Relevant bibliographies by topics / Programmed cell death ligand 1

Academic literature on the topic 'Programmed cell death ligand 1'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Programmed cell death ligand 1"

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Liu, Qiang, and Chun-Sheng Li. "Programmed Cell Death-1/Programmed Death-ligand 1 Pathway." Chinese Medical Journal 130, no. 8 (April 2017): 986–92. http://dx.doi.org/10.4103/0366-6999.204113.

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Jaafar, Jaafar, Eugenio Fernandez, Heba Alwan, and Jacques Philippe. "Programmed cell death-1 and programmed cell death ligand-1 antibodies-induced dysthyroidism." Endocrine Connections 7, no. 5 (May 2018): R196—R211. http://dx.doi.org/10.1530/ec-18-0079.

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Background Monoclonal antibodies blocking the programmed cell death-1 (PD-1) or its ligand (PD-L1) are a group of immune checkpoints inhibitors (ICIs) with proven antitumor efficacy. However, their use is complicated by immune-related adverse events (irAEs), including endocrine adverse events (eAEs). Purpose We review the incidence, time to onset and resolution rate of dysthyroidism induced by PD-1/PD-L1 Ab, and the clinical, biological and radiological findings. We aim to discuss the potential mechanisms of PD-1/PD-L1 Ab-induced dysthyroidism, and to propose a management algorithm. Methods We performed a literature search of available clinical trials regarding PD-1/PD-L1 Ab in the PubMed database. We selected all English language clinical trials that included at least 100 patients. We also present selected case series or reports, retrospective studies and reviews related to this issue. Findings In patients treated with PD-1 Ab, hypothyroidism occurred in 2–10.1% and hyperthyroidism occurred in 0.9–7.8%. When thyroiditis was reported separately, it occurred in 0.34–2.6%. Higher rates were reported when PD-1 Ab were associated with other ICI or chemotherapy. The median time to onset of hyperthyroidism and hypothyroidism after PD-1 Ab initiation was 23–45 days and 2–3.5 months, respectively. Regarding PD-L1 Ab, hypothyroidism occurred in 0–10% and hyperthyroidism in 0.5–2% of treated patients. The average time to onset of dysthyroidism after PD-L1 Ab was variable and ranged from 1 day after treatment initiation to 31 months. Conclusion Dysthyroidism occurs in up to 10% of patients treated with PD-1/PD-L1 Ab. Hypothyroidism and reversible destructive thyroiditis are the most frequent endocrine adverse events (eAE) in PD-1/PD-L1 treated patients. Immune and non-immune mechanisms are potentially involved, independently of the presence of thyroid antibodies.
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Verhoeff, Sarah R., Michel M. van den Heuvel, Carla M. L. van Herpen, Berber Piet, Erik H. J. G. Aarntzen, and Sandra Heskamp. "Programmed Cell Death-1/Ligand-1 PET Imaging." PET Clinics 15, no. 1 (January 2020): 35–43. http://dx.doi.org/10.1016/j.cpet.2019.08.008.

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Fang, Xiao-Na, and Li-Wu Fu. "Predictive Efficacy Biomarkers of Programmed Cell Death 1/Programmed Cell Death 1 Ligand Blockade Therapy." Recent Patents on Anti-Cancer Drug Discovery 11, no. 2 (April 15, 2016): 141–51. http://dx.doi.org/10.2174/1574892811666160226150506.

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Yu, Wesley Y., Timothy G. Berger, Jeffrey P. North, Zoltan Laszik, and Jarish N. Cohen. "Expression of programmed cell death ligand 1 and programmed cell death 1 in cutaneous warts." Journal of the American Academy of Dermatology 81, no. 5 (November 2019): 1127–33. http://dx.doi.org/10.1016/j.jaad.2019.02.063.

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Tamura, Akihiro, Makiko Yoshida, Nobuyuki Yamamoto, Nanako Nino, Naoko Nakatani, Takayuki Ichikawa, Sayaka Nakamura, et al. "Programmed Death-1 and Programmed Death-Ligand 1 Expression Patterns in Pediatric Lymphoma." Blood 132, Supplement 1 (November 29, 2018): 5316. http://dx.doi.org/10.1182/blood-2018-99-110732.

