scholarly journals Spontaneously formed tumorigenic hybrids of Meth A sarcoma and macrophages grow faster and are better vascularized than the parental tumor

2002 ◽  
Vol 100 (4) ◽  
pp. 407-413 ◽  
Author(s):  
Lill-Tove R. Busund ◽  
Mette K. Killie ◽  
Kristian Bartnes ◽  
Rolf Seljelid
Keyword(s):  
Parental Tumor ◽  
Meth A Sarcoma

scholarly journals Exosomes from Plasma of Neuroblastoma Patients Contain Doublestranded DNA Reflecting the Mutational Status of Parental Tumor Cells

2021 ◽  
Vol 22 (7) ◽  
pp. 3667
Author(s):  
Chiara Degli Esposti ◽  
Barbara Iadarola ◽  
Simone Maestri ◽  
Cristina Beltrami ◽  
Denise Lavezzari ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Acquired Resistance ◽  
Membrane Vesicles ◽  
Preschool Age ◽  
Molecular Diagnostic ◽  
Non Invasive ◽  
Mutational Status ◽  
Whole Exome ◽  
Parental Tumor ◽  
Intercellular Communications

Neuroblastoma (NB) is an aggressive infancy tumor, leading cause of death among preschool age diseases. Here we focused on characterization of exosomal DNA (exo-DNA) isolated from plasma cell-derived exosomes of neuroblastoma patients, and its potential use for detection of somatic mutations present in the parental tumor cells. Exosomes are small extracellular membrane vesicles secreted by most cells, playing an important role in intercellular communications. Using an enzymatic method, we provided evidence for the presence of double-stranded DNA in the NB exosomes. Moreover, by whole exome sequencing, we demonstrated that NB exo-DNA represents the entire exome and that it carries tumor-specific genetic mutations, including those occurring on known oncogenes and tumor suppressor genes in neuroblastoma (ALK, CHD5, SHANK2, PHOX2B, TERT, FGFR1, and BRAF). NB exo-DNA can be useful to identify variants responsible for acquired resistance, such as mutations of ALK, TP53, and RAS/MAPK genes that appear in relapsed patients. The possibility to isolate and to enrich NB derived exosomes from plasma using surface markers, and the quick and easy extraction of exo-DNA, gives this methodology a translational potential in the clinic. Exo-DNA can be an attractive non-invasive biomarker for NB molecular diagnostic, especially when tissue biopsy cannot be easily available.

scholarly journals Interleukin 2 gene transfer into tumor cells abrogates tumorigenicity and induces protective immunity.

1990 ◽  
Vol 172 (4) ◽  
pp. 1217-1224 ◽  
Author(s):  
B Gansbacher ◽  
K Zier ◽  
B Daniels ◽  
K Cronin ◽  
R Bannerji ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Tumor Cells ◽  
Interleukin 2 ◽  
Retroviral Vectors ◽  
Cytolytic Activity ◽  
Tumor Formation ◽  
Tumor Bearing ◽  
Low Levels ◽  
Parental Tumor ◽  
Observation Period

To study the effects of localized secretion of cytokines on tumor progression, the gene for human interleukin 2 (IL-2) was introduced via retroviral vectors into CMS-5 cells, a weakly immunogenic mouse fibrosarcoma cell line of BALB/c origin. Secretion of low levels of IL-2 from the tumor cells abrogated their tumorigenicity and induced a long-lasting protective immune response against a challenge with a tumorigenic dose of parental CMS-5 cells. Co-injection of IL-2-producing CMS-5 cells with unmodified tumor cells inhibited tumor formation even when highly tumorigenic doses of CMS-5 cells were used. Cytolytic activity in mice injected with parental CMS-5 cells was transient and was greatly diminished 3 wk after injection, as commonly observed in tumor-bearing animals. However, in mice injected with IL-2-producing cells, tumor-specific cytolytic activity persisted at high levels for the duration of the observation period (at least 75 d). High levels of tumor-specific cytolytic activity could also be detected in parental CMS-5 tumor-bearing animals 18 d after inoculation with tumor cells, if IL-2-producing CMS-5 cells but not unmodified parental tumor cells were used as targets. These studies highlight the potential advantages of localized secretion of cytokines mediated via gene transfer to induce potent anti-tumor immune responses.

