Correlation of Liver Growth and Function During Liver Regeneration and Hepatocarcinogenesis

Barbason, H.; Smoliar, V.; Cantfort, J. Van

doi:10.1007/978-3-642-67265-1_14

Cited by 13 publications

(8 citation statements)

References 18 publications

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“…This might be due to 2 effects: 1) in S phase the DNA is unwound for replication and there are single-stranded short pieces of it, so that the 3-MeDBC metabolites have easier access to the DNA strands, and 2) in the case of early (G1) injection detoxication is more advanced when the cells reach the S phase (about 24 h later), so that fewer reactive metabolites are available to bind to DNA, whereas in the case of the later injections the metabolites can react with DNA before being conjugated and eliminated. This also agrees with the mutually exclusive relationship between cell division and specific differentiated tissue function, as suggested by Barbason et al [1] and Craddock [3]. Indeed, the actively dividing ceils would not eliminate the carcinogen, so that the overall metabolism (we should not forget that we measure average activities in a large population of cells and not activities in specific cell types or stages) results in the existence of a larger proportion of reactive compounds available for DNA binding.…”

Section: Discussionsupporting

confidence: 89%

Effect of partial hepatectomy on the formation and elimination of 3‐methyldibenzo(c,g)carbazole and 5,9‐dimethyldibenzo(c,g)carbazole‐DNA adducts in mouse liver

Szafarz

Valéro

Périn

et al. 1990

Biology of the Cell

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Tritium-labeled 3-methyldibenzo(c,g)carbazole and 5,9-dimethyldibenzo(c,g)-carbazole, 2 organ-specific hepatocarcinogens in mice, were given intraperitoneally to partially hepatectomized animals at various times during the first cell division cycle following surgery. The former compound, more potent and cytotoxic, gave more striking results showing that the maximum number of adducts per unit weight of DNA in liver were formed when the carcinogen was given at the beginning of the S phase, which is evidence for the role of DNA replication in the initiation step of carcinogenesis. Elimination of these adducts led after several days to a residual number of lesions which was of the same order whatever the time of carcinogen administration. In the case of 5,9-dimethyldibenzo-carbazole there were fewer adducts formed after hepatectomy and their removal was much slower.

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Section: Discussionsupporting

confidence: 89%

Effect of partial hepatectomy on the formation and elimination of 3‐methyldibenzo(c,g)carbazole and 5,9‐dimethyldibenzo(c,g)carbazole‐DNA adducts in mouse liver

Szafarz

Valéro

Périn

et al. 1990

Biology of the Cell

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“…In the usually quiescent liver, regeneration following partial hepatectomy results in tight circadian gating of cell division at specific times of day (5). The central circadian clock, in the suprachiasmatic nuclei of the hypothalamus, interacts with the environment through the pineal, retina, and hypothalamic-adrenal axis to generate and maintain daily rhythms.…”

Section: Introductionmentioning

confidence: 99%

Circadian clock coordinates cancer cell cycle progression, thymidylate synthase, and 5-fluorouracil therapeutic index

Wood

Du-Quiton

You

et al. 2006

Molecular Cancer Therapeutics

100

101

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Dysregulated cellular proliferation is a characteristic property of cancer. We show that, despite this fact, cancers maintain high amplitude, circadian rhythms in their growth, DNA synthesis, and mitosis. These patterns are accompanied by the daily traverse of BMAL-1 protein between the cytoplasm, where it is produced, and nucleus, where it influences timing of cancer cell proliferation. This core clock gene product gates cancer cell proliferation by coordinating clock-controlled proteins, thymidylate synthase [thymidylate synthase activity (TSA) cell DNA replication], WEE-1 (cell mitosis), and vascular endothelial growth factor (growth). 5-Fluorouracil (5-FU) -induced host bone marrow and gut toxicity and tumor shrinkage following administration at six equispaced times of day allowed determination of circadian relationships among tumor growth, relevant clock, and clock-controlled proteins and dependence of 5-FU target availability (TSA) in normal and cancer tissues and resultant 5-FU toxic-therapeutic index. The time of day (hours after lights on) of low TSA in each tissue and tumor is respectively associated with greatest toxicity to that tissue and greatest tumor shrinkage. 5-FU treatment near daily awakening results in least damage to bone marrow and gut, greatest antitumor effect, and best survival. This time of day is associated with maximum tumor nuclear BMAL-1 and total cell WEE-1 protein. The described chain of events, for the first time, links cancer cell clock proteins, cancer cell DNA synthesis, proliferation, TSA, and 5-FU toxic-therapeutic index, explaining the dependence of cancer outcome on circadian timing of 5-FU.

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“…These functions are developmentally regulated; for example, albumin is expressed from the early stage of liver development (1), while enzymes required for metabolic functions are mostly absent until birth (2)(3)(4)(5)(6)(7)(8)(9). After the terminal differentiation, hepatocytes express numerous liver functions and do not proliferate except under pathologic states, such as liver regeneration and tumorigenesis (10,11).…”

mentioning

confidence: 99%

Cell Density-Dependent Regulation of Hepatic Development by a gp130-Independent Pathway

Kojima

Kinoshita

Kamiya

et al. 2000

Biochemical and Biophysical Research Communications

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Correlation of Liver Growth and Function During Liver Regeneration and Hepatocarcinogenesis

Cited by 13 publications

References 18 publications

Effect of partial hepatectomy on the formation and elimination of 3‐methyldibenzo(c,g)carbazole and 5,9‐dimethyldibenzo(c,g)carbazole‐DNA adducts in mouse liver

Effect of partial hepatectomy on the formation and elimination of 3‐methyldibenzo(c,g)carbazole and 5,9‐dimethyldibenzo(c,g)carbazole‐DNA adducts in mouse liver

Circadian clock coordinates cancer cell cycle progression, thymidylate synthase, and 5-fluorouracil therapeutic index

Cell Density-Dependent Regulation of Hepatic Development by a gp130-Independent Pathway

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