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Abstract Introduction The programmed death-1 (PD-1)-programmed death-ligand 1 (PD-L1) pathway is an inhibitory immune checkpoint that can suppress T-cell-mediated tumor cytotoxicity. Anti-PD-1 monoclonal antibodies have recently been recognized as promising therapy for adult patients with lymphoma, particularly in classical Hodgkin's lymphoma. However, little information is available regarding the expression patterns of PD-1 and PD-L1 in pediatric lymphoma. Therefore, this study aimed to investigate the expression patterns of PD-1 and PD-L1 in pediatric lymphoma. Methods Immunohistochemical analysis was performed on paraffin-embedded pretherapeutic tumor biopsies from 36 newly diagnosed pediatric patients (aged 0-15 years) with lymphoma or lymphoproliferative disorders treated at Kobe Children's Hospital (Kobe, Japan) from 2003 to 2018. Results Thirty-six samples comprising 11 of Burkitt lymphoma (BL), 7 of anaplastic large-cell lymphoma (ALCL), 6 of T-lymphoblastic lymphoma (T-LBL), 5 of diffuse large B-cell lymphoma (DLBCL), 3 of Hodgkin's lymphoma (HL), 2 of chronic active EBV-associated lymphoproliferative disorders (CAEBV-LPD), 1 of T cell/histiocyte rich B-cell lymphoma (T/HRBCL), and 1 of subcutaneous panniculitis-like T-cell lymphoma (SPTCL) were evaluated. PD-L1 and PD-1 staining results in each lymphoma type are explained below and in Table. Burkitt lymphoma None of the 11 samples stained for PD-L1 or PD-1 in BL cells. PD-1 was expressed in a small proportion of tumor-infiltrating lymphocytes (TIL) in 3 of the 11 samples. Anaplastic large-cell lymphoma PD-L1 was robustly expressed in ALCL cells in 5 of the 7 samples. However, PD-1 was not expressed in any ALCL cell samples but expressed in a small proportion of TIL in only 1 sample. T-lymphoblastic lymphoma None of the 6 samples stained for PD-L1 in T-LBL cells. PD-1 was stained in T-LBL cells in only 1 sample. Moreover, PD-1 was not stained in TIL in any samples. Diffuse large B-cell lymphoma None of the 3 samples with DLBCL-not otherwise specified (DLBCL-NOS) or 1 sample with DLBCL with IRF4 rearrangement expressed PD-L1 on tumor cells. Conversely, PD-L1 was overexpressed in tumor cells in 1 sample with DLBCL with an interfollicular pattern of proliferation (DLBCL-IF). However, PD-1 was not expressed in any DLBCL cell samples. PD-1 was expressed in a small proportion of TIL in 1 sample with DLBCL with IRF4 rearrangement. Hodgkin's lymphoma PD-L1 was overexpressed in HL cells in both nodular sclerosis classic HL (NScHL), whereas PD-L1 was not expressed in nodular lymphocyte predominant HL (NLPHL) cells. PD-1 was not expressed in HScHL or NLPHL cells but was expressed in a small proportion of TIL in 1 sample with NLPHL. Chronic active EBV-associated lymphoproliferative disorders PD-L1 was overexpressed in tumor cells in both samples with CAEBV-LPD. PD-1 was not expressed in tumor cells but was expressed in a small proportion of TIL in 1 sample. T cell/histiocyte-rich B-cell lymphoma PD-L1 was overexpressed on tumor cells in T/HRBCL. PD-1 was weakly expressed in a part of T/HRBCL cells but strongly expressed in TIL. Subcutaneous panniculitis-like T cell lymphoma PD-L1 was overexpressed in tumor cells in SPTCL. However, PD-1 was not expressed in SPTCL cells or TIL. Discussion In this pediatric cohort, PD-L1 was overexpressed in tumor cells in ALCL (5/7), DLBCL-IF (1/1), NScHL (2/2), CAEBV-LPD (2/2), T/HRBCL (1/1), and SPTCL (1/1), but not in BL, T-LBL, DLBCL-NOS, or NLPHL. While the PD-L1 expression in EBV-positive lymphoma cells has been reported before, this study demonstrated the PD-L1 overexpression in CAEBV-LPD. In addition, we demonstrated the PD-L1 overexpression on SPTCL and DLBCL-IF cells, whereas the PD-L1 overexpression in T/HRBCL cells was consistent with previous reports. This study demonstrated that the PD-1 expression in tumor cells was rare in pediatric lymphoma. In addition, PD-1 expressions in TIL tended to be low in pediatric lymphoma, except for NLPHL and T/HRBCL. Besides classic HL, PD-1 blockade might be a promising treatment strategy for ALCL, DLBCL-IF, CAEBV-LPD, T/HRBCL, and SPTCL in children. Indeed, anectodal reports showed promising efficacy in ALCL. Therefore, further investigations are required to assess the role of the PD-1-PD-L1 pathway in pediatric lymphoma. Disclosures No relevant conflicts of interest to declare.
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Zhang, Ni, Jingyao Tu, Xue Wang, and Qian Chu. "Programmed cell death-1/programmed cell death ligand-1 checkpoint inhibitors: differences in mechanism of action." Immunotherapy 11, no. 5 (April 2019): 429–41. http://dx.doi.org/10.2217/imt-2018-0110.

