Evidence map›Paper›PMID 24955214›Full record

ReviewGenes & cancer2014

SOD1, an unexpected novel target for cancer therapy.

Luena Papa, Giovanni Manfredi, Doris Germain

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
7.7field-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

90 citing papers in PubMed, 146 citations in OpenAlex.

  1. Copper, cuproptosis, and cancer: biology concepts of a novel cell death.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. From hemocuprein to CSRP: the many faces of Cu/Zn superoxide dismutase.Metallomics : integrated biometal science · 2026
    Review
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  18. Systemic and Ocular Associations of Keratoconus.Expert review of ophthalmology · 2024
    Article
  19. Article
  20. Article

30 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.

Luena PapaFrom the Department of Medicine, Division of Hematology/Oncology, Tisch Cancer Institute Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY.
Giovanni ManfrediThe Weill Cornell Medical College, Department of Neurology and Neuroscience, New York, New York.
Doris GermainFrom the Department of Medicine, Division of Hematology/Oncology, Tisch Cancer Institute Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY.
Icahn School of Medicine at Mount Sinai · USCornell University · US

Funding

TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
Mitochondria quality control in SOD1-ALSR01NS062055 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI MANFREDI, GIOVANNI · 2009 to 2019
$3.7M
The Pathogenic Mechanisms of Mutant SOD1 in MitochondriaR01NS051419 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI MANFREDI, GIOVANNI · 2006 to 2014
$3.0M
Mitochondrial inter membrane space-IMS unfolded protein response in familial ALSR01NS084486 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GERMAIN, DORIS A, MANFREDI, GIOVANNI · 2014 to 2018
$1.9M
Role of Skp2 and Skp2B in breast cancerR01CA109482 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GERMAIN, DORIS A · 2005 to 2009
$1.5M
NCI NIH HHS R01 CA109482NCI NIH HHS T32 CA078207NINDS NIH HHS R01 NS051419NINDS NIH HHS R01 NS062055NINDS NIH HHS R01 NS084486
6 · The paper itself

Abstract

Cancer cells have elevated levels of reactive oxygen species (ROS), which are generated in majority by the mitochondria. In the mitochondrial matrix, the manganese dismutase SOD2 acts as a major anti-oxidant enzyme. The deacetylase SIRT3 regulates the activity of SOD2. Recently, SIRT3 was reported to be decreased in 87% of breast cancers, resulting therefore in a decrease in the activity of SOD2 and an elevation in ROS. In addition to SIRT3, we recently reported that SOD2 itself is down-regulated in breast cancer cell lines upon activation of oncogenes, such as Ras. Since in absence of SOD2, superoxide levels are elevated and may cause irreversible damage, mechanisms must exist to retain superoxide below a critical threshold and maintain viability of cancer cells. The copper/zinc dismutase SOD1 localizes in the cytoplasm, the inter-membrane space of the mitochondria and the nucleus. Emerging evidences from several groups now indicate that SOD1 is overexpressed in cancers and that the activity of SOD1 may be essential to maintain cellular ROS under this critical threshold. This review summarizes the studies reporting important roles of SOD1 in cancer and addresses the potential cross-talk between the overexpression of SOD1 and the regulation of the mitochondrial unfolded protein response (UPR(mt)). While mutations in SOD1 is the cause of 20% of cases of familial amyotrophic lateral sclerosis (fALS), a devastating neurodegenerative disease, these new studies expand the role of SOD1 to cancer.

Indexed as

cancerfALSSIRT3SOD1SOD2

Identifiers

PMID24955214
PMCPMC4063254
OpenAlexW1591649477

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.