Effect of host immune status on the spontaneous metastasis of cloned cell lines of the 13762NF rat mammary adenocarcinoma

North, Susan M; Nicolson, Garth L.

doi:10.1038/bjc.1985.253

Cited by 7 publications

(3 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, experiments designed to manipulate host immune responses did not significantly influence the spontaneous metastatic potential of the highly metastatic 13762NF cell lines. These data could partially explain the poor immunogenicity of gp580 in viva and the lack of an effective anti-tumor immune response to MTLn3 cells growing in the syngeneic host (North and Nicolson, 19856).…”

Section: Not Determinedmentioning

confidence: 99%

Development and characterization of a syngeneic monoclonal antibody to a rat mammary tumor metastasis‐associated mucin like cell‐surface antigen (gp580)

North

Steck

Spohn

et al. 1988

Intl Journal of Cancer

View full text Add to dashboard Cite

A rat hybridoma producing IgM monoclonal antibody (MAb) GP21:56 was generated with specificity for a high-molecular-weight, mucin-like glycoprotein (gp580) present on highly metastatic 13762NF rat mammary adenocarcinoma cells. The hybridoma was made by fusing rat Y3 Ag1.2.3 myeloma cells with spleen cells from a rat immunized i.d. with purified gp580. The gp580 appeared to be of low immunogenicity in syngeneic F344 rats because a total of 27 fusions were required to produce one hybridoma with specificity for this glycoprotein. Immunoblotting of purified gp580 after electrophoresis in 1% agarose and antibody-binding assays using purified gp580 linked to microtiter plates confirmed that MAb GP21:56 bound specifically to gp580. Other MAbs made against breast mucins were negative for gp580 reactivity. Enzyme-linked immunoabsorbent assays (ELISA) and radiolabelled antibody binding assays demonstrated that MAb GP21:56 bound to 13762NF adenocarcinoma cell lines and clones in relation to their spontaneous metastatic potentials; significantly more MAb GP21:56 bound to highly metastatic MTLn3 cells than to low metastatic MTC cells, and MAb GP21:56 showed little reactivity towards the majority of other cell lines tested, whether of rodent or of human origin. Kinetic binding studies indicated that MAb GP21:56 does not have a high affinity for gp580 but, once bound, it shows high avidity for this sialogalactoprotein. Localization studies using frozen tissue sections of 13762NF tumors indicated that MAb GP21:56 reacts with tumor cells grown in vivo in an analogous manner to in vitro cultured cells. Using immunoperoxidase techniques, less than 50% of the highly metastatic MTLn3 tumor cells were stained, whereas approximately 20% of the intermediate metastatic MTF7 and MTLn2 cells and less than 10% of low metastatic MTC and MTPa cells were stained with MAb GP21:56. The cell-to-cell reactivity was heterogeneous and mainly associated with the tumor-cell surface and extracellular matrix.

show abstract

Section: Not Determinedmentioning

confidence: 99%

Development and characterization of a syngeneic monoclonal antibody to a rat mammary tumor metastasis‐associated mucin like cell‐surface antigen (gp580)

North

Steck

Spohn

et al. 1988

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Using radiolabeled cells, Fidler et al found that most do not survive (Fidler, 1970, 1973b; Fidler and Nicolson, 1977) because of hemodynamic sheer (Weiss, 1989, 1990; Weiss and Schmid-Schonbein, 1989; Weiss et al, 1985), anoikis (Kim et al, 1999; Phadke et al, 2008; Wong et al, 2001), or immune selection (Fidler, 1974; Gorelik et al, 1980; Hanna, 1985; North and Nicolson, 1985; Van Netten et al, 1993; Young and Newby, 1986). In contrast, using a fluorescent tag Naumov et al (1999, 2002) showed that a majority of cells not only survived but also extravasated.…”