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Zhao, Wanying, Yuanzheng Liang, and Liang Wang. "Advances in targeting programmed cell death 1/programmed cell death-ligand 1 therapy for hematological malignancies." Aging Pathobiology and Therapeutics 3, no. 4 (December 31, 2021): 84–94. http://dx.doi.org/10.31491/apt.2021.12.071.

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Programmed cell death 1 (PD-1) and programmed cell death-ligand 1 (PD-L1) are important immune checkpoints, and their interactions can mediate immune suppression in the tumor microenvironment. Targeting PD-1 and PD-L1 are immune checkpoint inhibitors that bind to PD-1 and PD-L1, respectively, to block the signal pathway between the two and increase the immune response. They are widely used in tumor treatment and have good efficacies for malignant melanoma, renal cell carcinoma, and non-small cell lung cancer, among others. In addition, for hematological malignancies, studies targeting PD-1 and PD-L1 have achieved gratifying results. This article briefly reviews the mechanisms of action and clinical and hematological malignancy applications of targeting PD-1 and PD-L1. Keywords: PD-1, PD-L1, mechanism of action, hematological malignancy
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Wang, Tianyu, Xiaoxing Wu, Changying Guo, Kuojun Zhang, Jinyi Xu, Zheng Li, and Sheng Jiang. "Development of Inhibitors of the Programmed Cell Death-1/Programmed Cell Death-Ligand 1 Signaling Pathway." Journal of Medicinal Chemistry 62, no. 4 (September 24, 2018): 1715–30. http://dx.doi.org/10.1021/acs.jmedchem.8b00990.

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Shen, Jacson K., Gregory M. Cote, Edwin Choy, Pei Yang, David Harmon, Joseph Schwab, G. Petur Nielsen, et al. "Programmed Cell Death Ligand 1 Expression in Osteosarcoma." Cancer Immunology Research 2, no. 7 (April 21, 2014): 690–98. http://dx.doi.org/10.1158/2326-6066.cir-13-0224.

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Dissertations / Theses on the topic "Programmed cell death ligand 1"

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Murata, Daiki. "High programmed cell death 1 ligand-1 expression: association with CD8+ T-cell infiltration and poor prognosis in human medulloblastoma." Kyoto University, 2018. http://hdl.handle.net/2433/233841.

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Liu, Bin. "PD-1/PD-L1 expression in a series of intracranial germinoma and its association with Foxp3+ and CD8+ infiltrating lymphocytes." Kyoto University, 2018. http://hdl.handle.net/2433/233842.

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Hamanishi, Junzo. "Programmed cell death 1 ligand 1 and tumor-infiltrating CD8+ T lymphocytes are prognostic factors of human ovarian cancer." Kyoto University, 2009. http://hdl.handle.net/2433/124273.

