Studies of dormant tumor cells

Abstract

An attempt was made to study dormant tumor cells in a syngeneic, immunologic, experimental tumor system. First, however, tumor cell dormancy was redemonstrated in the Walker 256 tumor‐Sprague‐Dawley rat model as it had been described by Fisher and Fisher. Walker 256 tumor‐cell suspensions were injected intraportally in Sprague‐Dawley rats (non‐inbred). Rats receiving subthreshold doses of tumor underwent serial liver massage beginning 4 or 12 weeks after injection. Control (non‐laparotomized) rats were followed 120 days, and livers were tumor‐negative at the time of sacrifice. Rats receiving subthreshold doses of 5 × 103, 2.5 × 104, and 1.25 × 105 cells were massaged four times at 4‐week intervals. In these groups, 85%, 73%, and 92%, respectively, developed liver metastases. An attempt to demonstrate dormant cells in syngeneic Fisher rats using a 3–4 benz(a)pyrene induced sarcoma was not successful. Ninety‐eight animals receiving subthreshold intraportal doses of this tumor serially underwent 6 liver massages at 4‐week intervals. In no instance were “dormant cells” stimulated to gross or microscopically discernible growth. The 3–4 benzpyrene sarcoma was shown to be highly immunogenic in Fisher rats. The Walker 256 tumor was not demonstrated immunogenic in Sprague‐Dawley rats. Possible explanations for these contrasting results are discussed.

Effects of Surgery and Chemotherapy on Metastatic Progression of Prostate Cancer: Evidence from the Natural History of the Disease Reconstructed through Mathematical Modeling

“…High sensitivity of tumor cells to the conditions of host microenvironment and the resulting selective affinity of tumor cells to specific organs and tissues has been known since 1889 under the name of “seed and soil hypothesis” [17]. However, it was uncovered by subsequent pioneering studies [18, 19] that even if seeded into a fertile “soil,” a tumor cell may remain dormant in a secondary site yet retain its clonogenic capacity. Direct evidence of prevalent breast tumor cell dormancy was presented in [20].…”

Inhibition of tumor implantation at sites of trauma by Arg-Gly-Asp containing proteins and peptides

“…Injury resulting from surgical [1][2][3][4][5][6][7][8][9][10] or mechanical [11,12] procedures, and exposure to radiation [13][14][15] or chemicals [16][17][18], including some anticancer drugs [19,20] increases tissue susceptibility to increased tumor implantation. Injury resulting from surgical [1][2][3][4][5][6][7][8][9][10] or mechanical [11,12] procedures, and exposure to radiation [13][14][15] or chemicals [16][17][18], including some anticancer drugs [19,20] increases tissue susceptibility to increased tumor implantation.…”

Stimulation of tumour angiogenesis by proximal wounds: spatial and temporal analysis by MRI

“…The concept that injuries promote tumour development at the injured site, in mice that were exposed to carcinogens, has already been suggested by Deelman (1927) and was later expanded to exposure to X-ray irradiation (Haran-Ghera et al, 1962), chemical (Fisher et al, 1967;Orr et al, 1986), mechanical (Fisher et al, 1967;Sugarbaker et al, 1971) or surgical (Paschkis et al, 1955;Fisher et al, 1967;Schackert and Fidler, 1989) trauma. Trauma increased the probability of tumour formation in the injured organ, without affecting the distribution to other sites, by promoting implantation and proliferation of circulating cancer cells (Murthy et al, 1991).…”