Evidence map›Paper›PMID 34900673›Full record

ReviewFrontiers in oncology2021

Biological Adaptations of Tumor Cells to Radiation Therapy.

Angeles Carlos-Reyes, Marcos A Muñiz-Lino, Susana Romero-Garcia, César López-Camarillo, Olga N Hernández-de la Cruz

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  8. Predictors of loss to follow-up after radiotherapy in cancer patients.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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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

5 authors at 2 institutions in 1 country.

Angeles Carlos-ReyesDepartment of Chronic-Degenerative Diseases, National Institute of Respiratory Diseases "Ismael Cosío Villegas", Mexico City, Mexico.
Marcos A Muñiz-LinoLaboratorio de Patología y Medicina Bucal, Universidad Autónoma Metropolitana Unidad Xochimilco, Mexico City, Mexico.
Susana Romero-GarciaDepartment of Chronic-Degenerative Diseases, National Institute of Respiratory Diseases "Ismael Cosío Villegas", Mexico City, Mexico.
César López-CamarilloPosgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Mexico, Mexico City.
Olga N Hernández-de la CruzPosgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Mexico, Mexico City.
Universidad Autónoma de la Ciudad de México · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiation therapy has been used worldwide for many decades as a therapeutic regimen for the treatment of different types of cancer. Just over 50% of cancer patients are treated with radiotherapy alone or with other types of antitumor therapy. Radiation can induce different types of cell damage: directly, it can induce DNA single- and double-strand breaks; indirectly, it can induce the formation of free radicals, which can interact with different components of cells, including the genome, promoting structural alterations. During treatment, radiosensitive tumor cells decrease their rate of cell proliferation through cell cycle arrest stimulated by DNA damage. Then, DNA repair mechanisms are turned on to alleviate the damage, but cell death mechanisms are activated if damage persists and cannot be repaired. Interestingly, some cells can evade apoptosis because genome damage triggers the cellular overactivation of some DNA repair pathways. Additionally, some surviving cells exposed to radiation may have alterations in the expression of tumor suppressor genes and oncogenes, enhancing different hallmarks of cancer, such as migration, invasion, and metastasis. The activation of these genetic pathways and other epigenetic and structural cellular changes in the irradiated cells and extracellular factors, such as the tumor microenvironment, is crucial in developing tumor radioresistance. The tumor microenvironment is largely responsible for the poor efficacy of antitumor therapy, tumor relapse, and poor prognosis observed in some patients. In this review, we describe strategies that tumor cells use to respond to radiation stress, adapt, and proliferate after radiotherapy, promoting the appearance of tumor radioresistance. Also, we discuss the clinical impact of radioresistance in patient outcomes. Knowledge of such cellular strategies could help the development of new clinical interventions, increasing the radiosensitization of tumor cells, improving the effectiveness of these therapies, and increasing the survival of patients.

Indexed as

cancerDNA-damage responseDNA repair pathwaysradioresistanceradiotherapy

Identifiers

PMID34900673
PMCPMC8652287
OpenAlexW3216462497

What Socratic 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 Socratic graph.