Evidence map›Paper›PMID 26927447›Full record

ReviewMedical oncology (Northwood, London, England)2016

KRAS, BRAF, and PIK3CA mutations, and patient prognosis in 126 pancreatic cancers: pyrosequencing technology and literature review.

Lei Zhou, Yoshifumi Baba, Yuki Kitano, Keisuke Miyake, Xiaobo Zhang, Kensuke Yamamura, Keisuke Kosumi, Takayoshi Kaida, Kota Arima, Katsunobu Taki and 8 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 12% of its field
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

19 citing papers in PubMed, 35 citations in OpenAlex.

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  12. Base excision repair deficiency signatures implicate germline and somaticCold Spring Harbor molecular case studies · 2019
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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

18 authors at 2 institutions in 2 countries.

Lei ZhouDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Yoshifumi BabaDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Yuki KitanoDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Keisuke MiyakeDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Xiaobo ZhangDepartment of Pancreatic and Thyroidal Surgery, China Medical University Shengjing Hospital, Shenyang, 110004, People's Republic of China.
Kensuke YamamuraDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Keisuke KosumiDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Takayoshi KaidaDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Kota ArimaDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Katsunobu TakiDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Takaaki HigashiDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Katsunori ImaiDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Daisuke HashimotoDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Yoichi YamashitaDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Akira ChikamotoDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Toru BeppuDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.
Xiaodong TanDepartment of Pancreatic and Thyroidal Surgery, China Medical University Shengjing Hospital, Shenyang, 110004, People's Republic of China.
Hideo BabaDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan. hdobaba@kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0003-3963-8653
Kumamoto University · JPChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The oncogenic hallmarks of pancreatic cancer (PC), such as the KRAS, BRAF, and PIK3CA mutations, have been widely investigated. However, almost all of the previous studies were limited by small sample sizes. In addition, previous data on the KRAS mutation and clinical outcomes in PC remain inconclusive. To clarify these data, we examined the mutation status of 126 PC patients and its relationship to clinical outcome. The frequencies of KRAS, BRAF, and PIK3CA mutations were determined from a non-biased database of 126 resected PCs and a high-throughput pyrosequencing assay. KRAS mutations were detected in 109 (86.5 %) of the 126 cases; the most common mutation was c.34G > T (p.G12C), which was present in 80 tumors, followed by c.35G > T (p.G12V) in 52 tumors. The KRAS mutation was not associated with any clinical or pathological features (p > 0.05 in all cases). In addition, the KRAS mutation was unrelated to overall survival (log rank p = 0.21) and cancer-specific survival (log rank p = 0.27). Importantly, the influence of KRAS mutation on patient outcome was not modified by any of the clinical or pathological variables (p for all interactions >0.05). Only one PIK3CA mutation (0.8 %) was detected on exon 9 RS3 (c.1633G > A, p.E545K). The BRAF mutation was not detected in PC. KRAS mutations appear to be unrelated to clinical outcome in PC. BRAF and PIK3CA mutations were extremely rare in PC, suggesting that they play a limited role in PC development.

Indexed as

MutationClass I Phosphatidylinositol 3-KinasesExonsFemaleHigh-Throughput Nucleotide SequencingHumansKaplan-Meier EstimateMalePancreatic NeoplasmsPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)BRAF protein, humanClass I Phosphatidylinositol 3-KinasesKRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)BRAFKRASMutationPancreatic cancerPIK3CA

Identifiers

PMID26927447
OpenAlexW2292075477

What OpenQuestion holds

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Registered trials

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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.