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McKendry, Richard. "Expression and function of programmed cell death Protein-1 (PD-1) and ligand PD-L1 in Chronic Obstructive Pulmonary Disease." Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/385139/.

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Sampangi, Sandeep. "Autologous human kidney proximal tubule epithelial cells (PTEC) modulate dendritic cell (DC), T cell and B cell responses." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82033/1/Sandeep_Sampangi_Thesis.pdf.

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This is a comprehensive study of human kidney proximal tubular epithelial cells (PTEC) which are known to respond to and mediate the pathological process of a range of kidney diseases. It identifies various molecules expressed by PTEC and how these molecules participate in down-regulating the inflammatory process, thereby highlighting the clinical potential of these molecules to treat various kidney diseases. In the disease state, PTEC gain the ability to regulate the immune cell responses present within the interstitium. This down-regulation is a complex interaction of contact dependent/independent mechanisms involving various immuno-regulatory molecules including PD-L1, sHLA-G and IDO. The overall outcome of this down-regulation is suppressed DC maturation, decreased number of antibody producing B cells and low T cell responses. These manifestations within a clinical setting are expected to dampen the ongoing inflammation, preventing the damage caused to the kidney tissue.
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van, der Linde Lea Isabell Shari [Verfasser], Lutz [Akademischer Betreuer] Welker, and Bernhard [Akademischer Betreuer] Schaaf. "Programmed Cell Death-Ligand 1 : Beitrag der Zytologie zur zielgerichteten Therapie von Lungenkarzinomen / Lea Isabell Shari van der Linde ; Akademische Betreuer: Lutz Welker, Bernhard Schaaf." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2021. http://d-nb.info/1228131252/34.

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Wise, Randi. "The role of the secretory pathway and cell surface proteolysis in the regulation of the aggressiveness of breast cancer cells." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/38199.

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Doctor of Philosophy
Biochemistry and Molecular Biophysics Interdepartmental Program
Anna Zolkiewska
Cancer cells exploit key signaling pathways in order to survive, proliferate, and metastasize. Understanding the intricacies of the aberrant signaling in cancer may provide new insight into how to therapeutically target tumor cells. The goal of my research was to explore the role of two modulators of transmembrane signaling, the secretory pathway and cell surface proteolysis, in the aggressiveness of breast cancer cells. To study the role of the secretory pathway, I focused on the family of endoplasmic reticulum (ER) chaperones. I found that several ER chaperones were upregulated in breast cancer cells grown under anchorage-independent conditions as mammospheres versus those grown under adherent conditions. Furthermore, certain members of the protein disulfide isomerase (PDI) family were consistently upregulated in two different cell lines at both the mRNA and protein levels. Knocking down these PDIs decreased the ability of the cells to form mammospheres. I demonstrated that the requirement for PDI chaperones in mammosphere growth is likely due to an increased flux of extracellular matrix (ECM) components through the ER. Next, I examined the role of cell surface proteolysis in modulating the aggressiveness of breast cancer cells. Cell-surface metalloproteases release soluble growth factors from cells and activate the corresponding growth factor receptors. I determined that specific metalloproteases (ADAM9 or ADAM12), modulate the activation of Epidermal Growth Factor Receptor (EGFR). I demonstrated that EGFR activation enhances the CD44⁺/CD24⁻ cell surface marker profile, which is a measure of cancer cell aggressiveness. I found that the MEK/ERK pathway, which is a downstream effector of EGFR activation, modulates the CD44⁺/CD24⁻ phenotype. When DUSP4, a negative regulator of the MEK/ERK pathway, is lost, activation of EGFR by metalloproteases no longer plays a significant role in cancer cell aggressiveness. This indicates that the ligand dependent activation of the EGFR/MEK/ERK pathway is a critical step in DUSP4-positive aggressive breast cancer. Finally, I examined the importance of metalloproteases in the regulation of Programmed-death ligand 1 (PD-L1), a transmembrane protein expressed by some cancer cells that plays a major role in suppressing the immune system. I demonstrated that cell-surface metalloproteases have the ability to cleave PD-L1 and release its receptor-binding domain to the extracellular environment. Collectively, these data indicate that (a) ER chaperones support anchorage-independent cell growth, (b) metalloproteases are important in regulation of an aggressive phenotype through the EGFR/MEK/ERK pathway, and (c) metalloproteases cleave PD-L1, a key component of immunosuppression in cancer.
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Richmond, Owen Benjamin. "Immune modulation mechanisms of porcine circovirus type 2." Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/73766.

