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Results for “metastatic potential”

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At least 19 recordsLinked to original sources
PubMed1979

Growth rate and chromosome number of tumor cell lines with different metastatic potential.

We investigated whether the metastatic potential of various tumor cell lines was related to chromosome counts or to rate of growth in vitro or in vivo. Clones of known metastatic potential derived from a C3H- fibrosarcoma induced by UV radiation (UV-2237) and from C57BL/6 B16 melanoma were tested for these characteristics. No correlation was found between the growth rate of these clones in monolayer culture or at a subcutaneous site and their ability to produce metastases. The cells from clones of UV-2237 were mainly in the diploid range with only one exception, and the B16 clones were all hyperploid. Thus, there was also no correlation between malignant behavior of the clones and gross changes in chromosome number.

Animals↗
PubMedDate not supplied

Metastatic potential of malignant tumours.

The term 'metastatic potential' is examined, together with some of the factors that may contribute to it. The evidence is drawn from clinical and experimental sources. Morphological factors include the site of the tumour, its size, histological appearances and pattern of local spread. The scope and limitations of each are discussed and the potential application of newer morphological techniques is noted. Certain non-morphological factors are considered: these are (1) the functional heterogeneity of tumour cell populations with resepct to the metastatic capacity; (2) the elaboration of certain tumour-associated products which may potentiate tumour spread; and (3) immunological factors in the form of local host cell infiltrates in and around primary tumours. The tumour-associated products include collagenases, prostaglandins and angiogenesis factor; their likely origin from tumour and host cells is stressed, together with their implications in physiological and pathological processes other than neoplasia. It is concluded that the metastatic potential of tumours cannot be assessed in the terms of conventional tumour pathology alone. A more functional approach is needed before the term 'metastatic potential' acquires solid conceptual or practical value.

Angiogenesis Inducing Agents↗
PubMed1979

Comparative studies of the metastatic potential of three transplantable rat mammary carcinomas of spontaneous origin.

The metastatic potential of 3 spontaneously arising mammary carcinomas (Sp4, Sp15 and Sp22) has been examined when transplanted in the form of a viable cell suspension into the tissue of origin. Primary tumours were excised at different times after implantation and it was found that the metastatic potential of the immunogenic tumour Sp4 was directly correlated with the size of the primary tumour when excised. By contrast, the incidence of metastases from the non-immunogenic tumours Sp15 and Sp22 was similar irrespective of the size of the primary tumour on excision. The pattern of metastasis also differed between the tumours, although here there was no relation to immunogenicity. Thus, resection en bloc of large primary Sp4 or Sp15 tumours plus regional lymph nodes could be completely curative, signifying initial spread of tumours via the lymphatics and only subsequently via the blood stream. On the other hand, resection en bloc of primary Sp22 tumours plus regional lymph nodes at a similar stage of primary tumour development was never curative, signifying early spread via the blood stream. Other studies showed that the metastatic potential of mammary carcinoma Sp4 was an innate characteristic of the tumour and not related to the tissue of implantation since in addition to metastasizing from the mammary pad it metastasized when implanted either s.c. or intradermally in a region devoid of mammary tissue. Furthermore, a rat sarcoma Mc7 showed a negligible tendency to metastasize when implanted either in the mammary pad or in the s.c. tissue, where it had been induced with methylcholanthrene.

Animals↗
PubMed1978

Control of melanogenesis in mouse melanoma cells of varying metastatic potential.

The control of melanin production, tyrosinase activity, and cell replication by melanocyte-stimulating hormone (MSH) and cyclic AMP (cAMP) was examined in differentially metastasizing B16 mouse melanoma variants. In B16-F1 cells (low metastatic potential), MSH or cAMP greatly elevated tyrosinase activity and melanin content while inhibiting cell replication. The same parameters in B16-F5 cells (intermediate metastatic potential) were altered to a much lesser degree, whereas B16-F10 cells (high metastatic potential) were not significantly affected by MSH or cAMP. Therefore, a correlation exists between loss of hormonal regulation and increased metastatic potential.

Animals↗
PubMed1976

Metastatic potential of metastases.

Nine cases of known metastases originating from other metastatic foci were documented at operation. The primary tumors included four melanomas, two osteosarcomas, a synovial sarcoma, an anaplastic lung carcinoma, and a rhadbomyosarcoma. Secondary metastatic sites to the regional lymph nodes were noted in the pulmonary hilum (one), mediastinum (one), pulmonary hilum and mediastinum (three), small bowel mesentary (two), retroperitoneum (one), and axilla (one). All patients were immunocompetent as evidenced by their ability to be sensitized to 2,4-dinitrochlorobenzene (DNCB) and/or their positive response to common skin test antigens. The metastatic potential of cells from metastases does not appear to differ from cells of the primary.

