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Alessandra Fabbri
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P2.09 - Pathology (ID 174)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Pathology
- Presentations: 1
- Now Available
- Moderators:
- Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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P2.09-05 - Clinical and Biological Characterization of Lung Enteric Adenocarcinoma (Now Available) (ID 1650)
10:15 - 18:15 | Author(s): Alessandra Fabbri
- Abstract
Background
Lung Enteric Adenocarcinoma (LEA) is a rare and poorly characterized variant of Lung Adenocarcinoma (LA), defined by an intestinal differentiation in ≥50% of tumor and ≥1 colorectal biomarker at Immunohistochemistry.
Method
We retrospectively identified the cases of LEA diagnosed at Fondazione IRCCS Istituto Nazionale dei Tumori (INT), Milan, Italy between 01/2013 and 12/2018. Next Generation Sequencing was performed with IonTorrent (ThermoFisher Scientific, Life Technologies) by using the commercial Hot Spot Cancer Panel (HCP) on DNA derived from formalin-fixed paraffin-embedded tissues. ALK and ROS-1 status was assessed with fluorescent in situ hybridization. PD-L1 expression was determined with DAKO22C3 assay. Biological data obtained from our cases were compared with those reported in Tumor Cancer Genome Atlas (TCGA) for LA, restricting the comparison only to the genes targeted by HCP.
Result
We identified 38 LEA cases. Main clinical and biological characteristics of the two populations are detailed in the table.
Variable/
gene mutation
INT LEA (N=38)
TCGA LA (N=660)
%
%
Gender
Female
34.1
51.9
Male
65.9
47.9
Unknown
0
0.2
Smoking status
Former/current
76.3
78.9
Never
15.8
14.1
Unknown
7.9
7.0
Disease stage
I
2.6
51.6
II
2.6
23.0
III
28.9
16.4
IV
65.9
4.7
Unknown
0
4.3
TP53
52.6
54.1
KRAS
34.2
32.4
STK11
23.7
15.8
CDKN2A
15.8
3.9
APC
7.9
4.8
CTNNB1
7.9
3.8
EGFR
7.9
15.8
KIT
5.3
2.1
PI3KCA
5.3
5.9
SMAD4
5.3
4.1
ATM
2.6
8.9
BRAF
2.6
8.2
FGFR
2.6
0.8
GNAS
2.6
3.8
NRAS
2.6
0.6
PDGFRA
2.6
7.4
RB1
2.6
5.8
SMO
2.6
2.7
Neither ALK nor ROS-1 rearrangements were detected in our case series. PD-L1 was negative in 23 cases, 1-49% in 9 cases, not evaluable in 6 cases. Microsatellite were stable except for 3 cases with low instability and 3 not evaluable cases.
Conclusion
Our series of LEA was small and differed from TCGA LA for a higher proportions of males and metastatic disease. Given these limitations, our LEA genetic profile showed some difference from that of TCGA LA. In particular, LEA showed a higher incidence of STK11, CTNNB1, FGFR, NRAS, KIT and CDKN2A mutations, and a lower incidence of ATM, BRAF, PDGFRA, RB-1 and EGFR mutations. PD-L1 expression, ALK and ROS-1 rearrangements were lower than literature data in LA. Most cases were microsatellite stable. In conclusion, further research is needed to understand the biology of LEA, which seems partially different from common LA.
