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C D Pasqualini

Publications and source records attributed to C D Pasqualini.

At least 37 records · Page 2Linked to original sources
PubMed1990

Correlation between seric antitumor activity and concomitant resistance in mice bearing nonimmunogenic tumors.

Serum from mice bearing five weakly immunogenic or nonimmunogenic tumors inducing concomitant resistance exhibited a growth-inhibitory activity on in vitro proliferation of the tumor cells. This activity was proportional to the intensity of concomitant resistance and correlated with the capacity to restrain metastatic development. It was not attributable to cytotoxic antibodies, was relatively nonspecific, and operated through a cytostatic and reversible mechanism. All attempts to transfer antitumor resistance in vivo by serum inoculation have failed, but this could be attained by parabiosis. Physical and chemical serum treatments suggest that heat-, acid-, and alkali-resistant peptide(s) with molecular weights ranging from 1000 to 3000 could account for this inhibitory effect.

Animals↗
PubMed1990

Popliteal lymph node enlargement induced in syngeneic hosts by T cells from foster-nursed mice.

Splenocytes from adult F1 mice were assayed for their capacity to induce popliteal lymph node enlargement (PLNE) when inoculated in the footpad of identical or reciprocal F1 hosts. The results obtained showed that: (i) T Lyt 1+ splenocytes from adult F1 hybrids were able to induce a significant PLNE when inoculated in reciprocal but not in identical F1 hosts. (ii) Foster-nursing of F1 hybrids on mothers from the paternal strain was able to induce permanent alterations in the ability of their T splenocytes to induce PLNE: Lyt 1+ splenocytes were able to induce significant PLNE in identical but not in reciprocal F1 hosts. Thus, the ability of T splenocytes from foster-nursed F1 hybrids to induce PLNE resembled that observed in reciprocal F1 hybrids nursed by their own mothers. (iii) PLNE was accompanied by cell proliferation involving host B and T lymphocytes. (iv) This PLNE could be detected using F1 hybrids from parental strains differing or not at H-2 antigens but involving a parental strain expressing the stimulatory Mlsa allele and a parental strain bearing the nonstimulatory Mlsb allele while it was not observed in F1 hybrids from parental strains sharing Mlsa antigens.

Animals↗
PubMed1989

Mammary adenocarcinomas induced by medroxyprogesterone acetate: hormone dependence and EGF receptors of BALB/c in vivo sublines.

Mammary adenocarcinomas were induced by medroxy-progesterone acetate (MPA) in female BALB/c mice. From 5 primary tumors, 9 different sublines were established by s.c. transplantation into syngeneic female mice; these developed after a long latent period (4-12 months). Each subline was transplanted both into 4 mice treated with 40mg of MPA depot (s.c. contralaterally to the tumor inoculum) and into 4 non-treated mice. Of the 9 sublines, 6 proved to be hormone-dependent (MPA-D) and 3 hormone-independent or autonomous (MPA-I). However, even the autonomous lines, when treated with MPA, showed a slight increase in growth. All MPA-D lines had a high content of ER (20-254 fmoles/mg of protein), PR (63-710), PRL-R (44-74) and low or non-detectable EGF-R. Of the 3 MPA-I sublines that were studied, 2 showed a high content of ER (16-125), PR (27-708), PRL-R (19-70) and EGF-R (29-65) while the other one had a low content of ER (0-36), PR (0-13), no EGF-R and moderate PRL-R (15-52). Spontaneous mammary tumors of BALB/c and C3H origin, which also showed an MPA-I pattern of tumor growth, had high levels of EGF-R. We postulate that MPA has a direct effect on mammary tumor cells in MPA-D lines and that the expression of EGF-R is correlated with an autonomous pattern of growth.

Adenocarcinoma↗
PubMed1989

[Antitumor concomitant immunity: a possible metastasis control mechanism].

