Evidence map›Paper›PMID 36260949›Full record

ArticleInternational journal of immunopathology and pharmacology

Influence of nitric oxide signaling mechanisms in cancer.

R Ramírez-Patiño, G Avalos-Navarro, L E Figuera, J J Varela-Hernández, L A Bautista-Herrera, J F Muñoz-Valle, M P Gallegos-Arreola

Open access · goldAbstract readEditorial
In one paragraph

Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. CD320 Receptor and Vitamin B12 as Potential Targets for Anti-Cancer Therapy.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
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

7 authors at 2 institutions in 1 country.

R Ramírez-PatiñoDepartamento de Ciencias Médicas y de la Vida, Centro Universitario de la Ciénega (CUCIÉNEGA), 42548Universidad de Guadalajara, Ocotlán Jalisco, México.
G Avalos-NavarroDepartamento de Ciencias Médicas y de la Vida, Centro Universitario de la Ciénega (CUCIÉNEGA), 42548Universidad de Guadalajara, Ocotlán Jalisco, México.ORCID 0000-0003-1121-607X
L E FigueraDivisión de Génetica, Centro de Investigación Biomédica de Occidente (CIBO), 42568Instituto Mexicano del Seguro Social (IMSS), Guadalajara Jalisco, México.ORCID 0000-0002-6096-4579
J J Varela-HernándezDepartamento de Ciencias Médicas y de la Vida, Centro Universitario de la Ciénega (CUCIÉNEGA), 42548Universidad de Guadalajara, Ocotlán Jalisco, México.
L A Bautista-HerreraDepartamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingeniería (CUCEI), 42566Universidad de Guadalajara, Guadalajara Jalisco, México.
J F Muñoz-ValleInstituto de Investigación en Ciencias Biomédicas (IICB), Centro Universitario de Ciencias de la Salud (CUCS) 42571Universidad de Guadalajara, Guadalajara Jalisco, México.ORCID 0000-0002-2272-9260
M P Gallegos-ArreolaDivisión de Génetica, Centro de Investigación Biomédica de Occidente (CIBO), 42568Instituto Mexicano del Seguro Social (IMSS), Guadalajara Jalisco, México.ORCID 0000-0003-4539-1693
Universidad de Guadalajara · MXMexican Social Security Institute · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) is a molecule with multiple biological functions that is involved in various pathophysiological processes such as neurotransmission and blood vessel relaxation as well as the endocrine system, immune system, growth factors, and cancer. However, in the carcinogenesis process, it has a dual behavior; at low doses, NO regulates homeostatic functions, while at high concentrations, it promotes tissue damage or acts as an agent for immune defense against microorganisms. Thus, its participation in the carcinogenic process is controversial. Cancer is a multifactorial disease that presents complex behavior. A better understanding of the molecular mechanisms associated with the initiation, promotion, and progression of neoplastic processes is required. Some hypotheses have been proposed regarding the influence of NO in activating oncogenic pathways that trigger carcinogenic processes, because NO might regulate some signaling pathways thought to promote cancer development and more aggressive tumor growth. Additionally, NO inhibits apoptosis of tumor cells, together with the deregulation of proteins that are involved in tissue homeostasis, promoting spreading to other organs and initiating metastatic processes. This paper describes the signaling pathways that are associated with cancer, and how the concentration of NO can serve a beneficial or pathological function in the initiation and promotion of neoplastic events.

Indexed as

NeoplasmsNitric OxideApoptosisCarcinogenesisHumansSignal TransductionNitric OxideangiogenesisCancerhomeostasismetastasisnitric oxidesignaling mechanisms

Identifiers

PMID36260949
PMCPMC9585559
OpenAlexW4306909234

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.