Evidence map›Paper›PMID 26859080›Full record

ArticleLeukemia2016

Targeting vasculogenesis to prevent progression in multiple myeloma.

M Moschetta, Y Mishima, Y Kawano, S Manier, B Paiva, L Palomera, Y Aljawai, A Calcinotto, C Unitt, I Sahin and 11 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. A Phase I/II Study of Evofosfamide, A Hypoxia-activated Prodrug with or without Bortezomib in Subjects with Relapsed/Refractory Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Trial
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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

21 authors at 11 institutions in 3 countries.

M MoschettaMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
Y MishimaMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
Y KawanoMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
S ManierMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
B PaivaClinica Universidad de Navarra, Centro de Investigaciones Medicas Aplicadas (CIMA), Pamplona, Spain.
L PalomeraHospital Clinico Universitario Lozano Blesa, Zaragoza. Spain.
Y AljawaiMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
A CalcinottoCellular Immunology Unit, IRCCS San Raffaele Scientific Institute, Milano, Italy.
C UnittDana Farber/Harvard Cancer Center, Boston, MA, USA.
I SahinMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
A SaccoMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
S GlaveyMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
J ShiDepartment of Biostatistics, Harvard School of Public Health, Boston, MA, USA.
M R ReaganMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
F ProsperClinica Universidad de Navarra, Centro de Investigaciones Medicas Aplicadas (CIMA), Pamplona, Spain.
M BelloneCellular Immunology Unit, IRCCS San Raffaele Scientific Institute, Milano, Italy.
M ChesiComprehensive Cancer Center, Mayo Clinic, Scottsdale, AZ, USA.
L P BergsagelComprehensive Cancer Center, Mayo Clinic, Scottsdale, AZ, USA.
A VaccaUniversity of Bari Medical School, Bari, Italy.
A M RoccaroMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
I M GhobrialMedical Oncology, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.
Dana-Farber Cancer Institute · USHarvard University · USClinica Universidad de Navarra · ESMayo Clinic in Arizona · USAzienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia · ITDana-Farber/Harvard Cancer Center · USHospital Clínico Universitario Lozano Blesa · ESIstituto di Ricovero e Cura a Carattere Scientifico San RaffaeleMaine Medical Center Research Institute · USUniversity of Bari Aldo Moro · ITVita-Salute San Raffaele University · IT

Funding

Stroma-mediated clonal evolution in Multiple MyelomaR01CA181683 · NCI · DANA-FARBER CANCER INST · PI GHOBRIAL, IRENE M. · 2014 to 2018
$1.8M
NCI NIH HHS R01 CA181683
6 · The paper itself

Abstract

The role of endothelial progenitor cell (EPC)-mediated vasculogenesis in hematological malignancies is not well explored. Here, we showed that EPCs are mobilized from the bone marrow (BM) to the peripheral blood at early stages of multiple myeloma (MM); and recruited to MM cell-colonized BM niches. Using EPC-defective ID1+/- ID3-/- mice, we found that MM tumor progression is dependent on EPC trafficking. By performing RNA-sequencing studies, we confirmed that endothelial cells can enhance proliferation and favor cell-cycle progression only in MM clones that are smoldering-like and have dependency on endothelial cells for tumor growth. We further confirmed that angiogenic dependency occurs early and not late during tumor progression in MM. By using a VEGFR2 antibody with anti-vasculogenic activity, we demonstrated that early targeting of EPCs delays tumor progression, while using the same agent at late stages of tumor progression is ineffective. Thus, although there is significant angiogenesis in myeloma, the dependency of the tumor cells on EPCs and vasculogenesis may actually precede this step. Manipulating vasculogenesis at an early stage of disease may be examined in clinical trials in patients with smoldering MM, and other hematological malignancies with precursor conditions.

Indexed as

AnimalsAntibodiesBone MarrowCell MovementClone CellsDisease ProgressionEndothelial CellsMiceMultiple MyelomaNeovascularization, PathologicSecondary PreventionVascular Endothelial Growth Factor Receptor-2AntibodiesKdr protein, mouseVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID26859080
OpenAlexW2293214575

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.