Evidence map›Paper›PMID 38764833›Full record

ReviewWorld journal of gastrointestinal oncology2024

Impact of STAT-signaling pathway on cancer-associated fibroblasts in colorectal cancer and its role in immunosuppression.

Damián Sánchez-Ramírez, Mónica G Mendoza-Rodríguez, Omar R Alemán, Fernando A Candanedo-González, Miriam Rodríguez-Sosa, Juan José Montesinos-Montesinos, Mauricio Salcedo, Ismael Brito-Toledo, Felipe Vaca-Paniagua, Luis I Terrazas

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastrointestinal oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. STAT3 Inhibition to Treat Ulcerative Colitis-Associated Colorectal Cancer.International journal of molecular sciences · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. 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

10 authors.

Damián Sánchez-RamírezUnidad de Investigacion en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autonoma de Mexico, Tlalnepantla 54090, Estado de Mexico, Mexico.
Mónica G Mendoza-RodríguezUnidad de Investigacion en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autonoma de Mexico, Tlalnepantla 54090, Estado de Mexico, Mexico.
Omar R AlemánDepartment of Biology, Facultad de Quimica, Universidad Nacional Autonoma de Mexico, Ciudad Universitaria, Mexico City 04510, Mexico.
Fernando A Candanedo-GonzálezDepartment of Pathology, National Medical Center Century XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Miriam Rodríguez-SosaUnidad de Investigacion en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autonoma de Mexico, Tlalnepantla 54090, Estado de Mexico, Mexico.
Juan José Montesinos-MontesinosLaboratorio de Células Troncales Mesenquimales, Unidad de Investigación Médica en Enfermedades Oncológicas, Hospital de Oncología Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Mauricio SalcedoUnidad de Investigacion en Biomedicina y Oncologia Genomica, Instituto Mexciano del Seguro Social, Mexico City 07300, Mexico.
Ismael Brito-ToledoServicio de Colon y Recto, Hospital de Oncología Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
Felipe Vaca-PaniaguaUnidad de Investigacion en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autonoma de Mexico, Tlalnepantla 54090, Estado de Mexico, Mexico.
Luis I TerrazasUnidad de Investigacion en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autonoma de Mexico, Tlalnepantla 54090, Estado de Mexico, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) remains one of the most commonly diagnosed and deadliest types of cancer worldwide. CRC displays a desmoplastic reaction (DR) that has been inversely associated with poor prognosis; less DR is associated with a better prognosis. This reaction generates excessive connective tissue, in which cancer-associated fibroblasts (CAFs) are critical cells that form a part of the tumor microenvironment. CAFs are directly involved in tumorigenesis through different mechanisms. However, their role in immunosuppression in CRC is not well understood, and the precise role of signal transducers and activators of transcription (STATs) in mediating CAF activity in CRC remains unclear. Among the myriad chemical and biological factors that affect CAFs, different cytokines mediate their function by activating STAT signaling pathways. Thus, the harmful effects of CAFs in favoring tumor growth and invasion may be modulated using STAT inhibitors. Here, we analyze the impact of different STATs on CAF activity and their immunoregulatory role.

Indexed as

Cancer-associated fibroblastsColorectal cancerImmunityImmunosuppressionSignal transducer and activator of transcription signaling

Identifiers

PMID38764833
PMCPMC11099434

What Socratic 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 Socratic graph.