See the published version of this preprint at World Journal of Surgical Oncology.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Xiang Wang
Corresponding Author
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Background: Several driver genetic alterations have been identified in micropapillary lung adenocarcinoma (MPA). However, the frequency of ROS1 rearrangements is yet unclear. Herein, we investigated the associations between clinicopathological and molecular characteristics of MPA compared with non-micropapillary lung adenocarcinoma (LA).
Methods: FFPE sections derived from lung adenocarcinoma patients who never received adjuvant chemotherapy or radiation therapy prior to surgical resection were collected from October 2016 to June 2019. EGFR mutations, ROS1 rearrangements and EML4-ALK fusions were identified in a set of 131 MPA and LA cases by using the Amplification Refractory Mutation System.
Results: EGFR mutations had occurred in 42 (76.4%) MPA patients and 42 (55.3%) LA patients. But interestingly, ROS1 rearrangement was present in 10.9% (6/55) MPA cases and 1.3% (1/76) LA cases. Moreover, 7.3% (4/55) MPA samples had multiple gene mutations, while only 1.3% (1/76) LA cases had double gene alterations.
Conclusions: A higher prevalence of ROS1 rearrangements or combined mutations of ROS1 and EGFR or EML4-ALK may play a critical role in the tumorigenesis of MPA. These finding provides a novel therapy strategy for the patients with malignant MPA through combining TKIs than one TKI.
Keywords
Lung adenocarcinoma, Micropapillary pattern, EGFR, ROS1, EML4-ALK
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CURRENT STATUS: Published
View the published article at World Journal of Surgical Oncology.
No community comments so far
Editorial decision: Accept
On 02 Jul, 2020
Editor assigned
On 29 Jun, 2020
Submission checks complete
On 28 Jun, 2020
Editor invited
On 28 Jun, 2020
No comments provided
Editorial decision: Major Revision
On 20 Jun, 2020
Review #2 received
Received 19 Jun, 2020
Reviewer #1 agreed
On 15 Jun, 2020
Reviewer #2 agreed
On 15 Jun, 2020
Review #1 received
Received 15 Jun, 2020
Editor assigned
On 14 Jun, 2020
Reviewers invited
Invitations sent on 14 Jun, 2020
Submission checks complete
On 13 Jun, 2020
Editor invited
On 13 Jun, 2020
Version 1
Posted 24 Feb, 2020
No comments provided
Editorial decision: Major Revision
On 22 May, 2020
Review #1 received
Received 21 May, 2020
Review #2 received
Received 09 May, 2020
Reviewer #3 agreed
On 27 Mar, 2020
Reviewer #2 agreed
On 21 Mar, 2020
Reviewer #1 agreed
On 09 Mar, 2020
Reviewers invited
Invitations sent on 21 Feb, 2020
Editor assigned
On 19 Feb, 2020
Submission checks complete
On 18 Feb, 2020
Editor invited
On 18 Feb, 2020
First submitted
On 17 Feb, 2020
Metrics
Comments: 0
PDF Downloads: ...
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Subject Areas
Oncology
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See the published version of this preprint at World Journal of Surgical Oncology.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Xiang Wang
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at World Journal of Surgical Oncology.
No community comments so far
Editorial decision: Accept
On 02 Jul, 2020
Editor assigned
On 29 Jun, 2020
Submission checks complete
On 28 Jun, 2020
Editor invited
On 28 Jun, 2020
No comments provided
Editorial decision: Major Revision
On 20 Jun, 2020
Review #2 received
Received 19 Jun, 2020
Reviewer #1 agreed
On 15 Jun, 2020
Reviewer #2 agreed
On 15 Jun, 2020
Review #1 received
Received 15 Jun, 2020
Editor assigned
On 14 Jun, 2020
Reviewers invited
Invitations sent on 14 Jun, 2020
Submission checks complete
On 13 Jun, 2020
Editor invited
On 13 Jun, 2020
Version 1
Posted 24 Feb, 2020
No comments provided
Editorial decision: Major Revision
On 22 May, 2020
Review #1 received
Received 21 May, 2020
Review #2 received
Received 09 May, 2020
Reviewer #3 agreed
On 27 Mar, 2020
Reviewer #2 agreed
On 21 Mar, 2020
Reviewer #1 agreed
On 09 Mar, 2020
Reviewers invited
Invitations sent on 21 Feb, 2020
Editor assigned
On 19 Feb, 2020
Submission checks complete
On 18 Feb, 2020
Editor invited
On 18 Feb, 2020
First submitted
On 17 Feb, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Oncology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at World Journal of Surgical Oncology.
Background: Several driver genetic alterations have been identified in micropapillary lung adenocarcinoma (MPA). However, the frequency of ROS1 rearrangements is yet unclear. Herein, we investigated the associations between clinicopathological and molecular characteristics of MPA compared with non-micropapillary lung adenocarcinoma (LA).
Methods: FFPE sections derived from lung adenocarcinoma patients who never received adjuvant chemotherapy or radiation therapy prior to surgical resection were collected from October 2016 to June 2019. EGFR mutations, ROS1 rearrangements and EML4-ALK fusions were identified in a set of 131 MPA and LA cases by using the Amplification Refractory Mutation System.
Results: EGFR mutations had occurred in 42 (76.4%) MPA patients and 42 (55.3%) LA patients. But interestingly, ROS1 rearrangement was present in 10.9% (6/55) MPA cases and 1.3% (1/76) LA cases. Moreover, 7.3% (4/55) MPA samples had multiple gene mutations, while only 1.3% (1/76) LA cases had double gene alterations.
Conclusions: A higher prevalence of ROS1 rearrangements or combined mutations of ROS1 and EGFR or EML4-ALK may play a critical role in the tumorigenesis of MPA. These finding provides a novel therapy strategy for the patients with malignant MPA through combining TKIs than one TKI.
Figure 1
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