TY - JOUR
T1 - Gemcitabine versus FOLFIRINOX in patients with advanced pancreatic adenocarcinoma hENT1-positive: everything was not too bad back when everything seemed worse
AU - Orlandi, A
AU - Calegari, M A
AU - Martini, M
AU - Cocomazzi, A
AU - Bagalà, C
AU - Indellicati, G
AU - Zurlo, V
AU - Basso, M
AU - Cassano, Alessandra
AU - Larocca, L M
AU - Barone, C
PY - 2016
Y1 - 2016
N2 - Purpose hENT1 is a transmembrane protein which acts\r\nas a nucleoside transporter and is the main mediator of\r\nGemcitabine (GEM) uptake into human cells. In this retrospective\r\nstudy we compared GEM versus FOLFIRINOX\r\nin patients with metastatic pancreatic cancer in which\r\nhENT1 evaluation was available.\r\nMethods 149 patients affected by unresectable metastatic\r\npancreatic cancer, treated in our institution from 2009 to\r\n2013, have been screened for inclusion in this retrospective\r\nstudy. Seventy patients, treated with GEM or FOLFIRINOX\r\nin first-line therapy, fulfilled clinical inclusion criteria\r\nfor survival analysis. Thirty-one patients were\r\navailable and contained sufficient quality/quantity RNA for\r\nevaluation of hENT1 expression by RT-PCR. The primary\r\nendpoint was OS and the secondary endpoint was PFS.\r\nResults The survival analysis, carried out on 70 patients\r\nregardless of hENT1 expression, showed a statistically longer\r\nOSandPFS in the group treated with FOLFIRINOX compared\r\nto GEM. Within the exploratory analysis, which included 31\r\npatients, no differences were found in hENT1 positive patients\r\ntreated with FOLFIRINOX compared to GEM in terms of OS\r\n(8.5 vs 7 months, HR: 0.89; 95 % CI 0.3–2.5; p = 0.8) and\r\nPFS (5.5 vs 5 months, HR: 0.8, 95 % CI 0.2–2.2; p = 0.61).\r\nGEM-treated hENT1 positive patients showed a statistically\r\nsignificant improvement both of OS (8 vs 2 months;\r\np = 0.0012) and PFS (5 vs 1 months; p = 0.0004) in comparison\r\nto GEM-treated hENT1 negative patients.\r\nConclusions In our exploratory analysis GEM seems as\r\neffective as FOLFIRINOX in terms of survival with a\r\nbetter safety profile in hENT1 positive metastatic pancreatic\r\ncancer.
AB - Purpose hENT1 is a transmembrane protein which acts\r\nas a nucleoside transporter and is the main mediator of\r\nGemcitabine (GEM) uptake into human cells. In this retrospective\r\nstudy we compared GEM versus FOLFIRINOX\r\nin patients with metastatic pancreatic cancer in which\r\nhENT1 evaluation was available.\r\nMethods 149 patients affected by unresectable metastatic\r\npancreatic cancer, treated in our institution from 2009 to\r\n2013, have been screened for inclusion in this retrospective\r\nstudy. Seventy patients, treated with GEM or FOLFIRINOX\r\nin first-line therapy, fulfilled clinical inclusion criteria\r\nfor survival analysis. Thirty-one patients were\r\navailable and contained sufficient quality/quantity RNA for\r\nevaluation of hENT1 expression by RT-PCR. The primary\r\nendpoint was OS and the secondary endpoint was PFS.\r\nResults The survival analysis, carried out on 70 patients\r\nregardless of hENT1 expression, showed a statistically longer\r\nOSandPFS in the group treated with FOLFIRINOX compared\r\nto GEM. Within the exploratory analysis, which included 31\r\npatients, no differences were found in hENT1 positive patients\r\ntreated with FOLFIRINOX compared to GEM in terms of OS\r\n(8.5 vs 7 months, HR: 0.89; 95 % CI 0.3–2.5; p = 0.8) and\r\nPFS (5.5 vs 5 months, HR: 0.8, 95 % CI 0.2–2.2; p = 0.61).\r\nGEM-treated hENT1 positive patients showed a statistically\r\nsignificant improvement both of OS (8 vs 2 months;\r\np = 0.0012) and PFS (5 vs 1 months; p = 0.0004) in comparison\r\nto GEM-treated hENT1 negative patients.\r\nConclusions In our exploratory analysis GEM seems as\r\neffective as FOLFIRINOX in terms of survival with a\r\nbetter safety profile in hENT1 positive metastatic pancreatic\r\ncancer.
KW - FOLFIRINOX
KW - Gemcitabine
KW - Metastatic pancreatic adenocarcinoma
KW - hENT1
KW - FOLFIRINOX
KW - Gemcitabine
KW - Metastatic pancreatic adenocarcinoma
KW - hENT1
UR - https://publicatt.unicatt.it/handle/10807/317581
UR - https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=84953380838&origin=inward
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84953380838&origin=inward
U2 - 10.1007/s12094-015-1471-z
DO - 10.1007/s12094-015-1471-z
M3 - Article
SN - 1699-048X
SP - N/A-N/A
JO - Clinical and Translational Oncology
JF - Clinical and Translational Oncology
IS - N/A
ER -