Evidence map›Paper›PMID 24969061›Full record

ArticleAsian journal of andrology

Lipogenic metabolism: a viable target for prostate cancer treatment?

Mengmeng Liang, David J Mulholland

Abstract readComment
In one paragraph

Article in Asian journal of andrology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Mengmeng Liang
David J MulhollandIcahn School of Medicine at Mount Sinai, New York, NY, USA.

Funding

Chronic inhibition of androgen receptor signaling leads to neuroendocrine prostate cancer by trans differentiation of stem/progenitor cellsR01CA197910 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MULHOLLAND, DAVID · 2015 to 2019
$2.0M
NCI NIH HHS R01 CA197910
6 · The paper itself

Abstract

Cancer cells often depend on altered metabolism compared with their normal counterparts. As observed in 1924 by Otto Warburg, cancer cells show preferential glucose consumption by way of aerobic glycolysis while normal cells generally assume mitochondrial oxidative phosphorylation. Another metabolic hallmark of carcinogenesis is altered lipid metabolism, whereby cancer cells may adopt enhanced de novo lipid production (lipogenesis). Enhanced lipid metabolism is also observed in individuals with metabolic syndromes potentially a consequence of increasing popularity of the Standard American Diet, composed of high levels of saturated fats and carbohydrates. A growing body of epidemiological data indicates a positive correlation between the occurrence of metabolic syndromes, such as cardiovascular disease, obesity, type-2 diabetes and associated hyperinsulemia, with the aggressiveness of cancer. Remarkably, it is estimated that for every 1% reduction in saturated fats, replaced by polyunsaturated, there would be a 2%-3% reduction in cardiovascular disease. Thus, it is conceivable that an equally remarkable attenuation in cancer progression might be achieved with such a reduction in lipid accumulation.

Indexed as

AnimalsCholesterol EstersHumansMalePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseCholesterol EstersPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN Phosphohydrolase

Identifiers

PMID24969061
PMCPMC4215688

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.