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C D Pasqualini

Publications and source records attributed to C D Pasqualini.

89 records · Page 5Linked to original sources
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Tumor necrosis can facilitate the appearance of metastases.

The non-metastatic murine mammary adenocarcinoma M3 and its metastatic variant MM3 were used to evaluate the role of intratumoral necrosis in cell detachment and metastasis. Accelular extracts from necrotic areas of both tumors increased in vitro cellular detachment from M3 but not from MM3 fragments. Furthermore, the in vivo inoculation of the necrotic extracts within non-metastatic M3 tumors gave rise to pulmonary metastases. Histological studies revealed in M3 a central necrosis limited by an uninterrupted peripheral ring of well preserved cells, while in MM3 necrotic and non-necrotic areas alternated. It is concluded that the distribution of necrosis within the primary tumor by facilitating cell detachment is, at least in part, responsible for the development of metastases.

Adenocarcinoma↗
PubMedDate not supplied

Inhibition of metastases by a serum factor associated to concomitant resistance induced by unrelated murine tumors.

Murine lung metatases growing undisturbed by the primary tumor were significantly inhibited by the concomitant resistance induced by a secondary subcutaneous implant of two unrelated tumors. Such inhibition was T-independent since it was also observed in nude mice; its full expression was dependent on the presence of the secondary tumor implant and it was exerted on both macroscopic and microscopic established metastases and not on the process of tumor cell dissemination from the primary tumor. Direct and indirect mechanisms seemed to be involved, the former affecting the metastatic cells per se by causing a decrease in proliferation and an increase in apoptosis while the latter affected neo-vascularization. These antitumor and antiangiogenic effects could be attributed to a serum factor induced by the unrelated tumors generating concomitant resistance. This factor proved to be heat, acid and alkaline resistant and dialysable; it was recovered in an HPLC column with maximum absorption at 215 and 266 nm; it was anionic at neutral pH, exhibiting free carboxil groups and one or more molecules of tyrosine, with a molecular weight between 870 and 1300 Dalton. Intravenous administration of this factor significantly inhibited lung metastases, decreasing mitosis and increasing apoptosis similar to that observed in the presence of the unrelated tumors.

Animals↗
PubMedDate not supplied

Two different types of concomitant resistance induced by murine tumors: morphological aspects and intrinsic mechanisms.

Concomitant resistance (CR) is the phenomenon according to which a tumor-bearing host inhibits the growth of a secondary implant of the same tumor at a distant site. Confirming and extending previous results of our laboratory, histological studies have revealed that two temporally separate peaks of CR can be detected throughout tumor evolution. The first peak induced by immunogenic small tumors, in euthymic but not in nude mice, is associated with extensive necrosis of the secondary tumor implant and a profuse infiltration of polymorphonuclear granulocytes and mononuclear cells resulting in its final destruction; these features correspond to a typical immunological rejection. The second peak of CR induced by both immunogenic and non-immunogenic large tumors, in euthymic as well as in nude mice, is characterized by a dormant tumor stage with scarce or null mononuclear infiltration, associated with a significant reduction of tumor mitotic index and of the number of PCNA+ cells along with an increase in apoptosis and an arrest in S phase. In previous reports we suggested that a 1000 D serum fraction from mice bearing large tumors could be responsible for the induction of this dormant tumor stage. In this study tumor cells incubated in vitro with that serum factor mimicked the inhibition and cellular alterations observed in vivo in the secondary tumor inhibited by the second peak of CR. Moreover, the passive transfer of this factor by the intra-peritoneal (i.p.) route induced an in vivo inhibition of an i.p. tumor reproducing the image characteristic of the second peak of CR. This represents a direct proof that this serum factor can restrain tumor growth in vivo and that it is, most probably, the effector of the second peak of CR.

Animals↗
PubMedDate not supplied

Thymectomy does not affect tumour rejection and cytophilic activity in a murine allogeneic lymphoma model.

An experimental model was devised in which an AKR lymphoma is conditioned to grow in BALB mice leading to reproducible tumor incidence which makes tumor-bearing (progressor) and tumor-rejecting (regressor) animals simultaneously available. The object of this paper was to determine the effect of neonatal thymectomy (xT) on allogeneic tumor incidence and on anti-tumor cytophilic activity. The latter was determined by the adherence of lymphoma cells to guinea pig peritoneal macrophages previously incubated with preheated mouse serum. The results obtained, in 2-3 month old animals, show no difference in lethal tumor incidence between xT and intact mice, 36% (14/39) vs. 39% (14/36). Neither did xT alter the significant increase in cytophilic antibodies detected in regressor serum, 115 +/- 15 (S.E.) vs. 106+/- 22 0/00 macrophages bearing tumor cells as compared to control values in either xT or normal serum, 53 +/- 3 vs 52 +/- 3. This background cytophilic activity was not significantly altered in progressor serum of either xT or intact mice, 36 +/- 5 vs 65 +/- 6. The specificity of the antitumor cytophilic antibodies was determined by the negative results obtained when a different tumor was used as target cell. It can be concluded that ant-tumor cytophilic antibodies are detectable in regressor but not in progressor serum. Thymectomy in this model does not alter either in vivo tumor incidence or humoral cytophilic activity. Since no thymic remnants were encountered at autopsy, it is postulated that AKR lymphoma cells, which proved to be neoplastic T cells, are capable of rendering T-immunocompetent a thymectomized allogeneic BALB host.

Animals↗