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Porcine circovirus associated disease (PCVAD) is an umbrella term for a multitude of diseases and syndromes that have a negative impact on the health and economics of pig production operations throughout the world. Porcine circovirus type 2 is the causative agent of PCVAD; however the presence of PCV2 alone is rarely enough to cause clinical disease. In order for the full development of PCVAD the presence of a co-infecting pathogen is required. The mechanisms by which co-infection leads to disease remain ongoing areas of research, but it is thought that host immune modulations by PCV2 or a co-infecting pathogen are critical in the pathogenesis of PCVAD. In the first study of this dissertation the ability of PCV2 to induce regulatory T-cells (Tregs) and alter cytokine production was evaluated in vivo. The addition of PCV2 to a multiple viral challenge resulted in a significant increase in Tregs. Levels of IL-10 and IFN-γ were also found to be altered when PCV2 was added to a multiple viral challenge. In further experiments, monocyte derived dendritic cells (MoDC) were infected with different combinations and strains of PCV2 and PRRSV in vitro and evaluated for expression levels of programmed death ligand-1 (PD-L1), IL-10, CD86, swine leukocyte antigen-1 (SLA-1), and swine leukocyte antigen-2 (SLA-2). Expression levels of PD-L1 were significantly increased in PCV2 and PRRSV co-infected MoDCs. SLA-1, SLA-2, and CD86 expression levels were significantly decreased in the MoDC treatment groups containing both PCV2 and virulent stains of PRRSV. MoDC IL-10 expression was significantly increased by PCV2 and virulent strains of PRRSV co-infection. Finally, we investigated the role of the PD-L1/programmed death ligand-1 (PD-1) axis in porcine lymphocyte anergy, apoptosis, and the induction of Tregs. Lymphocyte populations with normal PD-1 expression had significantly higher percentages of anergic and apoptotic lymphocytes, and CD4+CD25HighFoxP3+ Tregs when compared to a PD-1 deficient lymphocyte population. The findings from these studies indicate host immune modulation by PCV2 in vivo and the development of a regulatory phenotype of dendritic cell following PCV2/PRRSV co-infections in vitro that may contribute to a dysfunctional adaptive immune response and the overall pathogenesis of PCVAD.
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Sonnenburg, Anna [Verfasser]. "Optimierte In-vitro-Testung von Fremdstoffen auf hautsensibilisierendes Potenzial durch CRISPR/Cas9-vermittelten Knockout des Arylhydrocarbon-Rezeptors und Antikörperblockade des inhibitorischen Moleküls programmed cell death-ligand 1 / Anna Sonnenburg." Berlin : Freie Universität Berlin, 2021. http://d-nb.info/1238595820/34.

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Acheampong, Emmanuel. "Assessment of circulating tumour cells in lung cancer patients." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2022. https://ro.ecu.edu.au/theses/2554.

