Evidence map›Paper›PMID 30591192›Full record

ArticleCurrent problems in cancer2019

Epidermal growth factor receptor (EGFR), KRAS, and BRAF mutations in lung adenocarcinomas: A study from India.

Varsha Singh, Prerna Guleria, Prabhat Singh Malik, Anant Mohan, Sanjay Thulkar, R M Pandey, Kalpana Luthra, Sudheer Arava, Ruma Ray, Deepali Jain

Abstract read
In one paragraph

Article in Current problems in cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Observational
  4. Article
  5. Article
  6. Article
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

10 authors.

Varsha SinghDepartment of Pathology, All India Institute of Medical Sciences, New Delhi, India.
Prerna GuleriaDepartment of Pathology, All India Institute of Medical Sciences, New Delhi, India.
Prabhat Singh MalikDepartment of Medical Oncology, All India Institute of Medical Sciences, New Delhi, India.
Anant MohanDepartment of Pulmonary Medicine and Sleep Disorders, All India Institute of Medical Sciences, New Delhi, India.
Sanjay ThulkarDepartment of Radio-Diagnosis, All India Institute of Medical Sciences, New Delhi, India.
R M PandeyDepartment of Biostatistics, All India Institute of Medical Sciences, New Delhi, India.
Kalpana LuthraDepartment of Biochemistry, All India Institute of Medical Sciences, New Delhi, India.
Sudheer AravaDepartment of Pathology, All India Institute of Medical Sciences, New Delhi, India.
Ruma RayDepartment of Pathology, All India Institute of Medical Sciences, New Delhi, India.
Deepali JainDepartment of Pathology, All India Institute of Medical Sciences, New Delhi, India. Electronic address: deepalijain76@gmail.com.

Funding

Translational Research Enhancement CoreP30DK089502 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI ZACHOS, NICHOLAS CONSTANTINE · 2011 to 2020
$12.0M
DIARRHEAL DISEASES: A PHYSIOLOGIC APPROACH TO TREATMENTR01DK026523 · NIDDK · TUFTS MEDICAL CENTER · PI DONOWITZ, MARK · 1986 to 2016
$7.8M
NIDDK NIH HHS P30 DK089502NIDDK NIH HHS R01 DK026523
6 · The paper itself

Abstract

Mitogen-Activated Protein (MAP) Kinase pathway involves several oncogenic genes which can serve as potential targets for therapy. Therefore, aim of the present study is to analyze mutations in the MAP Kinase pathway in pulmonary adenocarcinoma (ADCA) of Indian patients along with clinico-pathologic correlation and determination of the survival status in patients receiving therapy. Blocks and slides of 125 pulmonary ADCA of last 5 years were retrieved. Histo-morphology and tumor content were determined. EGFR, KRAS, BRAF and MEK1 genes were analyzed using Sanger sequencing and Real-time polymerase chain reaction (PCR). Clinico-pathologic correlation and survival analysis were performed. Fifty-eight (46.4%) patients harbored genetic mutations of which 49 had single somatic mutations, 5 had multiple exonic and 4 showed coexisting EGFR and KRAS mutations. EGFR mutations were seen in 24.8%, KRAS in 19.2% and BRAF (non-V600E) in 2.4% cases. There was no difference in progression-free survival of wild- type/single mutations when compared with multiple/ coexisting mutations (P = 0.09). However, the P value may indicate borderline correlation. To conclude, EGFR and KRAS mutations may coexist in the same patient in lung ADCA. Multiple exonic mutations of KRAS gene formed substantial percentage of our cohort, requiring further exploration. Lung ADCA harbouring BRAF mutations are commonly non-V600E. Testing of all major genetic driver mutations of lung ADCA irrespective of histology and other demographic characteristics is necessary.

Indexed as

Adenocarcinoma of LungAdultAgedAged, 80 and overAntineoplastic AgentsDNA Mutational AnalysisErbB ReceptorsFemaleFollow-Up StudiesHumansIndiaKaplan-Meier EstimateLungLung NeoplasmsMaleMAP Kinase Signaling SystemAntineoplastic AgentsBRAF protein, humanEGFR protein, humanErbB ReceptorsKRAS protein, humanProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)

Identifiers

PMID30591192
PMCPMC6579716

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.