Adolescent↗
PubMed2026

Frequent mutations in the BIRC3 gene promote metastatic potential of nasopharyngeal carcinoma cells through the TRAF2-NF-κB pathway.

Nasopharyngeal carcinoma (NPC) is a head and neck cancer characterized by highly locoregionally invasive behavior attributable to the latent infection with Epstein-Barr virus (EBV) and genomic instability. It is well established that EBV-encoded oncogenic molecules actively contribute to the malignant behavior of NPC cells. However, the mechanism by which aberrant genomic alterations enable NPC cells to become aggressive remains largely unknown. In the present study, whole-exome sequencing (WES) revealed that the gene encoding the baculoviral IAP repeat-containing 3 (BIRC3) protein was frequently mutated in circulating tumor cells (CTCs) but not in paired primary tumor cells from patients with metastatic NPC. A minigene assay indicated that the c.637 A > G mutation disrupted normal mRNA splicing, resulting in the partial deletion of Exons 2 and 3 and altered stability of BIRC3 mRNA. In vitro experiments demonstrated that ectopic expression of the BIRC3c.637A>G mutant enhanced NPC cell invasive properties, including proliferation, resistance to apoptosis, migration, and invasion. Furthermore, overexpression of wild-type BIRC3 promoted invasive characteristics in NPC cells through the TRAF2-NF-κB signaling axis. In summary, BIRC3 acts as a regulator of the malignant features of NPC cells. Frequent BIRC3 mutations in CTCs, such as the c.637 A > G mutation, further enhance the metastatic potential of disseminated NPC cells by inducing aberrant alternative splicing. These findings suggest the therapeutic feasibility of targeting the BIRC3/TRAF2/NF-κB axis in the treatment of NPC.

Humans↗
PubMed1979

Prostaglandin D2 formation by malignant melanoma cells correlates inversely with cellular metastatic potential.

B16 malignant melanoma cell lines transform arachidonic acid and its transient metabolite, prostaglandin endoperoxide H2, into prostaglandin D2. The highly metastatic line, B16 F10, forms less prostaglandin D2 compared to the moderately metastatic parent line, B16 F1. Since platelet aggregation may be one factor involved in B16 metastasis and since prostaglandin D2 inhibits platelet aggregation, this prostaglandin could affect the outcome of platelet-tumour interactions, which may contribute ultimately to metastasis. Arachidonic acid metabolism may be another one of the intrinsic biochemical properties of tumor cells that affects their metastasis. Our results suggest that quantitative release of unusual prostaglandins must be considered in this context.

Arachidonic Acids↗
PubMed1979

[The metastatic potential of primary central nervous tumours (author's transl)].

Anatomical and clinical findings in 9 cases of primary brain tumors with metastases within (7 cases) or outside of (2 cases) the nervous system are reported. A review of the published literature revealed 248 cases of histologically-confirmed central nervous system tumors with metastases outside of the nervous system. These secondary sites are seen more frequently in adult males. Their frequency, in descending order, was gliomas (39,5 p. 100), meningeal tumors and sarcomas (28,2 p. 100), neuronal tumors (14,1 p. 100), lymphoma-microgliomas (12,5 p. 100), pineal body tumors (4 p. 100), and melanomas (1,6 p. 100). Ten cases out of 248 developed through a shunt. Nineteen cases were discovered without any surgical operation. There are still many unknown factors concerning their pathogenesis. It appears, however, than in some series of patients the prolongation of the survival-rate and the late effects of surgical operation are positive factors for metastatic dissemination.

Adult↗
PubMed1978

The regressing thin malignant melanoma: a distinctive lesion with metastatic potential.

To validate the supposition that thin malignant melanomas (less than 0.76 mm thick) of ordinarily low risk but with areas of regression may paradoxically metastasize, we observed 121 thin malignant melanomas over a six year period. Of these, 23 displayed readily apparent areas of regression, of which five (21.7%) metastasized. The incidence of metastases in their 98 counterparts without regression was 2.0% (2/98). The difference between the two is statistically significant (p = less than .01). Of the entire group of the two is statistically significant (p = less than .01). Of the entire group of thin melanomas, those with regression represented 19.0% (23/121) yet accounted for a disproportionate 71.4% (5/7) of all metastases. We conclude that regression is a relatively poor prognostic sign, whose occurrence within an otherwise thin melanoma represents a significant caveat to the current histologic staging system that equates thinness with low risk. We thus submit that patients whose malignant melanomas display regression be followed rigorously for evidence of metastases irrespective of the tumor's actual measured thickness or level of invasion.

Adult↗
PubMed1979

Transplantability and metastatic potential of chemically induced rat brain tumours.