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Lung cancer is among the most prevalent forms of cancer and remains the leading cause of cancer-associated deaths globally. Traditionally, lung cancers are classified as either non-small cell lung cancer (NSCLC) (85%) or small cell lung cancer (SCLC) (15%). About 60% of all cases are diagnosed at an advanced stage, at which the 5-year survival is only 4%. Anti-programmed cell death-1 and its ligand 1 (anti-PD-1/PD-L1) therapies have significantly improved the outcomes for lung cancer patients in recent years. However, prognosis and understanding of an individual patient’s lung cancer are often limited by tumour accessibility. Tissue biopsies are invasive, costly, and technically challenging procedures, posing risks to the patient. Circulating tumour cells (CTCs) are very attractive tumour surrogates that could serve as “liquid biopsy” with the advantage to be a low–to–null invasive and real-time approach compared to conventional tissue biopsies. Increasing evidence suggests that CTCs counts can serve as a prognostic biomarker for lung cancers. Notably, phenotypic, and molecular characterisation of CTCs may offer important clinical information for guiding personalised medicine. The studies in this dissertation assessed the potential of CTCs to provide information that could aid the management of lung cancer patients. We carried out a series of investigations covering a systematic review and meta-analysis of programmed cell death ligand-1 (PD-L1) expression on tumour samples and CTCs, a methodological study to improve phenotypic characterisation of CTCs for PD-L1 expression and its application in the clinical settings, and a study using singlecell genomics to uncover novel subpopulations of CTCs. The first chapter of the thesis includes an introduction to lung cancer and a thorough review of the literature on immunotherapy in lung cancer as well as CTCs. Chapter 2 describes a comprehensive review and meta-analysis of PD-L1 expression on tumour cells in SCLC from 27 studies enrolling a total of 27,292 patients. Our results revealed that the prevalence of PD-L1 expression in SCLC tumour cells was heterogeneous across studies. This heterogeneity was significantly moderated by factors such as cut-off values used for scoring PD-L1 staining by immunohistochemistry, and assessment of PD-L1 staining patterns as membranous and/or cytoplasmic. Following these findings, Chapter 3 covers a study carried out to address the feasibility to quantify PD-L1 expression on CTCs in SCLC patients. We develop an EpCAM targeting magnetic bead-based CTC isolation method as a surrogate for the CellSearch method, as this is the gold standard for CTC enumeration and the most used SCLC CTC isolation platform in the clinical setting. Using our immunomagnetic isolation technique, we compared detection rates of CTCs to those isolated using the microfluidic CTC enrichment device - Parsortix system, which separates cells by size exclusion. Detected CTCs were used to assess PD-L1 expression. We identified a subpopulation of EpCAM-negative SCLC CTCs, indicating that epitope-independent methods can detect additional CTCs missed by EpCAM basedcapture. The study also demonstrated that PD-L1 expression can be quantified on CTCs detected in SCLC patients. In parallel, we questioned whether blood is the alternative for PD-L1 expression in NSCLC patients based on several published studies that have assessed PD-L1 expression on CTCs in NSCLC patients. The review in Chapter 4 indicates that the analysis of PD-L1 on CTCs is feasible and PD-L1 expression could be detected before and after first-line therapy. However, there was limited evidence of whether PD-L1 expression on CTCs could predict response to anti-PD-1/PDL1 treatment. Chapter 5 describes a study in NSCLC patients to improve the detection of relevant CTC phenotypes and interrogate them for PD-L1 expression. We simultaneously identified circulating cells with epithelial origin and cells with mesenchymal features in patients with NSCLC by combining the Parsortix system with a modified sequential fluorescent quenching and restaining protocol. Nevertheless, none of the detected circulating cells expressed PD-L1 protein. Furthermore, a subset of mesenchymal-featured cells was confirmed as cancer cells via whole genome amplification (WGA) and low-pass whole-genome sequencing (LP-WGS) which revealed copy number alterations (CNAs) in several genomic regions. Lastly, the general discussion underscores how specific CTCs enrichment techniques are required for lung cancers according to their phenotypic characteristics. The results question the potential of CTCs for evaluating PD-L1 expression and the need for systematic clinical validation. Finally, the prospect of CTC genomic analysis is highlighted as it provides an opportunity to timely recognise patients harbouring deleterious alteration and new treatment targets. We conclude by proposing future directions building upon the findings presented in this thesis.
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Books on the topic "Programmed cell death ligand 1"

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Puthalakath, Hamsa, and Christine J. Hawkins, eds. Programmed Cell Death. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3581-9.

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Shi, Yun-Bo, Yufang Shi, Yonghua Xu, and David W. Scott, eds. Programmed Cell Death. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2.

