αvβ5-Integrins mediate early steps of metastasis formation

2005 ◽  
Vol 41 (7) ◽  
pp. 1065-1072 ◽  
Author(s):  
Andreas Enns ◽  
Timo Korb ◽  
Kerstin Schlüter ◽  
Peter Gassmann ◽  
Hans-Ullrich Spiegel ◽  
...  
Keyword(s):  
Metastasis Formation

Resident Memory T Cells in Tumor-Distant Tissues Fortify Against Metastasis Formation

2020 ◽  
Author(s):  
Laura S. Christian ◽  
liuyang wang ◽  
Haiyang Wu ◽  
Dachuan Deng ◽  
Bryan Lim ◽  
...  
Keyword(s):  
T Cells ◽  
Memory T Cells ◽  
Metastasis Formation ◽  
Resident Memory T Cells

scholarly journals Integrative Genomic Analyses of Patient-Matched Intracranial and Extracranial Metastases Reveal a Novel Brain-Specific Landscape of Genetic Variants in Driver Genes of Malignant Melanoma

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 731
Author(s):  
Renáta Váraljai ◽  
Susanne Horn ◽  
Antje Sucker ◽  
Daniela Piercianek ◽  
Verena Schmitt ◽  
...  
Keyword(s):  
Brain Metastases ◽  
Genetic Variants ◽  
Genetic Alterations ◽  
Metastasis Formation ◽  
Driver Genes ◽  
Targeted Next Generation Sequencing ◽  
Paired Samples ◽  
Melanoma Metastases ◽  
Frequent Event ◽  
Genetic Landscape

Background: Development of brain metastases in advanced melanoma patients is a frequent event that limits patients’ quality of life and survival. Despite recent insights into melanoma genetics, systematic analyses of genetic alterations in melanoma brain metastasis formation are lacking. Moreover, whether brain metastases harbor distinct genetic alterations beyond those observed at different anatomic sites of the same patient remains unknown. Experimental Design and Results: In our study, 54 intracranial and 18 corresponding extracranial melanoma metastases were analyzed for mutations using targeted next generation sequencing of 29 recurrently mutated driver genes in melanoma. In 11 of 16 paired samples, we detected nucleotide modifications in brain metastases that were absent in matched metastases at extracranial sites. Moreover, we identified novel genetic variants in ARID1A, ARID2, SMARCA4 and BAP1, genes that have not been linked to brain metastases before; albeit most frequent mutations were found in ARID1A, ARID2 and BRAF. Conclusion: Our data provide new insights into the genetic landscape of intracranial melanoma metastases supporting a branched evolution model of metastasis formation.

scholarly journals Immunological and Nonimmunological Effects of Indoleamine 2,3-Dioxygenase on Breast Tumor Growth and Spontaneous Metastasis Formation

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Vera Levina ◽  
Yunyun Su ◽  
Elieser Gorelik
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Growth Regulation ◽  
Breast Cancer Cell Lines ◽  
Tumor Escape ◽  
Metastasis Formation ◽  
Spontaneous Metastasis ◽  
Immunodeficient Mice ◽  
Indoleamine 2,3 Dioxygenase

The role of the tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase (IDO1), in tumor escape and metastasis formation was analyzed using two pairs ofIdo1+andIdo1−murine breast cancer cell lines.Ido1expression in 4T1 cells was knocked down by shRNA, andIdo1expression in NT-5 cells was upregulated by stable transfection. Growth ofIdo1−tumors and spontaneous metastasis formation were inhibited in immunocompetent mice. A higher level of cytotoxic T lymphocytes was generated by spleen cells from mice bearingIdo1−tumors thanIdo1+tumors. Tumor and metastatic growth was enhanced in immunodeficient mice, confirming an intensified immune response in the absence ofIdo1expression. However,Ido1+tumors grow faster thanIdo1−tumors in immunodeficient SCID/beige mice (lacking T, B, and NK cells) suggesting that someIdo1-controlled nonimmunological mechanisms may be involved in tumor cell growth regulation.In vitroexperiments demonstrated that downregulation ofIdo1in tumor cells was associated with decreased cell proliferation, increased apoptosis, and changed expression of cell cycle regulatory genes, whereas upregulation ofIdo1in the cells had the opposite effects. Taken together, our findings indicate thatIdo1expression could exert immunological and nonimmunological effects in murine breast tumor cells.

scholarly journals 873 Pharmacologic macrophage depletion affects metastasis formation by modulating systemic immune responses in a genetic pancreatic cancer model

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A926-A926
Author(s):  
Heidi Griesmann ◽  
Heidi Griesmann ◽  
Heidi Griesmann ◽  
Christof Drexel ◽  
Nada Milosevic ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
T Cells ◽  
Regulatory T Cells ◽  
Mouse Model ◽  
Immune Cells ◽  
Tumour Progression ◽  
Metastasis Formation ◽  
Macrophage Depletion ◽  
Genetic Mouse Model ◽  
Liposomal Clodronate

BackgroundTumour-associated macrophages (TAM) play an important role in mediating tumour progression. In pancreatic cancer, infiltrating macrophages have been identified not only in invasive tumours, but also in early preinvasive pancreatic intraepithelial neoplasias and are known to mediate tumour progression.MethodsWe aimed to study the impact of pharmacological macrophage depletion by liposomal clodronate in the genetic mouse model of pancreatic cancer (KPC mouse: LSL-KrasG12D/+;LSL-Trp53R172H/+;Pdx-1-Cre). KPC mice were treated with liposomal clodronate or control liposomes from week 8 to week 20. Tumour and metastasis formation as well as alterations in local and circulating immune cells and cytokines were analysed.ResultsTreatment with liposomal clodronate effectively reduced CD11b-positive macrophages both in the pancreas and other organs such as liver, lung and spleen. Tumour incidence and size was only slightly reduced. However, metastasis formation in the liver und lungs was markedly diminished after macrophage depletion. Reduced macrophage count was associated with significant alterations in circulating growth factors and mediators known to be secreted by macrophages and associated with angiogenesis, most prominently VEGF. Moreover, application of liposomal clodronate led to marked alterations in circulating immune cells, among them reduced regulatory T cells.ConclusionsPharmacological depletion of macrophages in a genetic mouse model of pancreatic cancer markedly reduced metastasis formation and is associated with modulated profile of both secreted mediators and regulatory T cells. Pharmacological modulation of infiltrating macrophages represents a promising avenue for antimetastatic therapeutic approaches.

scholarly journals Transketolase-Like 1 Expression Is Modulated during Colorectal Cancer Progression and Metastasis Formation

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e25323 ◽  
Author(s):  
Santiago Diaz-Moralli ◽  
Miriam Tarrado-Castellarnau ◽  
Cristina Alenda ◽  
Antoni Castells ◽  
Marta Cascante
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Metastasis Formation ◽  
Colorectal Cancer Progression
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