From clinical observations it is known that brain tumours in principle do not metastasize. An explanation for this phenomenon is not available. The few described cases of distant metastases from primary brain tumours all occurred after surgery of the central nervous system. Furthermore, the brain does not contain a lymphatic system. The major question in this matter is whether the inability of CNS tumours to metastasize is based on a specific tumour bound property or on specific local factors. Since an experimental model for this situation was not available we induced brain tumours in rats. About 130 WAG/Rij and Sprague Dawley rats (males and females) were treated with the neurocarcinogen ethylnitroso-urea (ENU) within 24 hours after birth. Tumours appeared at the age of 6 to 29 months. All tumours were removed after killing the host and transplanted subcutaneously into syngeneic rats. Histologically the tumours were mostly oligodendrogliomas, schwannomas and several mixed glial tumours. Metastases from these primary tumours were not observed. The transplanted tumours showed distant metastases in 52% of the cases. Metastases occurred mainly in lungs, liver and lymph nodes. From these observations it is concluded that the absence of metastases from primary brain tumours is probably not related to a specific property of brain tumours. Further research is emphasized on specific local factors.

Animals↗
PubMed1978

Hormonal activation of adenylate cyclase in mouse melanoma metastatic variants.

The ability of melanocyte stimulating hormone (MSH), adrenocorticotropic hormone (ACTH), and prostaglandin E1 (PGE1) to stimulate the accumulation of cyclic AMP was examined in intact mouse melanoma cells of varying metastatic potential. F1 cells (low metastatic potential) had significantly greater cyclic AMP levels in response to all three hormones than F5 (intermediate metastatic potential) and F10 (high metastatic potential) cells. The ranking of the response was as follows: MSH, F1 greater than F5 greater than F10, ACTH, F1 greater than F5 greater F10, PGE, F1 greater than F10 greater F5. In contrast to the above, the degree of hormonal stimulation of adenylate cyclase in broken cell preparations was virtually identical in all three melanoma cell lines. Control enzyme activity was depressed in both F5 and F10 relative to F1. The conflicting results between studies of intact vs. broken cell preparations could not be explained by increased cyclic AMP phosphodiesterase activity in F5 and F10 cells. We conclude that as the melanoma cells increase in metastatic potential, there is a significant loss in the ability of their cyclic AMP system to respond appropriately to hormonal stimuli.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1978

Induction of a tumor with greatly increased metastatic growth potential by injection of cells from a low-metastatic H-2 heterozygous tumor cell line into an H-2 incompatible parental strain.

An H-2 heterozygous sarcoma, MDAY, originally induced with methylcholanthrene in an (A X DBA/2)F1 ((H-2a X H-2d) hybrid host was selected for growth in the H-2d homoxygous parental DBA/2 strain by serial intraperitoneal transplantation of ascites tumor cells. An apparent variant, designated MDAY-D2, was obtained which showed the expected loss of the private and public H-2Kk haplotype antigens normally associated with the A strain parent and the original MDAY tumor. Comparison of the original and variant lines revealed a wide variety of a cell surface antigen and receptor differences. Both tumors were found to be highly anaplastic and histologically unclasssifiable. Examination of the two tumor lines growing in vivo revealed a remarkable difference in their metastatic growth potential. The original MDAY line showed little propensity to spread to any organ site, with the occasional exception of liver, after subcutaneous inoculation of (A X DBA/2)F1 mice. In striking contrast, there was a rapid and massive spread of MDAY-D2 to liver, spleen, lungs and kidneys within 12-16 days: liver and spleen could be totally replaced by tumor within 2-3 weeks. These characteristics were observed in both (A X DBA/2)F1 and DBA/2 mice. The tendency to metastasize, as well as loss of the H-2Kk haplotype, appeared stable and irreversible. Although the precise origin of MDAY-D2 is not clear, its metastasizing properties are unique, making it a useful and desirable model to study the biology of metastasis.

Animals↗
PubMed2026

Biomarkers of metastatic disease in pheochromocytoma and paraganglioma.

Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors with variable metastatic potential. While metastatic disease occurs in approximately 10-20% of cases, its prediction remains a major clinical challenge, as no histological system has been universally validated to reliably identify aggressive tumors at diagnosis. This review aims to provide a comprehensive and updated overview of current and emerging biomarkers of metastatic risk in PPGL, encompassing histopathological scoring systems, genetic and molecular markers, biochemical phenotyping, liquid biopsy approaches, and imaging-based biomarkers. Among established markers, germline SDHB mutation status, loss of SDHB expression by immunohistochemistry, elevated plasma 3-methoxytyramine, and histopathological scoring systems, such as GAPP and COPPS, represent the most clinically validated tools for risk stratification. Emerging biomarkers - including somatic alterations in ATRX and TERT, genomic instability indices, tumor immune microenvironment characterization, circulating tumor DNA, and oncometabolite quantification - show promise in refining prognostic assessment but require prospective validation before routine clinical implementation. Accurate risk stratification in PPGL demands a multiparametric and dynamic approach, integrating clinical, genetic, biochemical, and molecular parameters. Future progress will depend on large prospective international cohorts, standardized biomarker platforms, and biomarker-driven clinical trial designs to translate emerging molecular knowledge into improved patient outcomes.

