ArticleProceedings of the National Academy of Sciences of the United States of America2001
A growth-constrained environment drives tumor progression invivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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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.
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Who cites it
25 citing papers in PubMed, 55 citations in OpenAlex.
- Stem cell-based therapeutic strategies for liver aging.Liver research (Beijing, China) · 2025Review
- Cell competition in primary and metastatic colorectal cancer.Oncogenesis · 2024Review
- The sculpting of somatic mutational landscapes by evolutionary forces and their impacts on aging-related disease.Molecular oncology · 2022Review
- Detection of hepatocarcinogens by combination of liver micronucleus assay and histopathological examination in 2-week or 4-week repeated dose studies.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- Aging and Cancer: The Waning of Community Bonds.Cells · 2021Review
- Cell competition in liver carcinogenesis.World journal of hepatology · 2020Review
- Regenerative Medicine: Shedding Light on the Link between Aging and Cancer.Cell transplantation · 2017Review
- Article
- Rat-derived amniotic epithelial cells differentiate into mature hepatocytes in vivo with no evidence of cell fusion.Stem cells and development · 2015Article
- The effect of environmental chemicals on the tumor microenvironment.Carcinogenesis · 2015Review
- Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.Carcinogenesis · 2015Review
- Inhibition effects of scorpion venom extracts (Buthus matensii Karsch) on the growth of human breast cancer MCF-7 cells.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2014Article
- Article
- DNA damage checkpoints in stem cells, ageing and cancer.Nature reviews. Molecular cell biology · 2012Review
- Tumor heterogeneity: mechanisms and bases for a reliable application of molecular marker design.International journal of molecular sciences · 2012Review
- The growth pattern of transplanted normal and nodular hepatocytes.Histochemistry and cell biology · 2011Article
- c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.Cancer biology & therapy · 2011Review
- Ionizing radiation and hematopoietic malignancies: altering the adaptive landscape.Cell cycle (Georgetown, Tex.) · 2010Article
- Comfrey (Symphytum Officinale. l.) and Experimental Hepatic Carcinogenesis: A Short-term Carcinogenesis Model Study.Evidence-based complementary and alternative medicine : eCAM · 2010Article
- Irradiation selects for p53-deficient hematopoietic progenitors.PLoS biology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently have shown that selective growth of transplanted normal hepatocytes can be achieved in a setting of cell cycle block of endogenous parenchymal cells. Thus, massive proliferation of donor-derived normal hepatocytes was observed in the liver of rats previously given retrorsine (RS), a naturally occurring alkaloid that blocks proliferation of resident liver cells. In the present study, the fate of nodular hepatocytes transplanted into RS-treated or normal syngeneic recipients was followed. The dipeptidyl peptidase type IV-deficient (DPPIV(-)) rat model for hepatocyte transplantation was used to distinguish donor-derived cells from recipient cells. Hepatocyte nodules were chemically induced in Fischer 344, DPPIV(+) rats; livers were then perfused and larger (>5 mm) nodules were separated from surrounding tissue. Cells isolated from either tissue were then injected into normal or RS-treated DPPIV(-) recipients. One month after transplantation, grossly visible nodules (2--3 mm) were seen in RS-treated recipients transplanted with nodular cells. They grew rapidly, occupying 80--90% of the host liver at 2 months, and progressed to hepatocellular carcinoma within 4 months. By contrast, no liver nodules developed within 6 months when nodular hepatocytes were injected into the liver of recipients not exposed to RS, although small clusters of donor-derived cells were present in these animals. Taken together, these results directly point to a fundamental role played by the host environment in modulating the growth and the progression rate of altered cells during carcinogenesis. In particular, they indicate that conditions associated with growth constraint of the host tissue can drive tumor progression in vivo.
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Registered trials
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.