Evidence map›Paper›PMID 24755613›Full record

ArticleCancer biology & therapy2014

Vemurafenib and panitumumab combination tailored therapy in BRAF-mutated metastatic colorectal cancer: a case report.

Carlo Capalbo, Paolo Marchetti, Anna Coppa, Antonella Calogero, Emanuela Anastasi, Amelia Buffone, Francesca Belardinilli, Matteo Gulino, Paola Frati, Carlo Catalano and 3 more

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

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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

13 authors at 4 institutions in 4 countries.

Carlo CapalboDepartment of Molecular Medicine; Sapienza University of Rome; Rome, Italy; Medical Oncology; IDI IRCCS; Rome, Italy.
Paolo MarchettiMedical Oncology; IDI IRCCS; Rome, Italy; Department of Clinical and Molecular Medicine; Sapienza University of Rome; Rome, Italy.
Anna CoppaDepartment of Experimental Medicine; Sapienza University of Rome; Rome, Italy.
Antonella CalogeroDepartment of Medical-Surgical Sciences and Biotechnologies; Sapienza University of Rome; Rome, Italy.
Emanuela AnastasiDepartment of Molecular Medicine; Sapienza University of Rome; Rome, Italy.
Amelia BuffoneDepartment of Molecular Medicine; Sapienza University of Rome; Rome, Italy.
Francesca BelardinilliDepartment of Molecular Medicine; Sapienza University of Rome; Rome, Italy.
Matteo GulinoDepartment of Anatomical, Histological, Forensic Medicine and Orthopedic Science; Forensic Medicine Section; Sapienza University of Rome; Rome, Italy.
Paola FratiDepartment of Anatomical, Histological, Forensic Medicine and Orthopedic Science; Forensic Medicine Section; Sapienza University of Rome; Rome, Italy; Neuromed IRCCS; Pozzilli, Italy.
Carlo CatalanoDepartment of Radiological, Oncological and Pathological Sciences; Sapienza University of Rome; Rome, Italy.
Enrico CortesiDepartment of Radiological, Oncological and Pathological Sciences; Sapienza University of Rome; Rome, Italy.
Giuseppe GianniniDepartment of Molecular Medicine; Sapienza University of Rome; Rome, Italy.
Alberto GulinoNeuromed IRCCS; Pozzilli, Italy; Department of Molecular Medicine; Center for Life Nanoscience@Sapienza; Italian Institute of Technology and Istituto Pasteur; Fondazione Cenci-Bolognetti; Sapienza University of Rome; Rome, Italy.
Sapienza University of Rome · ITPathological Society · GBCenter for NanoScience · DEIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the knowledge on cancer genetic alterations progresses, it fosters the need for more personalized therapeutic intervention in modern cancer management. Recently, mutations in KRAS, BRAF, and PIK3CA genes have emerged as important mechanisms of resistance to EGFR-targeted therapy in metastatic colorectal cancer (mCRC). Here we report the first case of a mCRC patient whose disease had progressed on standard lines of treatment and for which we devised a personalized therapeutic approach consisting of vemurafenib (Zelboraf) and panitumumab (Vectibix), based on the following molecular profile: BRAF(V600E)-mutant, amplified EGFR (double positive) and WT KRAS, WT PIK3CA, not-amplified HER2 (triple negative). This new combination therapy was well tolerated and resulted in a strong control of the disease. In particular, the vemurafenib-panitumumab combination appears to limit the typical toxicity of single agents, since no cutaneous toxic effects typically associated with vemurafenib were observed. Here we report the first clinical evidence that the combination of an anti-EGFR (panitumumab) and an inhibitor of BRAF(V600E) (vemurafenib) is well tolerated and results in a strong disease control in an extensively pretreated mCRC patient.

Indexed as

AdenocarcinomaAntibodies, MonoclonalAntineoplastic Combined Chemotherapy ProtocolsColorectal NeoplasmsHumansIndolesMaleMiddle AgedMutationPanitumumabProto-Oncogene Proteins B-rafSulfonamidesVemurafenibAntibodies, MonoclonalBRAF protein, humanIndolesPanitumumabProto-Oncogene Proteins B-rafSulfonamidesVemurafenibBRAFcolorectal cancercutaneous toxicityEGFRpanitumumabpersonalized medicinetarget therapyvemurafenib

Identifiers

PMID24755613
PMCPMC4100983
OpenAlexW1977775137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.