Concomitant immunity (CI) is defined as the lack or retardation or proliferation of a secondary tumor implant at a distant site; it has been given an immunological interpretation. Our experiments were designed to investigate CI in association with spontaneous tumors with or without metastases. In BALB/c mice, various syngeneic tumors, of undetectable immunogenicity, induced CI, preventing the development of a secondary implant of the same and occasionally of another tumor, indicating some degree of nonspecificity. This CI could also be observed in young and adult nude mice with high and low NK level, and in those treated with silica, discarding and participation of T lymphocytes, NK cells and macrophages, respectively. The lack of development of the secondary implant was not due to tumor rejection--contrarily to observations in allogeneic systems with immunogenic tumor--but to cytostasis. This "dormant tumor" state is observed together with the absence of host cell infiltration. The creation of a local inflammatory reaction abrogated CI, resulting in rapid tumor growth. On the other hand, an inflammatory reaction created by a foreign body inhibited the development of a tumor implant in the contralateral flank and tumor growth could be inhibited by piroxicam; furthermore, the tumor itself diminished the inflammatory reaction created by a foreign body at a distant site. Considering metastases as natural secondary implants, two mammary adenocarcinomas with a common origin were compared, one with 0 and the other with 100% metastatic incidence. The non-metastatic tumor induced stronger and earlier CI against both tumors and prevented the development of experimental and spontaneous metastases; moreover; its surgical extirpation led to the appearance of lung metastases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Role of concomitant resistance in the development of murine lung metastases.

An attempt was made to explain the distinct lung metastatic patterns of 2 mammary adenocarcinomas with a common BALB/c origin: M3, which does not induce spontaneous metastases, and MM3 with an almost 100% incidence. No difference between the 2 tumors was detected with respect to host mononuclear cell content, degree of immunogenicity or lung-colony-forming ability. Conversely, there was a marked difference in the capacity to induce concomitant resistance: M3-bearing mice induced stronger and earlier resistance against i.v. challenge of both M3 and MM3 tumor cells than MM3-bearing mice; this resistance was expressed as lower number of lung metastases and lower tumor-cell proliferation in metastatic nodules. M3 was also able to control the development of spontaneous metastases: metastases developed in all M3-excised mice, compared with none in M3-bearing mice, while MM3-bearing mice also bearing a secondary M3 tumor developed fewer metastases than mice bearing MM3 only. This anti-metastatic effect does not appear to depend on classical immunological mechanisms since no difference could be detected between the 2 tumors in response to T cells, NK, macrophages or antibodies.

Adenocarcinoma↗
PubMed1988

Maternal influence on the immune response: SMLC reactions between identical and reciprocal F1 hybrids and the role of lactation.

Identical and reciprocal adult F1 mice from different strain combinations, either nursed on their own mothers or foster-nursed on mothers from the paternal strain, were used to carry out SMLC assays. The results obtained showed that: (1) in vitro proliferation of F1 T cells was significantly different when splenocytes from identical versus reciprocal hybrids were used as the stimulatory population, splenocytes from one of the members of the reciprocal pair being able to induce higher proliferative responses of T cells from both identical and reciprocal F1 hybrids; (2) foster-nursing of F1 hybrids on mothers from the paternal strain was able to induce permanent alterations in the ability of their splenocytes to stimulate the proliferation of responder F1 T cells. The stimulatory ability of splenocytes from foster-nursed hybrids was indistinguishable from that observed in the reciprocal F1 combination nursed by its own mother. The existence of a maternal effect acting through milk on the outcome of self recognition in the litter is discussed.

Animals↗
PubMed1987

Neonatal cells in the immunoregulation of parental alloreactivity.

The ability of neonatal murine F1 cells to regulate parental graft vs. host (GvH) reactions was investigated. Neonatal F1 splenocytes were able to decrease significantly the deleterious effects of systemic GvH reactions induced either with maternal or paternal splenocytes in a third party strain. Both neonatal F1 splenocytes or thymocytes were able to decrease local GvH reactions induced with maternal splenocytes towards paternal histocompatibility antigens. In the same experimental conditions, however, neonatal F1 cells were unable to decrease local GvH reactions induced with paternal splenocytes towards maternal histocompatibility antigens; using different numbers of neonatal F1 cells not only was no suppressive effect detected but even, a significant increase in GvH was registered. Similar results were obtained when mortality assays were carried out. It can be concluded that neonatal F1 mice differ in their capacity for regulating parental alloreactive T reactions against self histocompatibility antigens either of maternal or paternal origin.

