Evidence map›Paper›PMID 26336083›Full record

ArticleThe oncologist2015

Comprehensive Genomic Profiling of Advanced Esophageal Squamous Cell Carcinomas and Esophageal Adenocarcinomas Reveals Similarities and Differences.

Kai Wang, Adrienne Johnson, Siraj M Ali, Samuel J Klempner, Tanios Bekaii-Saab, Jeffrey L Vacirca, Depinder Khaira, Roman Yelensky, Juliann Chmielecki, Julia A Elvin and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The oncologist, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
8.6field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. No significant association between PIK3CA mutation and survival of esophageal squamous cell carcinoma: A meta-analysis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017
    Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Molecular mechanisms associated with chemoresistance in esophageal cancer.Cellular and molecular life sciences : CMLS · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. [Influence of molecular pathology on oncological surgery of tumors of the upper gastrointestinal tract].Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen · 2021
    Review
  20. 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

14 authors at 3 institutions in 1 country.

Kai WangFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA kwang@foundationmedicine.com.
Adrienne JohnsonFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Siraj M AliFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Samuel J KlempnerFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Tanios Bekaii-SaabFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Jeffrey L VacircaFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Depinder KhairaFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Roman YelenskyFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Juliann ChmieleckiFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Julia A ElvinFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Doron LipsonFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Vincent A MillerFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Philip J StephensFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Jeffrey S RossFoundation Medicine, Inc., Cambridge, Massachusetts, USA; Division of Hematology-Oncology, University of California Irvine, Orange, California, USA; The Ohio State University-James Cancer Hospital, Columbus, Ohio, USA; National Translational Research Group, New York, New York, USA; Albany Medical College, Albany, New York, USA.
Foundation Medicine (United States)University of California, Irvine · USThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinomas (ESCCs) and esophageal adenocarcinomas (EACs) account for >95% of esophageal malignancies and represent a major global health burden. ESCC is the dominant histology globally but represents a minority of U.S. cases, with EAC accounting for the majority of U.S. CASES: The patient outcomes for advanced ESCC and EAC are poor, and new therapeutic options are needed. Using a sensitive sequencing assay, we compared the genomic profiles of ESCC and EAC with attention to identification of therapeutically relevant genomic alterations.

methodsNext-generation sequencing-based comprehensive genomic profiling was performed on hybridization-captured, adaptor ligation-based libraries to a median coverage depth of >650× for all coding exons of 315 cancer-related genes plus selected introns from 28 genes frequently rearranged in cancer. Results from a single sample were evaluated for all classes of genomic alterations (GAs) including point mutations, short insertions and deletions, gene amplifications, homozygous deletions, and fusions/rearrangements. Clinically relevant genomic alterations (CRGAs) were defined as alterations linked to approved drugs and those under evaluation in mechanism-driven clinical trials.

resultsThere were no significant differences by sex for either tumor type, and the median age for all patients was 63 years. All ESCCs and EACs were at an advanced stage at the time of sequencing. All 71 ESCCs and 231 EACs featured GAs on profiling, with 522 GAs in ESCC (7.4 per sample) and 1,303 GAs in EAC (5.6 per sample). The frequency of clinically relevant GAs in ESCC was 94% (2.6 per sample) and 93% in EAC (2.7 per sample). CRGAs occurring more frequently in EAC included KRAS (23% EAC vs. 6% ESCC) and ERBB2 (23% EAC vs. 3% ESCC). ESCC samples were enriched for CRGA in PIK3CA (24% ESCC vs. 10% EAC), PTEN (11% ESCC vs. 4% EAC), and NOTCH1 (17% ESCC vs. 3% EAC). Other GAs that differed significantly between histologic tumor types included SMAD4 (14% EAC vs. 1% ESCC), RB1 (14% ESCC vs. 2% EAC), SOX2 (18% ESCC vs. 1% EAC), and NFE2L2 (24% ESCC vs. 1% EAC).

conclusionESCC and EAC share similarly high frequencies of overall and clinically relevant genomic alterations; however, the profiles of genomic alterations in the two diseases differ widely, with KRAS and ERBB2 far more frequently altered in EAC compared with ESCC and with mammalian target of rapamycin (MTOR) pathway genes (PIK3CA and PTEN) and NOTCH1 more frequently altered in ESCC compared with EAC. Comprehensive genomic profiling highlights the promise of identifying clinically relevant genomic alterations in both ESCC and EAC and suggests new avenues for molecularly directed therapies in esophageal cancer.

Indexed as

TranscriptomeAdenocarcinomaAdultAgedAged, 80 and overCarcinoma, Squamous CellEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedMutationAdenocarcinomaComprehensive genomic profilingEsophageal cancerNext-generation sequencingSquamous cellTargeted therapy

Identifiers

PMID26336083
PMCPMC4591943
OpenAlexW2144333719

What OpenQuestion holds

Textmetadata
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.