Cellular Proliferation in Carcinogenesis*

Oehlert, W.

doi:10.1111/j.1365-2184.1973.tb01621.x

Cited by 22 publications

(9 citation statements)

References 19 publications

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“…Although cell division is crucial for the transformation of a normal cell into a tumor cell, direct correlation of tumor incidence in a given tissue to its normal rate of cell turnover cannot always be made (Oehlert 1973). The liver, which in most adult animals has a very low rate of cell turnover, is a good example of this.…”

Section: Introductionmentioning

confidence: 99%

Heat induced liver cell proliferation in the livebearing fish Poeciliopsis

1993

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Section: Introductionmentioning

confidence: 99%

Heat induced liver cell proliferation in the livebearing fish Poeciliopsis

1993

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Section: Introductionmentioning

confidence: 99%

“…Genetic damage can also occur through deletions or rearrangements at the chromosome level and through changes in chromosome number. In addition, cell killing and the resulting change in cell proliferation rate play an important role in carcinogenesis [Cole and Nowell, 1965;Oehlert, 1973;Shami et al, 19821. Most automotive emissions research has been conducted on samples from either engines or vehicles operated in controlled laboratory conditions, with the exhaust entering a dilution tunnel and particles collected on a filter. Laboratory samples may be collected using different dilution ratios, exposure times to exhaust gases, and exposure temperatures which may not represent environmental conditions.…”

Section: Introductionmentioning

confidence: 99%

A comparison of genotoxicity of automotive exhaust particles from laboratory and environmental sources

Brooks

Dutcher

et al. 1984

Environ. mutagen

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This research (1) ranked the genotoxicity of methylene chloride extracts of laboratory and environmentally collected particles and (2) evaluated the role of collection location and sample composition on genotoxic potency. Samples of exhaust from a spark-ignition automobile, light-duty diesel automobile, and a heavy-duty diesel engine operated in a laboratory on a dynamometer were studied, as well as samples taken in a highway tunnel and outside the same tunnel. The tunnel samples were collected 30 m inside or 56 m outside the exit portal at times when between 70%-95% of the traffic consisted of diesel trucks. In the Ames Salmonella mutagenicity assay, each extract produced a dose-dependent increase in mutagenicity in strain TA-98 without addition of liver S-9 fraction. Extracts from two tunnel samples collected 1 yr apart, and extracts of particles collected outside the tunnel had similar mutagenic activity. The order of mutagenic activity per microgram of extract in TA-98 without S-9 from the lowest to the highest was environmental sample less than or equal to tunnel less than heavy-duty diesel less than light-duty diesel less than spark ignition. Addition of S-9 or testing in Salmonella strains resistant to the mutagenicity of nitroaromatic compounds (TA-98 NR and TA-98 1,8-DNP6) decreased the mutagenic response. With cell killing, sister chromatid exchanges, and mutations as endpoints in Chinese hamster ovary cells (CHO), the order of potency was tunnel less than light-duty less than spark-ignition samples. All three extracts induced a similar amount of mitotic delay per microgram with or without S-9. Enhanced chromosome aberration frequency was detected only in cells exposed to extracts from spark-ignition exhaust. The data indicated that genotoxic activity was detected in each particle extract, that the potency ranking was similar using different genetic endpoints, and that the magnitude of the genotoxic potency was similar.

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“…So ist das maligne Wachstum unter anderem dadurch charak terisiert, daß die neoplastische Zelle den Kontrollmechanismen, die die Proliferation normaler Zellen regulieren, nicht oder in ungenügendem Maße unterliegt. Eine Zellproliferation ist wahrscheinlich eine notwendige Vor aussetzung für die Entwicklung eines Tumors [Oehlert, 1973], Die Umwandlung einer gesunden in eine maligne Zelle (Trans formation) kann im Stadium der stimulierten Zellproliferation erfolgen. Werden die Zellen in einem früheren Stadium trans formiert, ohne sich danach zu vermehren, spricht man von «dormant cells».…”

Section: Introductionunclassified

“…Dafür spricht die Tatsache, daß schon eine einmalige Gabe einer karzinogenen Substanz Krebs auslösen kann und daß die Wirkung über längere Z eit gespeichert bleibt. Promotoren weisen ein vielfältiges Spektrum physiologischer Wirkung auf, eine wesentliche davon ist die Stimulierung der Zellproliferation [Oehlert, 1973].…”

Section: Introductionunclassified

Wachstumsregulation und Tumorpromotion in der Rattenleber durch Steroidhormone

Wiest¹

1981

Oncol Res Treat

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Kortikosteron hemmt die Zellproliferation in der Leber adulter Ratten und synchronisiert die Teilung der Leberzellen nach partieller Hepatektomie. Kortikosteron kann zumindest vorübergehend aus dem Kreislauf durch Adrenalektomie entfernt werden oder durch Progesteron mit-tels kompetitiver Hemmung seines zytoplasmatischen Rezeptors in der Leberzelle inaktiviert werden. Die Folge davon ist eine erhöhte zelluläre Proliferation. Es wurde untersucht, inwieweit diese Situation die Entwicklung von chemisch induzierten Lebertumoren beeinflußt. Tiere, die gleichzeitig mit Diäthylnitrosamin und proliferationsstimulierenden Steroiden aus der Gruppe der Gestagene, Androgene oder Östrogene behandelt wurden, starben signifikant früher an Hepatomen. Es kann daher eine tumorpromovierende Wirkung dieser Substanzen angenommen werden.

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Cellular Proliferation in Carcinogenesis*

Cited by 22 publications

References 19 publications

Heat induced liver cell proliferation in the livebearing fish Poeciliopsis

Heat induced liver cell proliferation in the livebearing fish Poeciliopsis

A comparison of genotoxicity of automotive exhaust particles from laboratory and environmental sources

Wachstumsregulation und Tumorpromotion in der Rattenleber durch Steroidhormone

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