SDHB↗
PubMed1978

Tumor heterogeneity and the biology of cancer invasion and metastasis.

The development of a metastasis is dependent on an interplay between host factors and intrinsic characteristics of malignant tumor cells. The process of metastasis is highly selective, and the metastatic lesion represents the end point of many destructive events that only a few cells can survive. Neoplasms, which are predominantly heterogeneous, contain a variety of subpopulations of cells with differing metastatic potential. Furthermore, metastatic cell variants have been shown to preexist in murine neoplasms of old and recent origin. The possible existence of highly metastatic variant cells within a primary tumor suggests that we no longer should consider a neoplasm to be a uniform entity. Efforts to design effective therapeutic agents and procedures against malignant tumors should be directed toward the few but fatal metastatic subpopulations of cells.

Animals↗
PubMed1979

Metastatic colonization potential of primary tumour cells in mice.

A model has been developed for studying the capability of cells from primary murine mammary tumours to establish colonies in distant organs. The model involves the i.v. inoculation of disaggregated tumour cells into autologous and syngeneic recipients. The results show that the metastatic colonization potential of cells from a given tumour is consistent within the animals of an inoculated batch. Also, the findings are uniform in the autologous host and the syngeneic recipients. Tumours vary in their colonization potential and can be classified in 2 main groups designated high and low. These findings indicate that: (i) cells from 37% of mammary tumours can heavily colonize the lungs when inoculated i.v., even though the incidence of metastatic spread of these tumours in the undisturbed animal is almost zero. Thus, the relative infrequency of spontaneous metastasis from murine mammary tumours is not due to inability of the tumour cells to survive and colonize once free in the blood stream; and (ii) the colonization potential of the tumours is an intrinsic property of the tumour cells rather than of the host, whose prior acquaintance with the cells does not seem to confer resistance to colonization. The model presents opportunities for identification of possible differences between tumours of high and low colonization potential, and is being used to study cellular properties which favour colonization of distant organs by comparison of observations in vitro with the behaviour of cells from the same tumour in vivo.

Animals↗
PubMed2026

A Phosphoproteomic Platform Identifies Erythrocyte Membrane Protein Band 4.1-Like 3-Mediated Lipid Droplet Remodeling Linked to Liver Cancer Invasion and Migration.

Aberrant lipid metabolism is a hallmark of hepatocellular carcinoma (HCC), yet the regulatory mechanisms governing lipid droplet (LD) dynamics and their contribution to tumor progression remain poorly understood. Here, we developed an ultrasensitive phosphoproteomic platform using high-affinity HPDA@Ti4+ nanospheres to map LD-associated phosphorylation events across six HCC cell lines. By correlating phosphoproteomic signatures with LD morphology, we identified distinct regulatory signatures associated with LD size and abundance. Functional perturbation screens identified two distinct phosphoprotein modules controlling LD size: silencing SH3KBP1, SLK, EHD2, EPB41L3, and NEXN reduced LD size in Huh1 cells, whereas silencing CPD, BET1, UFL1, RRP1B, OGFR, and CD2BP2 enlarged LDs in Huh7 cells. Notably, we identified EPB41L3 as a critical metabolic-metastatic link; its loss decreased LD size and accelerated HCC migration and invasion, correlating with poor clinical prognosis. Crucially, we identified five key phosphorylation sites on EPB41L3 essential for its function; substituting these with alanine completely abolished its regulatory control over both LD size and HCC metastatic potential. Together, these findings delineate a phosphorylation-based regulatory network controlling the LD architecture and metastatic potential in HCC. Our study not only identifies potential therapeutic targets but also establishes a generalizable phosphoproteomic framework for interrogating lipid signaling in cancer metabolism.

Humans↗
PubMed1979

Properties of metastatic and nonmetastatic cloned subpopulations of an ultraviolet-light-induced murine fibrosarcoma of recent origin.

The present studies were designed to evaluate whether tumor cell properties such as growth rate, chromosome number, anchorage-independent growth, susceptibility to lymphocyte- or macrophage-mediated lysis in vitro, and antigenicity in vivo correlated with metastatic potential. A murine fibrosarcoma of recent origin induced in a C3H- mouse by chronic irradiation with ultraviolet light was used. Cells from the parent tumor and its clones were grown in culture. No single property of tumor cells that was measured in vitro or in vivo predicted or correlated with their metastatic potential. In order for metastasis to occur, all steps of the process must be completed. Therefore, interruption of the sequence at any stage can prevent the production of visible metastasis. It was concluded that the search for a single property common to all metastatic cells in a large variety of neoplasms is likely to be unproductive.

Animals↗