Evidence map›Paper›PMID 25639873›Full record

ReviewOncogene2015

The tumor microenvironment shapes hallmarks of mature B-cell malignancies.

K H Shain, W S Dalton, J Tao

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
8.0field-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

63 citing papers in PubMed, 99 citations in OpenAlex.

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  16. Complex genetic and histopathological study of 15 patient-derived xenografts of aggressive lymphomas.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  17. Review
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  19. Bone-Targeted Bortezomib Inhibits Bortezomib-Resistant Multiple Myeloma in Mice by Providing Higher Levels of Bortezomib in Bone.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  20. Review

3 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

K H ShainDepartment of Malignant Hematology and Chemical Biology and Molecular Medicine Program, Tampa, FL, USA.
W S DaltonDepartment of Malignant Hematology and Chemical Biology and Molecular Medicine Program, Tampa, FL, USA.
J TaoDepartment of Hematopathology and Laboratory Medicine, Moffitt Cancer Center and Research Institute at the University of South Florida, Tampa, FL, USA.
University of Tampa · USMoffitt Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Integrative Molecular Epidemiology WorkshopR25CA174664 · NCI · AMERICAN ASSOCIATION FOR CANCER RESEARCH · PI Shelley S Tworoger · 2013 to 2026
$2.8M
Tageting BAFF and BAFF-Induced Non-Canonical NF-kB Pathways for Enhancing Mantle R01CA137123 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI TAO, JIANGUO · 2009 to 2013
$1.3M
NCI NIH HHS P30 CA076292NCI NIH HHS P30-CA076292NCI NIH HHS R01 CA137123NCI NIH HHS R01CA137123NCI NIH HHS R25 CA174664
6 · The paper itself

Abstract

B-cell tumorigenesis results from a host of known and unknown genetic anomalies, including non-random translocations of genes that normally function as determinants of cell proliferation or cell survival to regions juxtaposed to active immunoglobulin heavy chain enhancer elements, chromosomal aneuploidy, somatic mutations that further affect oncogenic signaling and loss of heterozygosity of tumor-suppressor genes. However, it is critical to recognize that even in the setting of a genetic disease, the B-cell/plasma cell tumor microenvironment (TME) contributes significantly to malignant transformation and pathogenesis. Over a decade ago, we proposed the concept of cell adhesion-mediated drug resistance to delineate a form of TME-mediated drug resistance that protects hematopoietic tumor cells from the initial effect of diverse therapies. In the interim, it has been increasingly appreciated that TME also contributes to tumor initiation and progression through sustained growth/proliferation, self-renewal capacity, immune evasion, migration and invasion as well as resistance to cell death in a host of B-cell malignancies, including mantle cell lymphoma, diffuse large B-cell lymphoma, Waldenstroms macroglobulinemia, chronic lymphocytic leukemia and multiple myeloma. Within this review, we propose that TME and the tumor co-evolve as a consequence of bidirectional signaling networks. As such, TME represents an important target and should be considered integral to tumor progression and drug response.

Indexed as

B-LymphocytesCarcinogenesisCell ProliferationCell SurvivalHumansLeukemia, Lymphocytic, Chronic, B-CellLymphoma, Large B-Cell, DiffuseLymphoma, Mantle-CellMultiple MyelomaSignal TransductionTumor Microenvironment

Identifiers

PMID25639873
PMCPMC4688902
OpenAlexW2030086461

What OpenQuestion holds

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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.