By Oscar Sudilovsky (auth.), Oscar Sudilovsky, Henry C. Pitot, Lance A. Liotta (eds.)
The objective! of this convention was once to not outline the 2 parts which are being certain, that can be a good nigh very unlikely proposition. really, its concentration was once to pay attention to the mechanistic similarities among promoting and development. Are the components concerned in the obstacles a continuum? Are those simultaneous techniques? Or are a few of the affected cells within the level of promoting whilst whilst others have gone through irreversi ble alterations tha. t place them within the level of development? Or are those levels a similar factor, yet referred to as via various names? To discover such suggestions we assembled investigators with quite a few again grounds and requested them to in particular tackle those and different questions about "The Boundaries", in the context of the consultation to which they con tributed. The convention lasted and a part days, from Wednesday to Friday. there have been a minimum of 4 audio system in line with consultation with morning and after midday classes every day, other than on Friday while the assembly ended at midday. the 1st day, every one speaker had 25 mins to offer a place, through 5 mins of debate. on the finish of the consultation there have been forty or 50 mins of trade on all of the matters tested. For the rest days, there have been 25 mins of presentation and quarter-hour of discussion.
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Extra resources for Boundaries between Promotion and Progression during Carcinogenesis
J CRIBRIFORMl 1- I'&H~"J '--IADELMAI 1 j J PAPILLARY 1 COMEDO 1 j CYST FIBROADENOMA 1 1 J INVASIVE Ca I 1METASTASES 1 Fig. 1. Chart representing two different pathogenetic pathways for benign and malignant lesions. Malignant lesions originate from TEB and appear earlier than benign lesions originated from AB. The earliest lesion detected after OMBA administration is the lOP. 11. The distribution of cell populations in the mammary gland during carcinogenesis varies in TEBs, but not in ABs or lobules.
Amer. Assoc. Cancer Res. 25:78 (1984). G. J. Patskan, J. C. Pelling, R. S. Nairn, and T. J. Slaga, Altered oncogene expression in mouse skin squamous cell carcinomas, presented at the Pennsylvania State University Fourth Summer Symposium in Molecular Biology (1985). H. Hennings, R. Shores, M. L. Wenk, E. F. Spangler, R. Tarone, and S. H. Yuspa, Malignant conversion of mouse skin tumours is increased by tumour initiators and unaffected by tumour promoters, Nature 304:67-69 (1983). J. F. O'Connell, A.
Mice were sacrificed at week 60. In SOITle mice, metastases developed in both lymph nodes and lung. 3 15 3 20 4-NQO 2 3 17 3 18 Acetone 0 3 23 3 13 Lung Lymph Node Site of Metastases 8 Percent Metastases TPA Treatment Number of Carcinoma-bearing Mice with Metastases Metastases from Epidermal Squamous Cell Carcinomas Number of Mice with Squamous Cell Carcinomas Table 2. programmed with a given probability of conversion. Treatment of papillomabearing mice with a genotoxic agent, such as 4-NQO, urethane or cisplatin, increases the rate of malignant conversion.
Boundaries between Promotion and Progression during Carcinogenesis by Oscar Sudilovsky (auth.), Oscar Sudilovsky, Henry C. Pitot, Lance A. Liotta (eds.)