Evidence map›Paper›PMID 17173673›Full record

ArticleTheoretical biology & medical modelling2006

The biological sense of cancer: a hypothesis.

Raúl A Ruggiero, Oscar D Bustuoabad

Abstract read
In one paragraph

Article in Theoretical biology & medical modelling, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Editorial: Ageing and Carcinogenesis.Frontiers in oncology · 2022
    Article
  3. Article
  4. Lessons from Hippocrates: Time to Change the Cancer Paradigm.International journal of chronic diseases · 2020
    Review
  5. Mathematical modeling of solid cancer growth with angiogenesis.Theoretical biology & medical modelling · 2012
    Article
  6. Biphasic effect of a primary tumor on the growth of secondary tumor implants.Journal of cancer research and clinical oncology · 2010
    Article
  7. 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.

Raúl A RuggieroDivisión Medicina Experimental, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina de Buenos Aires, Pacheco de Melo 3081, 1425 Buenos Aires, Argentina. ruloruggiero@yahoo.com.ar
Oscar D Bustuoabad

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMost theories about cancer proposed during the last century share a common denominator: cancer is believed to be a biological nonsense for the organism in which it originates, since cancer cells are believed to be ones evading the rules that control normal cell proliferation and differentiation. In this essay, we have challenged this interpretation on the basis that, throughout the animal kingdom, cancer seems to arise only in injured organs and tissues that display lost or diminished regenerative ability. HYPOTHESIS: According to our hypothesis, a tumor cell would be the only one able to respond to the demand to proliferate in the organ of origin. It would be surrounded by "normal" aged cells that cannot respond to that signal. According to this interpretation, cancer would have a profound biological sense: it would be the ultimate way to attempt to restore organ functions and structures that have been lost or altered by aging or noxious environmental agents. In this way, the features commonly associated with tumor cells could be reinterpreted as progressively acquired adaptations for responding to a permanent regenerative signal in the context of tissue injury. Analogously, several embryo developmental stages could be dependent on cellular damage and death, which together disrupt the field topography. However, unlike normal structures, cancer would have no physiological value, because the usually poor or non-functional nature of its cells would make their reparative task unattainable.

conclusionThe hypothesis advanced in this essay might have significant practical implications. All conventional therapies against cancer attempt to kill all cancer cells. However, according to our hypothesis, the problem might not be solved even if all the tumor cells were eradicated. In effect, if the organ failure remained, new tumor cells would emerge and the tumor would reinitiate its progressive growth in response to the permanent regenerative signal of the non-restored organ. Therefore, efficient anti-cancer therapy should combine an attack against the tumor cells themselves with the correction of the organ failure, which, according to this hypothesis, is fundamental to the origin of the cancer.

Indexed as

Cell DifferentiationCell ProliferationAdaptation, PhysiologicalCellular SenescenceEmbryonic DevelopmentHumansNeoplasms

Identifiers

PMID17173673
PMCPMC1764731

What OpenQuestion holds

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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.