Tumori Journal Abstract Book - October 2020 - 145

H - Genitourinary Tumours	
Ribera D.1, Buonerba C.1, Di Lorenzo G.1, Zappavigna S.2, Scafuri
L.1, Giuliano M.1, Bruzzese D.1, Morra R.1, Facchini S.2, Iaccarino S.1,
Costabile F.1, Onofrio L.1, Viggiani M.1, De Placido P.1, Marretta A.L.1,
Pietroluongo E.1, Morelli F.2, Facchini G.3, Caraglia M.4, De Placido S.1
1

AOU Federico II, Napoli; 2S. Giovanni di Dio Hospital, ASL Napoli 2Nord,
Oncology Unit, Frattamaggiore, Italy; 3IRCCS Pascale, Napoli; 4Department of
Pharmaceutical and Biomedical Sciences, University of Salerno, Fisciano, Italy

Background: Since demonstration of enzalutamide efficacy in mCRPC men after failure of docetaxel, enzalutamide has proven to be effective in PCa patients in an
increasing number of clinical settings. CTCs count has
shown prognostic value in patients with advanced PCa
regardless of the systemic treatment administered, the
majority of available data in mCRPC populations selected
for a certain treatment has been obtained in patients receiving abiraterone, with only limited data available in populations receiving enzalutamide Presence of ARV-7+ CTCs
has been associated with resistance to enzalutamide and
abiraterone.
Material (patients) and methods: CTCs in the peripheral
blood were assessed within 28 days to the start of enzalutamide and after 12 weeks. Radiographic evaluation was
performed by whole body CT scan with and without contrast and bone scan every 12 weeks. Continued surgical or
medical castration was required during enzalutamide treatment. Anti-cytokeratin 8/18 and anti-CD45 antibodies
were used to identify neoplastic cells in peripheral blood.
Moreover, we evaluated the levels of PTEN and AR-V7 in
prostate cancer cells in order to validate these antibodies.
Results: A total of 53 patients were enrolled since
September 2016 to October 2018 at three participating
centers. Median (interquartile range) CTCs count at baseline was 5 (3;8). CTCs count, PTEN- CTC count, ARV-7+
CTC count were associated with both PFS and OS at univariate analysis. At baseline, >=5 vs. <5 CTCs were associated with worse PFS (HR = 2.35; 95%CI: 1.14-4.84;
p=0.021) and OS (HR = 3.08; 95%CI: 1.45-6.54;
p=0.003); >=2 vs. <2 PTEN- CTCs were associated with
worse PFS (HR = 3.96; 95%CI: 1.8-8.72; p= 0.001) and
OS (HR =2.36; 95%CI: 1.12-5; p =0.025); >= 1 vs. < 0
ARV7+ CTCs was also associated with worse PFS (HR =
5.05; 95%CI:2.4-10.64; p <0.001) and OS (HR = 2.25;
95%CI:1.1 - 4.58;p=0.026).
Conclusions: ARV-7+ CTC count, which ranged from 0
to 20, was associated with rPFS as a continuous variable
also (HR 1.25 (1.13 to 1.37) <0.001), which may suggest
that additional information may be provided by counting
circulating ARV-7+ cells and not by just assessing presence vs. absence. Furthermore, our results show that flow
cytometry has potential to assess PTEN status in CTCs as
a prognostic and possibly predictive marker in patients
treated with enzalutamide. In conclusion our data add supporte the role of flow cytometry not only in enumeration
but also in molecular profiling of CTCs.

145

H16
Is cabozantinib efficient in
metastatic HLRCC papillary renal
cell carcinoma?
Cerbone L.1, Carril-Ajuria L.2, Colomba-Blameble E.3, Crouzet L.4,
Laguerre B.4, Thibault C.5, Vicier C.6, Caron O.3, Richard S.7, De
Velasco G.2, Flechon A.8, Saldana C.9, Ronan F.3, Boccardo F.10,
Escudier B.3, Albiges L.3
1

Department de Medicine Oncologique, Institut Gustave Roussy, FR, Villejuif;
Hospital Universitario XII Octubre, Madrid; 3Institut Gustave Roussy,
Villejuif; 4Centre Eugene Marquis, Rennes; 5Hopital Europeen Georges
Pompidou, Paris; 6Institut Paoli-Calmette, Marseille; 7Hopital Kremlin-Bicetre,
Kremlin Bicetre; 8Centre Leon Berard, Lyon; 9APHP Hopital Henri Modor,
Creteil; 10Università degli Studi di Genova, Genova
2

Background: Hereditary Leiomyomatosis and RCC
(HLRCC) is a rare autosomal dominant inherited disorder
confering an increased risk to develop cutaneous and uterine
leiomyomas and type 2 pRCC, caused by a germline mutation in FH, a Krebs cycle enzyme. Data on efficacy of systemic therapy in FH mutated pRCC population is limited.
Recently the combination of Erlotinib and Bevacizumab
proved a great efficacy in this specific subgroup of patients
in a phase 2 trial. However, this data is still partial, with
limited applicability to routine clinical practice. Cabozantinib
(CABO), a potent tyrosine-kinase inhibitor (TKI), has
become the standard of care after failure of first line in
ccRCC and achieved an Overall Response Rate of 27% in
all-comers pRCC patients (pts). The aim of this study is to
describe the activity of CABO in HLRCC pts.
Methods: We included all FH mutated pRCC pts treated
with CABO for metastatic disease from December 2014 to
February 2020 in a multicentric retrospective study. Clinical,
laboratory and survival data were retrospectively reviewed.
Disease control rate (DCR) was defined as complete response
(CR) + partial response (PR) + stable disease (SD)
(CR+PR+SD). Objective response rate (ORR) as CR+PR.
Time to treatment failure (TTF) was definded as time from
CABO initiation to discontinuation of treatment for any reason and Overall Survival (OS) as time from CABO initiation
to the date of last follow-up (FUP) or death. OS and TTF
were estimated by Kaplan-Meier method. We reported the
rates of grade 3-4 toxicities per CTCAE v 5.0.
Results: Overall, 10 patients with metastatic pRCC FH
mutated treated with CABO were included in this study.
Median age was 38 (28-56) years, 3(30%) were male, and
5(50%) had prior nephrectomy. Performance status was ⩾
80% in 50%. IMDC risk group was good, intermediate and
poor in respectively 30%, 40%, and 30%. Among them,
40% had a family history of kidney cancer. Fifty% received
CABO as second line and 50% received CABO as a third
line. ORR and DCR were 50% and 80% respectively. TTF
and OS were 13.8 months (95% IC: 9.50-18.12) and 23.2
months (95%IC: 7.08-39.32) respectively. The median follow up was 23.2 months (95%IC: 5.7-34.1). Grade 3-4



Tumori Journal Abstract Book - October 2020

Table of Contents for the Digital Edition of Tumori Journal Abstract Book - October 2020

Contents
Tumori Journal Abstract Book - October 2020 - Cover1
Tumori Journal Abstract Book - October 2020 - Cover2
Tumori Journal Abstract Book - October 2020 - I
Tumori Journal Abstract Book - October 2020 - II
Tumori Journal Abstract Book - October 2020 - Contents
Tumori Journal Abstract Book - October 2020 - IV
Tumori Journal Abstract Book - October 2020 - V
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