Evidence map›Paper›PMID 34719756›Full record

ReviewJournal of the Egyptian National Cancer Institute2021

Reviewing cancer's biology: an eclectic approach.

Ibrahim Diori Karidio, Senay Hamarat Sanlier

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of the Egyptian National Cancer Institute, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. MED12 dysregulation: insights into cancer and therapeutic resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  9. AhR and STAT3: A Dangerous Duo in Chemical Carcinogenesis.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Role of LMO7 in cancer (Review).Oncology reports · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Observational
  17. Review
  18. Frontiers in pharmacology · 2024
    Article
  19. NovelJournal of enzyme inhibition and medicinal chemistry · 2023
    Article
  20. 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

2 authors at 1 institution in 1 country.

Ibrahim Diori KaridioDepartment of Biochemistry, Faculty of Science, E Block, Ege University, Erzene Mahallesi, Bornova, 35040, Izmir, Turkey. kardio_ib@outlook.fr.ORCID http://orcid.org/0000-0002-7551-7480
Senay Hamarat SanlierDepartment of Biochemistry, Faculty of Science, E Block, Ege University, Erzene Mahallesi, Bornova, 35040, Izmir, Turkey.
Ege University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer refers to a group of some of the worldwide most diagnosed and deadliest pathophysiological conditions that conquered researchers' attention for decades and yet begs for more questions for a full comprehension of its complex cellular and molecular pathology. MAIN BODY: The disease conditions are commonly characterized by unrestricted cell proliferation and dysfunctional replicative senescence pathways. In fact, the cell cycle operates under the rigorous control of complex signaling pathways involving cyclins and cyclin-dependent kinases assumed to be specific to each phase of the cycle. At each of these checkpoints, the cell is checked essentially for its DNA integrity. Genetic defects observed in these molecules (i.e., cyclins, cyclin-dependent kinases) are common features of cancer cells. Nevertheless, each cancer is different concerning its molecular and cellular etiology. These could range from the genetic defects mechanisms and/or the environmental conditions favoring epigenetically harbored homeostasis driving tumorigenesis alongside with the intratumoral heterogeneity with respect to the model that the tumor follows.

conclusionsThis review is not meant to be an exhaustive interpretation of carcinogenesis but to summarize some basic features of the molecular etiology of cancer and the intratumoral heterogeneity models that eventually bolster anticancer drug resistance for a more efficient design of drug targeting the pitfalls of the models.

Indexed as

Epithelial-Mesenchymal TransitionNeoplasmsBiologyCell ProliferationHumansSignal TransductionCancer epigeneticsCancer stem cellCancer stem cell plasticityEpithelial-mesenchymal transition (EMT)Lonal evolution modelMesenchymal-epithelial transition (MET)Microbiota

Identifiers

PMID34719756
PMCPMC13316913
OpenAlexW3210591228

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.