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  1. Article: Dysregulation of Peripheral Blood Mononuclear Cells and Immune-Related Proteins during the Early Post-Operative Immune Response in Ovarian Cancer Patients.

    Ulevicius, Jonas / Jasukaitiene, Aldona / Bartkeviciene, Arenida / Dambrauskas, Zilvinas / Gulbinas, Antanas / Urboniene, Daiva / Paskauskas, Saulius

    Cancers

    2023  Volume 16, Issue 1

    Abstract: Surgical treatment is a cornerstone of ovarian cancer (OC) therapy and exerts a substantial influence on the immune system. Immune responses also play a pivotal and intricate role in OC progression. The aim of this study was to investigate the dynamics ... ...

    Abstract Surgical treatment is a cornerstone of ovarian cancer (OC) therapy and exerts a substantial influence on the immune system. Immune responses also play a pivotal and intricate role in OC progression. The aim of this study was to investigate the dynamics of immune-related protein expression and the activity of peripheral blood mononuclear cells (PBMCs) in OC patients, both before surgery and during the early postoperative phase. The study cohort comprised 23 OC patients and 20 non-cancer controls. A comprehensive analysis of PBMCs revealed significant pre-operative downregulation in the mRNA expression of multiple immune-related proteins, including interleukins, PD-1, PD-L1, and HO-1. This was followed by further dysregulation during the first 5 post-operative days. Although most serum interleukin concentrations showed only minor changes, a distinct increase in IL-6 and HO-1 levels was observed post-operatively. Reduced metabolic and phagocytic activity and increased production of reactive oxygen species (ROS) were observed on day 1 post-surgery. These findings suggest a shift towards immune tolerance during the early post-operative phase of OC, potentially creating a window for treatment. Further research into post-operative PBMC activity could lead to the development of new or improved treatment strategies for OC.
    Language English
    Publishing date 2023-12-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16010190
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Targeting AHR Increases Pancreatic Cancer Cell Sensitivity to Gemcitabine through the ELAVL1-DCK Pathway.

    Stukas, Darius / Jasukaitiene, Aldona / Bartkeviciene, Arenida / Matthews, Jason / Maimets, Toivo / Teino, Indrek / Jaudzems, Kristaps / Gulbinas, Antanas / Dambrauskas, Zilvinas

    International journal of molecular sciences

    2023  Volume 24, Issue 17

    Abstract: The aryl hydrocarbon receptor (AHR) is a transcription factor that is commonly upregulated in pancreatic ductal adenocarcinoma (PDAC). AHR hinders the shuttling of human antigen R (ELAVL1) from the nucleus to the cytoplasm, where it stabilises its target ...

    Abstract The aryl hydrocarbon receptor (AHR) is a transcription factor that is commonly upregulated in pancreatic ductal adenocarcinoma (PDAC). AHR hinders the shuttling of human antigen R (ELAVL1) from the nucleus to the cytoplasm, where it stabilises its target messenger RNAs (mRNAs) and enhances protein expression. Among these target mRNAs are those induced by gemcitabine. Increased AHR expression leads to the sequestration of ELAVL1 in the nucleus, resulting in chemoresistance. This study aimed to investigate the interaction between AHR and ELAVL1 in the pathogenesis of PDAC in vitro.
    MeSH term(s) Humans ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; ELAV-Like Protein 1/genetics ; Gemcitabine ; Pancreas ; Pancreatic Hormones ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Receptors, Aryl Hydrocarbon/genetics ; RNA, Messenger/genetics ; Deoxycytidine Kinase/drug effects ; Deoxycytidine Kinase/metabolism ; Pancreatic Neoplasms
    Chemical Substances ELAV-Like Protein 1 ; ELAVL1 protein, human ; Gemcitabine ; Pancreatic Hormones ; Receptors, Aryl Hydrocarbon ; RNA, Messenger ; Deoxycytidine Kinase (EC 2.7.1.74)
    Language English
    Publishing date 2023-08-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241713155
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Association between

    Bartkeviciene, Arenida / Jasukaitiene, Aldona / Zievyte, Inga / Stukas, Darius / Ivanauskiene, Sandra / Urboniene, Daiva / Maimets, Toivo / Jaudzems, Kristaps / Vitkauskiene, Astra / Matthews, Jason / Dambrauskas, Zilvinas / Gulbinas, Antanas

    Cancers

    2023  Volume 15, Issue 18

    Abstract: Pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), has an immune suppressive environment that allows tumour cells to evade the immune system. The aryl-hydrocarbon receptor (AHR) is a transcription factor that can be activated by ... ...

    Abstract Pancreatic cancer, particularly pancreatic ductal adenocarcinoma (PDAC), has an immune suppressive environment that allows tumour cells to evade the immune system. The aryl-hydrocarbon receptor (AHR) is a transcription factor that can be activated by certain exo/endo ligands, including kynurenine (KYN) and other tryptophan metabolites. Once activated, AHR regulates the expression of various genes involved in immune responses and inflammation. Previous studies have shown that AHR activation in PDAC can have both pro-tumorigenic and anti-tumorigenic effects, depending on the context. It can promote tumour growth and immune evasion by suppressing anti-tumour immune responses or induce anti-tumour effects by enhancing immune cell function. In this study involving 30 PDAC patients and 30 healthy individuals, peripheral blood samples were analysed. PDAC patients were categorized into Low (12 patients) and High/Medium (18 patients)
    Language English
    Publishing date 2023-09-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15184639
    Database MEDical Literature Analysis and Retrieval System OnLINE

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