Evidence map›Paper›PMID 25742458›Full record

ReviewNature medicine2015

Anemia: progress in molecular mechanisms and therapies.

Vijay G Sankaran, Mitchell J Weiss

Open access · greenAbstract readReview
In one paragraph

Review in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 1 pooled it
17.5field-weighted citation impact, top 1% 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

138 citing papers in PubMed, 1 synthesis or guideline pooled it, 264 citations in OpenAlex.

  1. Pooled it
  2. Risk prediction models based on hematological/body parameters for chemotherapy-induced adverse effects in Chinese colorectal cancer patients.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2021
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78 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

2 authors at 2 institutions in 1 country.

Vijay G Sankaran1] Division of Hematology and Oncology, The Manton Center for Orphan Disease Research, Boston Children's Hospital, Boston, Massachusetts, USA. [2] Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA. [3] Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts, USA.
Mitchell J WeissDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Boston Children's Hospital · USSt. Jude Children's Research Hospital · US

Funding

Translational and clinical studies targeting y-globin modulationU01HL117720 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI SANKARAN, VIJAY GANESH · 2013 to 2017
$7.4M
Systematic Genetic Dissection of Human ErythropoiesisR01DK103794 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI Vijay Ganesh Sankaran · 2014 to 2026
$5.9M
Trim58 and the Ubiquitin Proteasome System in Erythro-megakaryopoiesisR01DK061692 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI WEISS, MITCHELL J · 2002 to 2018
$5.6M
Mechanisms of Heterocellular Signaling at the Myoenothelial JunctionR01HL088554 · NHLBI · UNIVERSITY OF VIRGINIA · PI ISAKSON, BRANT E, WEISS, MITCHELL J · 2008 to 2017
$3.8M
Regulation of erythropoiesis by the miR-144/451 microRNA locusR01DK092318 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI WEISS, MITCHELL J · 2012 to 2016
$1.8M
Identifying Genome-wide Association Study-Nominated Regulators of ErythropoiesisR21HL120791 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI SANKARAN, VIJAY GANESH · 2014 to 2015
$477k
NHLBI NIH HHS R01 HL088554NHLBI NIH HHS R21 HL120791NHLBI NIH HHS U01 HL117720NIDDK NIH HHS R01 DK061692NIDDK NIH HHS R01 DK0923128NIDDK NIH HHS R01 DK092318NIDDK NIH HHS R01 DK103794NIDDK NIH HHS R01 DK61692
6 · The paper itself

Abstract

Anemia is a major source of morbidity and mortality worldwide. Here we review recent insights into how red blood cells (RBCs) are produced, the pathogenic mechanisms underlying various forms of anemia, and novel therapies derived from these findings. It is likely that these new insights, mainly arising from basic scientific studies, will contribute immensely to both the understanding of frequently debilitating forms of anemia and the ability to treat affected patients. Major worldwide diseases that are likely to benefit from new advances include the hemoglobinopathies (β-thalassemia and sickle cell disease); rare genetic disorders of RBC production; and anemias associated with chronic kidney disease, inflammation, and cancer. Promising new approaches to treatment include drugs that target recently defined pathways in RBC production, iron metabolism, and fetal globin-family gene expression, as well as gene therapies that use improved viral vectors and newly developed genome editing technologies.

Indexed as

Genetic TherapyAnemiaFetal HemoglobinHematinicsHemoglobinopathiesHumansInflammationNeoplasmsRenal Insufficiency, ChronicFetal HemoglobinHematinics

Identifiers

PMID25742458
PMCPMC4452951
OpenAlexW2014865621

What OpenQuestion holds

Textmetadata
LicenceTDM
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.