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De Gara, Laura, and Vittoria Locato, eds. Plant Programmed Cell Death. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7668-3.

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Shi, Yufang, John A. Cidlowski, David Scott, Jia-Rui Wu, and Yun-Bo Shi, eds. Molecular Mechanisms of Programmed Cell Death. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-5890-0.

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Khosravi-Far, Roya, and Eileen White. Programmed Cell Death in Cancer Progression and Therapy. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6554-5.

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Moerdler, Scott, and Xingxing Zang. PD-1/PDL-1 Inhibitors as Immunotherapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0010.

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Programmed death 1 (PD-1), a member of the B7-CD28 immunoglobulin superfamily, and its ligands PD-L1/PD-L2 inhibit T-cell activation. They also play a key role in the tumor microenvironment, allowing for cancer immune escape. PD-1 is induced on a variety of immune cells, including tumor-infiltrating lymphocytes (TILs), while PD-L1 is found on many types of solid tumors including ovarian cancer and some TILs. The use of immunocheckpoint inhibitors like anti-PD-1 and anti-PD-L1 therapies has been shown to reactivate the immune system to attack tumor cells. Ovarian cancers have been shown to be responsive to anti-PD-1 and anti-PD-L1 therapies, though immunocheckpoint inhibitors are not enough. Current research is evaluating combination therapies to improve response rates.
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Book chapters on the topic "Programmed cell death ligand 1"

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Duke, Richard C., Paul B. Nash, Mary S. Schleicher, Cynthia Richards, Jodene Moore, Evan Newell, Alex Franzusoff, and Donald Bellgrau. "CD95 (Fas) Ligand." In Programmed Cell Death, 159–67. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_16.

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Tan, Kuan Onn, Shing-Leng Chan, Naiyang Fu, and Victor C. Yu. "MAP-1 Is a Putative Ligand for the Multidomain Proapoptotic Protein Bax." In Molecular Mechanisms of Programmed Cell Death, 123–30. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-5890-0_11.

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Parra, Edwin Roger, and Sharia Hernández Ruiz. "Western Blot as a Support Technique for Immunohistochemistry to Detect Programmed Cell Death Ligand 1 Expression." In Methods in Molecular Biology, 49–57. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1278-1_5.

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Parra, Edwin Roger, and Sharia Hernández Ruiz. "Detection of Programmed Cell Death Ligand 1 Expression in Lung Cancer Clinical Samples by an Automated Immunohistochemistry System." In Methods in Molecular Biology, 35–47. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1278-1_4.

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Austen, K. F., and W. Owen. "Regulation of Eosinophil Programmed Cell Death and the Subsequent Priming of Ligand Mediated Functions by the Eosinophil-Directed Hematopoietins." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 255–59. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_50.

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Shen, Jie. "Programmed Cell Death." In Encyclopedia of Gerontology and Population Aging, 1–6. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_430-1.

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Mehlhorn, Heinz. "Programmed cell death." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4209-1.

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Tata, Jamshed R. "How Hormones Regulate Programmed Cell Death during Amphibian Metamorphosis." In Programmed Cell Death, 1–11. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_1.

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Scott, David W., Tommy Brunner, Dubravka Donjerković, Sergei Ezhevsky, Terri Grdina, Douglas Green, Yufang Shi, and Xiao-rui Yao. "Murder and Suicide." In Programmed Cell Death, 91–103. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_10.

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Zheng, Dexian, Yanxin Liu, Yong Zheng, Ying Liu, Shilian Liu, Baoping Wang, Markus Metzger, Emiko Mizoguchi, and Cox Terhorst. "Molecular Mechanisms of T Lymphocyte Apoptosis Mediated by CD3." In Programmed Cell Death, 105–12. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_11.

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Conference papers on the topic "Programmed cell death ligand 1"

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Lim, Seung-Oe, Chia-Wei Li, and Mien-Chie Hung. "Abstract 4713: Deubiquitination and stabilization of programmed cell death-ligand 1 by CSN5." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4713.