IDENTIFICATION OF A CLASS I MHC-ASSOCIATED PEPTIDE DERIVED FROM THE METH A SARCOMA AND RECOGNIZED BY CD8+ T CELLS

1993 ◽  
Vol 14 (4) ◽  
pp. 369
Author(s):  
A Frassanito ◽  
J I Mayordomo ◽  
W J Storkus ◽  
M T Lotze ◽  
R DeLeo ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Class I ◽  
Class I Mhc ◽  
Meth A Sarcoma

scholarly journals Conditionally Reprogrammed Cells from Patient-Derived Xenograft to Model Neuroendocrine Prostate Cancer Development

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1398 ◽  
Author(s):  
Xinpei Ci ◽  
Jun Hao ◽  
Xin Dong ◽  
Hui Xue ◽  
Rebecca Wu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Ex Vivo ◽  
Cancer Cell Line ◽  
Marker Genes ◽  
Patient Derived Xenograft ◽  
Pdx Model ◽  
Neuroendocrine Prostate Cancer ◽  
Parental Tumor

Neuroendocrine prostate cancer (NEPC) is a lethal subtype of prostate cancer. It develops mainly via NE transdifferentiation of prostate adenocarcinoma in response to androgen receptor (AR)-inhibition therapy. The study of NEPC development has been hampered by a lack of clinically relevant models. We previously established a unique and first-in-field patient-derived xenograft (PDX) model of adenocarcinoma (LTL331)-to-NEPC (LTL331R) transdifferentiation. In this study, we applied conditional reprogramming (CR) culture to establish a LTL331 PDX-derived cancer cell line named LTL331_CR_Cell. These cells retain the same genomic mutations as the LTL331 parental tumor. They can be continuously propagated in vitro and can be genetically manipulated. Androgen deprivation treatment on LTL331_CR_Cells had no effect on cell proliferation. Transcriptomic analyses comparing the LTL331_CR_Cell to its parental tumor revealed a profound downregulation of the androgen response pathway and an upregulation of stem and basal cell marker genes. The transcriptome of LTL331_CR_Cells partially resembles that of post-castrated LTL331 xenografts in mice. Notably, when grafted under the renal capsules of male NOD/SCID mice, LTL331_CR_Cells spontaneously gave rise to NEPC tumors. This is evidenced by the histological expression of the NE marker CD56 and the loss of adenocarcinoma markers such as PSA. Transcriptomic analyses of the newly developed NEPC tumors further demonstrate marked enrichment of NEPC signature genes and loss of AR signaling genes. This study provides a novel research tool derived from a unique PDX model. It allows for the investigation of mechanisms underlying NEPC development by enabling gene manipulations ex vivo and subsequent functional evaluations in vivo.

scholarly journals PD38-07 GENETIC MUTATIONS IN PATIENT-DERIVED BLADDER TUMOR ORGANOIDS MIMIC PARENTAL TUMOR SAMPLES

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Justin T. Matulay ◽  
Lamont J. Barlow ◽  
Mark V. Silva ◽  
Chee Wai Chua ◽  
Mitchell C. Benson ◽  
...  
Keyword(s):  
Bladder Tumor ◽  
Genetic Mutations ◽  
Parental Tumor ◽  
Tumor Organoids

Macroscopic and microscopic early effects of tumour necrosis factor on murine Meth A sarcoma, and relation to curative activity

1989 ◽  
Vol 157 (1) ◽  
pp. 65-73 ◽  
Author(s):  
Paul A. van de Wiel ◽  
Nanne Bloksma ◽  
C. Frieke Kuper ◽  
Frans M. Hofhuis ◽  
Jan. M. Willers
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Early Effects ◽  
Necrosis Factor ◽  
Meth A Sarcoma
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