Evidence map›Paper›PMID 32193223›Full record

ArticleCancer discovery2020

The Evolutionary Origins of Recurrent Pancreatic Cancer.

Hitomi Sakamoto, Marc A Attiyeh, Jeffrey M Gerold, Alvin P Makohon-Moore, Akimasa Hayashi, Jungeui Hong, Rajya Kappagantula, Lance Zhang, Jerry P Melchor, Johannes G Reiter and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
6.7field-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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.

  1. Pooled it
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  4. Observational
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 4 institutions in 1 country.

Hitomi Sakamoto *Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID https://orcid.org/0000-0002-5688-7806
Marc A Attiyeh *Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID https://orcid.org/0000-0002-9949-1449
Jeffrey M Gerold *Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts.
Alvin P Makohon-MooreSloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Akimasa HayashiSloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Jungeui HongSloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Rajya KappagantulaSloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Lance ZhangSloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Jerry P MelchorSloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, New York.
Johannes G ReiterCanary Center for Cancer Early Detection, Department of Radiology, Stanford University, Palo Alto, California.ORCID https://orcid.org/0000-0002-0170-7353
Alexander HeydeProgram for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts.
Craig M BielskiMarie-Josee and Henry R. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York.
Alexander V PensonHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID https://orcid.org/0000-0003-2429-2370
Mithat GönenDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
Debyani ChakravartyMarie-Josee and Henry R. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York.
Eileen M O'ReillyHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.
Laura D WoodDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland.
Ralph H HrubanDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland.
Martin A NowakProgram for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts.ORCID https://orcid.org/0000-0001-5489-0908
Nicholas D SocciBioinformatics Core, Memorial Sloan Kettering Cancer Center, New York, New York.
Barry S TaylorHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.
Christine A Iacobuzio-DonahueHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York. iacobuzc@mskcc.org.ORCID https://orcid.org/0000-0002-4672-3023
Memorial Sloan Kettering Cancer Center · USEvolutionary Genomics (United States) · USJohns Hopkins University · USPalo Alto University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI JAFFEE, ELIZABETH M. · 1993 to 2022
$54.6M
Training Program in Bioinformatics and Integrative GenomicsT32HG002295 · NHGRI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Peter J Park · 2001 to 2026
$15.8M
Interrogating the Evolutionary Dynamics of Cancer for Clinical Benefit and ActionabilityR35CA220508 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI IACOBUZIO-DONAHUE, CHRISTINE A · 2018 to 2024
$6.9M
Translational Research in Oncology Training ProgramT32CA160001 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SAWYERS, CHARLES L. · 2011 to 2020
$2.0M
(PQB6) Genetics of Subclonal Evolution in Pancreatic CancerR01CA179991 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI IACOBUZIO-DONAHUE, CHRISTINE A · 2013 to 2016
$1.3M
Inferring the roots of metastases and their effects on patient survivalR00CA229991 · NCI · STANFORD UNIVERSITY · PI REITER, JOHANNES G · 2019 to 2021
$743k
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA062924NCI NIH HHS R00 CA229991NCI NIH HHS R01 CA179991NCI NIH HHS R35 CA220508NCI NIH HHS T32 CA160001NHGRI NIH HHS T32 HG002295
6 · The paper itself

Abstract

Surgery is the only curative option for stage I/II pancreatic cancer; nonetheless, most patients will experience a recurrence after surgery and die of their disease. To identify novel opportunities for management of recurrent pancreatic cancer, we performed whole-exome or targeted sequencing of 10 resected primary cancers and matched intrapancreatic recurrences or distant metastases. We identified that recurrent disease after adjuvant or first-line platinum therapy corresponds to an increased mutational burden. Recurrent disease is enriched for genetic alterations predicted to activate MAPK/ERK and PI3K-AKT signaling and develops from a monophyletic or polyphyletic origin. Treatment-induced genetic bottlenecks lead to a modified genetic landscape and subclonal heterogeneity for driver gene alterations in part due to intermetastatic seeding. In 1 patient what was believed to be recurrent disease was an independent (second) primary tumor. These findings suggest routine post-treatment sampling may have value in the management of recurrent pancreatic cancer. SIGNIFICANCE: The biological features or clinical vulnerabilities of recurrent pancreatic cancer after pancreaticoduodenectomy are unknown. Using whole-exome sequencing we find that recurrent disease has a distinct genomic landscape, intermetastatic genetic heterogeneity, diverse clonal origins, and higher mutational burden than found for treatment-naïve disease.

Indexed as

Carcinoma, Pancreatic DuctalEvolution, MolecularExome SequencingHumansNeoplasm MetastasisNeoplasm Recurrence, LocalPancreatic Neoplasms

Identifiers

PMID32193223
PMCPMC7323937
OpenAlexW3011715213

What OpenQuestion holds

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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.