Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bilineal differentiated liver carcinoma cells generates highly aggressive escape variants

ABSTRACT: Bilineal differentiated liver carcinoma cells generates highly aggressive escape variants

PROVIDER: PRJNA888145 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Bilineal differentiated liver carcinoma cells generates highly aggressive escape variants

Project description:Background & Aims: Combined HCC/iCCA is a rare liver tumor type. We generated a transgenic mouse model (AlfpCre+-Trp53fl/fl/Alb-HBs+ tg mouse) which developed next to HCC combined HCC/iCCA (cHCC/iCCA). We compared bilineal differentiated liver carcinoma cell lines generated from primary liver tumors of AlfpCre+-Trp53fl/fl/Alb-HBs+ tg mice and transplanted them into C57BL/6J mice to monitor there agressiveness. We compared the geneexpression profile from those primary liver carcinoma cell lines with IFNγ treatment (pCCL-IFNγ) and without treatment (pCCL) with explanted primary carcinoma cell line (pCCL-ex). Results: Here we describe that elimination of HBs+ in pCCL by HBs/(Kb/S190-197)-specific CD8 T cells describes a potential immune escape mechanism for highly aggressive cHCC/iCCA-type liver carcinomas.

2023-05-23 | GSE215059 | GEO

CD8 T cell-mediated depletion of HBV surface-antigen-expressing, bilineal-differentiated liver carcinoma cells generates highly aggressive escape variants.

Project description:The expression of viral antigens in chronic hepatitis B virus (HBV) infection drives continuous liver inflammation, one of the main risk factors to develop liver cancer. HBV developed immune-suppressive functions to escape from the host immune system, but their link to liver tumor development is not well understood. Here, we analyzed if and how HBV surface antigen (HBs) expression in combined hepatocellular-cholangiocarcinoma (cHCC/iCCA) cells influences their antigenicity for CD8 T cells. We randomly isolated liver tumor tissues from AlfpCre+-Trp53fl/fl/Alb-HBs+ tg mice and established primary carcinoma cell lines (pCCL) that showed a bilineal (CK7+/HNF4α+) cHCC/iCCA phenotype. These pCCL uniformly expressed HBs (HBshi), and low levels of MHC-I (MHC-Ilo), and were transiently convertible to a high antigenicity (MHC-Ihi) phenotype by IFN-γ treatment. HBshi/pCCL induced HBs/(Kb/S190-197)-specific CD8 T cells and developed slow-growing tumors in subcutaneously transplanted C57Bl/6J (B6) mice. Interestingly, pCCL-ex cells, established from HBshi/pCCL-induced and re-explanted tumors in B6 but not those in immune-deficient Rag1-/- mice showed major alterations, like an MHC-Ihi phenotype, a prominent growth-biased gene expression signature, a significantly decreased HBs expression (HBslo) and a switch to fast-growing tumors in re-transplanted B6 or PD-1-/- hosts with an unlocked PD-1/PD-L1 control system. CD8 T cell-mediated elimination of HBshi/pCCL, together with the attenuation of the negative restraints of HBs in the tumor cells, like ER-stress, reveals a novel mechanism to unleash highly aggressive HBslo/pCCL-ex immune-escape variants. Under certain conditions, HBs-specific CD8 T-cell responses thus potentiate tumor growth, an aspect that should be considered for therapeutic vaccination strategies against chronic HBV infection and liver tumors.

| S-EPMC10228399 | biostudies-literature

Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Project description:Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

| PRJNA1085286 | ENA

Highly Immunogenic Cancer Cells Require Activation of the WNT Pathway for Immunological Escape

Project description:Highly Immunogenic Cancer Cells Require Activation of the WNT Pathway for Immunological Escape

| PRJNA753524 | ENA

BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas

Project description:BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas

| PRJNA539867 | ENA

BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [MethylationEPIC]

Project description:BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [MethylationEPIC]

| PRJNA539865 | ENA

BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [MethylationEPIC]

Project description:The strong association between BAP1 mutations and highly aggressive Class 2 uveal melanoma (UM) suggests that epigenetic alterations may play a significant role in tumor progression. Thus, we characterized the impact of BAP1 loss on methylomic repatterning in UM.

2020-04-04 | GSE130295 | GEO

BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [RNA-Seq]

2020-04-04 | GSE130356 | GEO

BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [BeadChip 450K]

2020-04-04 | GSE130354 | GEO

BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [RNA-Seq]

Project description:BAP1 loss triggers DNA methylomic repatterning in highly aggressive Class 2 uveal melanomas [RNA-Seq]

| PRJNA539871 | ENA