invasion and the number and position of metastatic