Section: Introductionmentioning

confidence: 99%

Metastasis Suppressor Genes

Hurst

Welch

2011

International Review of Cell and Molecular Biology

118

View full text Add to dashboard Cite

The molecular mechanisms and genetic programs required for cancer metastasis are sometimes overlapping, but components are clearly distinct from those promoting growth of a primary tumor. Every sequential, rate-limiting step in the sequence of events leading to metastasis requires coordinated expression of multiple genes, necessary signaling events, and favorable environmental conditions or the ability to escape negative selection pressures. Metastasis suppressors are molecules that inhibit the process of metastasis without preventing growth of the primary tumor. The cellular processes regulated by metastasis suppressors are diverse and function at every step in the metastatic cascade. As we gain knowledge into the molecular mechanisms of metastasis suppressors and cofactors with which they interact, we learn more about the process, including appreciation that some are potential targets for therapy of metastasis, the most lethal aspect of cancer. Until now, metastasis suppressors have been described largely by their function. With greater appreciation of their biochemical mechanisms of action, the importance of context is increasingly recognized especially since tumor cells exist in myriad microenvironments. In this review, we assemble the evidence that selected molecules are indeed suppressors of metastasis, collate the data defining the biochemical mechanisms of action, and glean insights regarding how metastasis suppressors regulate tumor cell communication to–from microenvironments.

show abstract

“…Using an animal model for metastatic breast cancer based on the rat 13762NF mammary adenocarcinoma, we have asked certain questions concerning the role of adhesive, invasive, and growth properties of highly metastatic cells in specific organ colonization. The 13762NF adenocarcinoma system fulfills several criteria that are important in a tumor model for breast cancer, such as its similarity to malignant human breast adenocarcinomas in cytoskeletal [10,11] and cell surface [12][13][14][15] components, antigens [16,17], enzymes [18][19][20], and mode of spread [12,18]. We have developed in vitro assays for malignant cell adhesion and invasion of syngeneic organ tissues [19] as well as the ability of malignant cells to respond to soluble growth stimulators and inhibitors released by syngeneic organ tissues [20,21].…”

Section: Introductionmentioning

confidence: 99%

Differential organ tissue adhesion, invasion, and growth properties of metastatic rat mammary adenocarcinoma cells

Nicolson

1988

Breast Cancer Res Tr

View full text Add to dashboard Cite

Metastatic lines and clones of the rat 13762NF mammary adenocarcinoma have been established that show reproducible spontaneous metastasis from the mammary fat pad to regional lymph node and lung. Poorly (MTC) and highly (MTLn3) metastatic cloned lines derived from tumor growing in the mammary fat pad (MTC) and its spontaneous lung metastasis (MTLn3) were tested in vitro for their abilities to attach to and invade into syngeneic organ tissue and to survive and grow in medium conditioned by target and nontarget syngeneic organ tissues. The highly metastatic MTLn3 cells adhered to and invaded target lung tissue at significantly higher rates than the MTC cells, and bound to and invaded other organ tissues although at lower rates than lung tissue. Similarly, the MTLn3 cells showed significantly higher growth stimulation by lung-conditioned medium than medium conditioned by other tissues. Poorly metastatic MTC cells were not significantly stimulated by any of the organ-conditioned media. The results are consistent with previous proposals that explain preferential organ metastasis in terms of 'seed and soil', and further suggest that metastasis of mammary tumors to specific organ secondary sites is mediated by specific properties, such as those involved in tumor-cell organ-cell adhesion, invasion, and growth.

show abstract

Effect of host immune status on the spontaneous metastasis of cloned cell lines of the 13762NF rat mammary adenocarcinoma

Cited by 7 publications

References 19 publications

Development and characterization of a syngeneic monoclonal antibody to a rat mammary tumor metastasis‐associated mucin like cell‐surface antigen (gp580)

Development and characterization of a syngeneic monoclonal antibody to a rat mammary tumor metastasis‐associated mucin like cell‐surface antigen (gp580)

Metastasis Suppressor Genes

Differential organ tissue adhesion, invasion, and growth properties of metastatic rat mammary adenocarcinoma cells

Contact Info

Product

Resources

About