Acute Changes in Calcitonin Levels in Lung Cancer Patients Treated with C. Parvum: Do These Reflect in Vivo Killing of Tumour Cells?

Metastasis ◽  
1980 ◽  
pp. 346-350
Author(s):  
H. D. Mitcheson ◽  
C. J. Hillyard ◽  
I. MacIntyre ◽  
J. E. Castro
2010 ◽  
Vol 8 (7) ◽  
pp. 182
Author(s):  
A.A. van der Veldt ◽  
M. Lubberink ◽  
E.F. Comans ◽  
H.N. Greuter ◽  
A. van Lingen ◽  
...  

1997 ◽  
Vol 20 (5) ◽  
pp. 354-364 ◽  
Author(s):  
Yuh-Min Chen ◽  
Wen-Kuang Yang ◽  
Jacqueline Whang-Peng ◽  
Wen-Ying Tsai ◽  
Yi-Mei Hung ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
pp. 215
Author(s):  
Florence Bonnet-Magnaval ◽  
Leïla Halidou Diallo ◽  
Valérie Brunchault ◽  
Nathalie Laugero ◽  
Florent Morfoisse ◽  
...  

Stau1 is a pluripotent RNA-binding protein that is responsible for the post-transcriptional regulation of a multitude of transcripts. Here, we observed that lung cancer patients with a high Stau1 expression have a longer recurrence free survival. Strikingly, Stau1 did not impair cell proliferation in vitro, but rather cell migration and cell adhesion. In vivo, Stau1 depletion favored tumor progression and metastases development. In addition, Stau1 depletion strongly impaired vessel maturation. Among a panel of candidate genes, we specifically identified the mRNA encoding the cell adhesion molecule Thrombospondin 1 (THBS1) as a new target for Staufen-mediated mRNA decay. Altogether, our results suggest that regulation of THBS1 expression by Stau1 may be a key process involved in lung cancer progression.


2000 ◽  
Vol 98 (2) ◽  
pp. 167-174 ◽  
Author(s):  
Susanne LEIJ-HALFWERK ◽  
Pieter C. DAGNELIE ◽  
J. Willem O. VAN DEN BERG ◽  
J. H. Paul WILSON ◽  
Paul E. SIJENS

Stable-isotope tracers were used to assess whether levels of phosphomonoesters (PME) and phosphodiesters (PDE) in the livers of lung cancer patients, as observed by 31P magnetic resonance (MR) spectroscopy, reflect elevated whole-body glucose turnover and gluconeogenesis from alanine. Patients with advanced non-small-cell lung cancer without liver metastases (n = 24; weight loss 0–24%) and healthy control subjects (n = 13) were studied after an overnight fast. 31P MR spectra of the liver in vivo were obtained, and glucose turnover and gluconeogenesis from alanine were determined simultaneously using primed-constant infusions of [6,6-2H2]glucose and [3-13C]alanine. Liver PME concentrations were 6% higher in lung cancer patients compared with controls (not significant); PME levels in patients with ⩾ 5% weight loss were significantly higher than in patients with < 5% weight loss (P < 0.01). PDE levels did not differ between the groups. In lung cancer patients, whole-body glucose production was 19% higher (not significant) and gluconeogenesis from alanine was 42% higher (P < 0.05) compared with healthy subjects; turnover rates in lung cancer patients with ⩾ 5% weight loss were significantly elevated compared with both patients with < 5% weight loss and healthy subjects (P < 0.05). PME levels were significantly correlated with glucose turnover and gluconeogenesis from alanine in lung cancer patients (r = 0.48 and r = 0.48 respectively; P < 0.05). In conclusion, elevated PME levels in lung cancer patients appear to reflect increased glucose flux and gluconeogenesis from alanine. These results are consistent with the hypothesis that elevated PME levels are due to contributions from gluconeogenic intermediates.


2012 ◽  
Vol 48 ◽  
pp. S187-S188
Author(s):  
A. Benedikova ◽  
J. Srovnal ◽  
J. Klein ◽  
P. Skalicky ◽  
M. Szkorupa ◽  
...  

2019 ◽  
Vol 1 (Supplement_1) ◽  
pp. i7-i7
Author(s):  
Michael Offin ◽  
Morana Vojnic ◽  
Zebing Liu ◽  
Allan Lui ◽  
Evan Siau ◽  
...  

Abstract BACKGROUND: CNS metastases occur in 20–50% of lung cancer patients during their disease; leptomeningeal disease (LMD) representing 5–8%, classically carries a poor prognosis with a median overall survival ranging from 1–11 months. There is a paucity of patient-derived preclinical disease models using tumor cells isolated from the CSF. Models that faithfully recapitulate the biology of CNS tumors would offer new insights into the biology of the disease as well as provide the basis for developing more effective therapy. METHODS: To create more representative preclinical models to study LMD we isolated tumor cells from CSF of 5 patients with cytologically proven LMD and implanted the cells into the subcutaneous flank of immune-compromised mice. Where possible, cell lines were also generated from PDX tissues. Models were characterized by next generation sequencing (NGS), growth rates, expression of driver oncogenes and sensitivity to small molecule inhibitors. RESULTS: To date, one PDX (LUAD-0048A) and cell line model were successfully derived from CSF samples (NSCLC patient with MET amplification) and 4 are pending. MET amplification and mRNA over-expression were confirmed by quantitative PCR in the PDX tissue and the cell line. Western blot analysis indicated that over-expressed MET was phosphorylated in both PDX tissue and cell line. These results were confirmed by immunohistochemistry. Growth of LUAD-0048A cells were unaffected by 3 MET inhibitors (crizotinib, cabozantinib, glesatinib). Similarly, MET inhibitors did not induce apoptosis in the cells. CONCLUSION: LMD represents an aggressive metastatic event in lung cancer patients. Here we were able to successfully establish a PDX from the CSF of a patient with LMD and trial targeted therapies in vivo. Translational collaborations where patients with clinical suspicion of LMD undergo CSF sampling, NGS/ctDNA analysis, and PDX modeling are crucial in improving our understanding of this metastatic compartment and investigating novel treatment paradigms.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Hui Xu ◽  
Wenjing Zhou ◽  
Fan Zhang ◽  
Linhui Wu ◽  
Juan Li ◽  
...  

AbstractPDS5B (precocious dissociation of sisters 5B) plays a pivotal role in carcinogenesis and progression. However, the biological functions of PDS5B in lung cancer and its underlying mechanisms are not fully elucidated. In the present study, we used MTT assays, wound-healing assays, and transwell migration and invasion approach to examine the cell viability, migration, and invasion of non-small cell lung cancer (NSCLC) cells after PDS5B modulation. Moreover, we investigated the function of PDS5B overexpression in vivo. Furthermore, we detected the expression of PDS5B in tissue samples of lung cancer patients by immunohistochemical study. We found that upregulation of PDS5B repressed cell viability, migration, and invasion in NSCLC cells, whereas downregulation of PDS5B had the opposite effects. We also observed that PDS5B overexpression retarded tumor growth in nude mice. Notably, PDS5B positively regulated LATS1 expression in NSCLC cells. Strikingly, low expression of PDS5B was associated with lymph node metastasis in lung cancer patients. Our findings suggest that PDS5B might be a therapeutic target for lung cancer.


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