Evidence map›Paper›PMID 27486759›Full record

ArticleOncotarget2016

Chemo-immunotherapy induces tumor regression in a mouse model of spontaneous mammary carcinogenesis.

Eleonora Aricò, Paola Sestili, Giulia Carpinelli, Rossella Canese, Serena Cecchetti, Giovanna Schiavoni, Maria Teresa D'Urso, Filippo Belardelli, Enrico Proietti

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 5 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

9 authors at 1 institution in 1 country.

Eleonora AricòDepartment of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Paola SestiliDepartment of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Giulia CarpinelliDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
Rossella CaneseDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
Serena CecchettiDepartment of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
Giovanna SchiavoniDepartment of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Maria Teresa D'UrsoDepartment of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Filippo BelardelliDepartment of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Enrico ProiettiDepartment of Haematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Istituto Superiore di Sanità · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-specific immune tolerance represents an obstacle for the development of effective anti-tumor immune responses through cancer vaccines. We here evaluated the efficacy of chemo-immunotherapy in breaking tumor-specific immune tolerance in an almost incurable mouse model of spontaneous carcinogenesis.Transgenic HER-2/neu mice bearing large mammary tumors received the adoptive transfer of splenocytes and serum isolated from immune donors, with or without pre-conditioning with cyclophosphamide. Treatment efficacy was assessed by monitoring tumor growth by manual inspection and by magnetic resonance imaging. The same chemo-immunotherapy protocol was tested on tumor-free HER-2/neu mice, to evaluate the effects on tumor emergence.Our data show that chemo-immunotherapy hampered carcinogenesis and caused the regression of large mammary tumor lesions in tumor-bearing HER-2/neu mice. The complete eradication of a significant number of tumor lesions occurred only in mice receiving cyclophosphamide shortly before immunotherapy, and was associated with increased serum anti HER-2/p185 antibodies and tumor leukocyte infiltration. The same protocol significantly delayed the appearance of mammary tumors when administered to tumor-free HER-2/neu mice, indicating that this chemo-immunotherapy approach acted through the elicitation of an effective anti-tumor immune response. Overall, our data support the immune-modulatory role of chemotherapy in overcoming cancer immune tolerance when administered at lymphodepleting non-myeloablative doses shortly before transfer of antigen-specific immune cells and immunoglobulins. These findings open new perspectives on combining immune-modulatory chemotherapy and immunotherapy to overcome immune tolerance in cancer patients.

Indexed as

Disease Models, AnimalAnimalsAntineoplastic Agents, AlkylatingCell Line, TumorCyclophosphamideErb-b2 Receptor Tyrosine KinasesFemaleHumansImmunotherapy, AdoptiveMammary Neoplasms, ExperimentalMice, 129 StrainMice, TransgenicRatsTreatment OutcomeAntineoplastic Agents, AlkylatingCyclophosphamideErb-b2 Receptor Tyrosine KinasesACTcancerchemotherapyHER-2 miceimmunotherapy

Identifiers

PMID27486759
PMCPMC5312346
OpenAlexW2491826241

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.