We propose that the rate of growth for some epithelia, such as SW-13 and MDCK, is proportional to the level of intrinsic progranulin gene expression, and that elevated progranulin gene expression confers a transformed phenotype on epithelial cells including anchorage independence in vitro and growth as tumors in nude mice.
Differential granulin expression in tumor samples and the antiproliferative effects of its antisense down-regulation suggest that GEP may be a new autocrine growth factor and molecular target for epithelial ovarian cancer.
IFN-alpha controls hormone secretion and symptoms in human gastroenteropancreatic neuroendocrine tumors (GEP-NET) but it rarely induces a measurable tumor size reduction.
Functional studies on Hep-2 cell lines demonstrated that the attenuation of PC cell-derived growth factor expression levels led to diminished cell proliferation rates (P<0.001), anchorage-independent growth in vitro (P<0.001), tumor forming in vivo (P<0.01) and resistance to apoptosis (P<0.001).
Gastroenteropancreatic neuroendocrine tumors (GEP NETs) are relatively rare neoplasias arising from the embryonic neural crest, neuroectoderm and endoderm.
A characteristic of human gastroenteropancreatic neuroendocrine tumors (GEP-NET) is a minute unobtrusive primary tumor which often cannot be detected by common physical examinations.
In contrast, the cumulative actuarial 5-year probability of metastatic death was 8.0 % for those with an insufficient/unsatisfactory aspirate for GEP classification or GEP class 1 tumor, versus 45.0 % for those with a GEP class 2 tumor (log rank P = 0.005).
Hierarchical clustering using all GEP genes showed that majority (61 of 71) of tumor samples clustered by patient, indicating greater interpatient heterogeneity (IPH) than ITH.
This study aimed to determine the expression of progranulin (PGRN) in hepatocellular carcinoma (HCC) cells in response to interleukin 6 (IL-6), a non-cellular component of the tumor microenvironment, and the molecular mechanism of PGRN oncogenic activity in hepatocarcinogenesis.
In studies of mixed adeno-neuroendocrine carcinomas (MANECs) the molecular features of GEP-NEC largely resemble their carcinoma/adenocarcinomas tumor counterparts.
Gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN) are relatively rare tumors that arise from the diffuse neuroendocrine system, and the biggest advances in molecular biology have helped in understanding these biological diversity of tumors over the past decades.
In this chapter, we outlined our experimental procedures in determining the feasibility of novel mAb in the preclinical cancer model, with an example of progranulin (PGRN/GEP) mAb against hepatocellular carcinoma (HCC) tumor in mouse model.
An in vivo study confirmed that the combined use of the two drugs displayed more potent antitumor activity compared to mice treated with cisplatin and GRN A alone; the inhibitory rate of tumor growth was 65.46% and 68.94%, respectively, in mice treated with GRN A and cisplatin.
This chapter describes a number of approaches to measure the transcription level of the GRN gene and to detect and analyze PGRN expression in cancer cells and in the local environment of the tumor, in mouse and human samples.
Transcriptome analysis of GEP-NET-derived cells, perturbed with a library of 107 compounds, identified the HDAC class I inhibitor entinostat as a potent inhibitor of master regulator activity for 42% of metastatic GEP-NET patients, abrogating tumor growth in vivo.
When scoring is correlated to patient outcome, we have demonstrated that a patient with tumorPGRN/GP88/GEP staining of "3+" has a fivefold increased risk of disease recurrence within 5 years.
Gastroenteropancreatic neuroendocrine tumours (GEP NET) are a heterogeneous group of rare tumours that have distinct effects on the body due to their tumour location and potential to secrete hormones and peptides.
We failed to find any association between the BALF content of progranulin or BCA-1 and the stage of tumor or prospectively assessed treatment response.