Evidence map›Paper›PMID 33796913›Full record

ArticleJournal of cancer research and clinical oncology2021

Comprehensive analysis of the clinicopathological features, targetable profile, and prognosis of mucinous adenocarcinoma of the lung.

Daisuke Ueda, Masaoki Ito, Yasuhiro Tsutani, Ana Giménez-Capitán, Ruth Román-Lladó, Ana Pérez-Rosado, Cristina Aguado, Kei Kushitani, Yoshihiro Miyata, Koji Arihiro and 4 more

Abstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Diagnostic gastrointestinal markers in primary lung cancer and pulmonary metastases.Virchows Archiv : an international journal of pathology · 2024
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Daisuke UedaDepartment of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima, Japan.
Masaoki ItoDepartment of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima, Japan.ORCID http://orcid.org/0000-0001-7296-4624
Yasuhiro TsutaniDepartment of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima, Japan.
Ana Giménez-CapitánPangaea Oncology, Laboratory of Molecular Biology, Quirón-Dexeus University Institute, Barcelona, Spain.
Ruth Román-LladóPangaea Oncology, Laboratory of Molecular Biology, Quirón-Dexeus University Institute, Barcelona, Spain.
Ana Pérez-RosadoPangaea Oncology, Laboratory of Molecular Biology, Quirón-Dexeus University Institute, Barcelona, Spain.
Cristina AguadoPangaea Oncology, Laboratory of Molecular Biology, Quirón-Dexeus University Institute, Barcelona, Spain.
Kei KushitaniDepartment of Pathology, Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan.
Yoshihiro MiyataDepartment of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima, Japan.
Koji ArihiroDepartment of Anatomical Pathology, Hiroshima University Hospital, Hiroshima, Japan.
Miguel Angel Molina-VilaPangaea Oncology, Laboratory of Molecular Biology, Quirón-Dexeus University Institute, Barcelona, Spain.
Rafael RosellLaboratory of Cellular and Molecular Biology, Institute for Health Science Research Germans Trias I Pujol (IGTP), Badalona, Spain.
Yukio TakeshimaDepartment of Pathology, Graduate School of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan.
Morihito OkadaDepartment of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima, Japan. morihito1217@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe clinicopathological or genetic features related to the prognosis of mucinous adenocarcinoma are unknown because of its rarity. The clinicopathological or targetable features were investigated for better management of patients with mucinous adenocarcinoma of the lung.

methodsWe comprehensively evaluated the clinicopathological and genetic features of 60 completely resected mucinous lung adenocarcinomas. Targetable genetic variants were explored using nCounter and polymerase chain reaction, PD-L1 and TTF-1 expression were evaluated using immunohistochemistry. We analyzed the prognostic impact using the Kaplan-Meier method and log-rank test.

resultsOf the 60 enrolled patients, 13 (21.7%) had adenocarcinoma in situ/minimally invasive adenocarcinoma, and 47 (78.3%) had invasive mucinous adenocarcinoma (IMA). Fifteen patients (25%) showed a pneumonic appearance on computed tomography (CT). CD74-NRG1 fusion, EGFR mutations, and BRAF mutation were detected in three (5%), four (6.7%), and one (1.7%) patient(s), respectively. KRAS mutations were detected in 31 patients (51.7%). Two patients (3.5%) showed immunoreactivity for PD-L1. No in situ or minimally invasive cases recurred. IMA patients with pneumonic appearance had significantly worse recurrence-free survival (RFS) and overall survival (OS) (p < 0.001). Furthermore, IMA patients harboring KRAS mutations had worse RFS (p = 0.211). Multivariate analysis revealed that radiological pneumonic appearance was significantly associated with lower RFS (p < 0.003) and OS (p = 0.012). KRAS mutations served as an unfavorable status for RFS (p = 0.043).

conclusionMucinous adenocarcinoma had a low frequency of targetable genetic variants and PD-L1 immunoreactivity; however, KRAS mutations were frequent. Pneumonic appearance on CT imaging and KRAS mutations were clinicopathological features associated with a worse prognosis.

Indexed as

Adenocarcinoma, MucinousAgedAged, 80 and overFemaleHumansLung NeoplasmsMaleMiddle AgedMutationNeoplasm Recurrence, LocalPrognosisProgression-Free SurvivalProto-Oncogene Proteins p21(ras)Retrospective StudiesKRAS protein, humanProto-Oncogene Proteins p21(ras)KRASMucinous adenocarcinomanCounterNRG1PD-L1

Identifiers

PMID33796913
PMCPMC11802007

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.