Animals↗
PubMed1987

Mouse mammary tumors induced by medroxyprogesterone acetate: immunohistochemistry and hormonal receptors.

Mammary adenocarcinomas induced by medroxyprogesterone acetate (MPA) in female BALB/c mice were investigated as to their morphology and immunohistochemistry and their content of steroid, prolactin (PRL), and epidermal growth factor (EGF) receptors. Histologically, these tumors were mainly of ductal origin, since hyperplastic alveolar nodules were observed only in 3 cases. No viral particles were encountered in electron microscopic studies. Estrogen and/or progesterone, PRL, and EGF receptors were detected in MPA-induced tumors, as well as in the occasional spontaneous mammary tumors of multiparous females. EGF was detected, by a radioimmunoassay, in the cystic fluid of 12 mammary adenocarcinomas. MPA treatment was found to induce uterine secretory changes, glandular cystic hyperplasia, and eventually deciduomas that stained strongly for desmin and to a lesser degree for vimentin, suggesting a muscular differentiation. Consequently, MPA-induced adenocarcinomas can be considered as ductal tumors that possess estrogen and/or progesterone, PRL, and EGF receptors. Whether MPA induces tumor growth directly via progesterone receptors remains to be investigated.

Adenocarcinoma↗
PubMed1986

Induction of mammary adenocarcinomas by medroxyprogesterone acetate in BALB/c female mice.

In a previous paper we reported that medroxyprogesterone acetate (MPA) decreased the incidence of foreign body tumorigenesis in BALB/c mice but that mammary adenocarcinomas appeared in some of the females. The experiment was repeated in 245 virgin females as follows: (1) 40 mice treated with 40 mg of MPA depot s.c. every 2 months during a whole year; (2) 117 mice bearing a foreign body (FB) and treated with MPA; (3) 46 mice bearing a FB; (4) 42 non-treated mice. Mammary adenocarcinomas developed in 16/40 in group 1 and 30/117 in group 2; no mammary tumors appeared in either control groups. The tumors were infiltrating adenocarcinomas often affecting more than one mammary gland; metastases were occasionally observed. Animals killed after 1 year of MPA treatment presented deciduomas. MPA also decreased the incidence of FB-induced sarcomas, confirming previous results.

Adenocarcinoma↗
PubMed1986

Histologic aspects of concomitant resistance induced by nonimmunogenic murine tumors.

Concomitant resistance to a second tumor implant was induced in both conventional and nude BALB/c mice by two nonimmunogenic syngeneic tumors of spontaneous origin, an epidermoid carcinoma and a lymphoid leukemia. In the secondary tumor, which was significantly inhibited by concomitant resistance, histologic examination revealed the presence of well-preserved tumor cells without any sign of necrosis and without any host cell infiltration, contrasting with classical immunologic rejection. Tumor cell proliferation as evaluated by the number of mitoses per high-power field was significantly inhibited in the secondary tumor as compared with the corresponding controls. No effect of concomitant resistance could be detected on primary tumor growth.

Animals↗
PubMed1986

Inhibitory effect of medroxyprogesterone acetate on foreign body tumorigenesis in mice.

This paper reports on the investigation of the effect of medroxyprogesterone acetate (MPA) on foreign body tumorigenesis that resulted from sc implantation of a glass cylinder. Adult BALB/c mice of both sexes bearing the foreign body were separated into groups. Group 1 received 40 mg MPA sc every 2 months during 1 year, in the vicinity of the glass cylinder; group 2 received the same MPA treatment in the contralateral flank; and group 3 received no hormonal treatment. Sarcomas developed in 4 of 39, 9 of 41, and 17 of 39 mice, respectively. With the use of an evaluation based on the number of high-risk mice per time interval, the MPA inhibitory effect was found to be statistically significant in both groups: 26, 53, and 79% tumor incidence, respectively. A decrease in the rate of tumor development also was observed but only in mice treated with MPA in situ. An unexpected side effect of continuous MPA administration in females was the appearance of adenocarcinomas.

Adenocarcinoma↗