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Yamane, Hiromichi, Hideko Isozaki, Nobuaki Ochi, Kenichiro Kudo, Yoshihiro Honda, Tomoko Yamagishi, Toshio Kubo, Katsuyuki Kiura, and Nagio Takigawa. "Abstract 1323: Both programmed cell death protein 1 and programmed death-ligand 1 molecules can be expressed on the cell surface of small-cell lung cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1323.

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Mir, P. Seyed, A. S. Berghoff, M. Preusser, G. Ricken, J. Riedl, F. Posch, L. Hell, et al. "Programmed Cell Death Ligand 1 and Venous Thromboembolism in Patients with Primary Brain Tumors." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680130.

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Hwang, Ilseon, Keon Uk Park, Jin Young Kim, Hun-Mo Ryoo, and Yun-Han Lee. "Abstract 3927: Programmed cell death ligand 1 expression in resected colorectal adenocarcinomas: association with micrometastasis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3927.

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Hung, Jung-Jyh, Yu-Chung Wu, and Wen-Hu Hsu. "Abstract A145: The prognostic significance of programmed cell death-ligand 1 expression in pulmonary squamous cell carcinoma." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a145.

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Takahashi, Miho, Satoshi Watanabe, Ko Sato, Tomohiro Tanaka, Yu Saida, Junko Baba, Aya Ohtsubo, et al. "Abstract 3206: Programmed death receptor-1/programmed death receptor ligand-1 blockade improves priming of antitumor effector T cells after cytotoxic therapies." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3206.

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Charpidou, Andriani, Vasilios Patriarcheas, Ioannis Vathiotis, Eleni Kokotou, Nikos Syrigos, Maria Mani, Lamprini Stournara, and Ioannis Gkiozos. "Immune-related adverse events as a predictor marker of response to programmed cell death 1/programmed death-ligand 1 axis inhibitors in patients with non-small cell lung cancer." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2305.

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Haile, Samuel, Sonia P. Dalal, Virginia Clements, Koji Tamada, and Suzanne Ostrand-Rosenberg. "Abstract 462: Soluble CD80 restores T-cell activation and overcomes tumor cell programmed death ligand-1-mediated suppression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-462.

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Heo, Jun Hyeok, Hye Young Kim, Ki Chung Park, Sung Joon Hong, Kang Su Cho, and Kyung Seok Han. "Abstract B41: Expression of programmed cell death ligand 1/2 and BCG immunotherapy in bladder cancer." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b41.

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McLaughlin, Joseph, Kurt A. Schalper, Daniel E. Carvajal-Hausdorf, Vasiliki Pelekanou, Vamsidhar Velcheti, Herbert Haack, Matthew R. Silver, Roy Herbst, Patricia LoRusso, and David L. Rimm. "Abstract 1310: Programmed death ligand-1 (PD-L1) heterogeneity in non-small cell lung cancer (NSCLC)." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1310.

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Reports on the topic "Programmed cell death ligand 1"

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Xiao, Youchao, Jiaqi Hao, Xingguang Ren, Hubin Duan, Chunyan Hao, Huan Wang, Xin Yang, et al. Programmed cell death ligand 1 is a prognostic factor for glioblastoma: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2020. http://dx.doi.org/10.37766/inplasy2020.7.0079.

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Liu, Shu, Xin Zhang, Wenhan Yang, and Shun Xu. Association of Patient Sex with Efficacy of Programmed Death-1/Ligand-1 Inhibitors in Advanced Non–small-cell Lung Cancer: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2021. http://dx.doi.org/10.37766/inplasy2021.1.0005.

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Peng, Xinya, Congchao Jia, Luling Huang, Xiaomeng Zhang, Xingxin Wen, Hao Chi, and Ligang Chen. The Clinicopathological and Prognostic Value of Programmed Death-Ligand 1 in Gallbladder cancer: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0078.

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Coplin, David L., Shulamit Manulis, and Isaac Barash. roles Hrp-dependent effector proteins and hrp gene regulation as determinants of virulence and host-specificity in Erwinia stewartii and E. herbicola pvs. gypsophilae and betae. United States Department of Agriculture, June 2005. http://dx.doi.org/10.32747/2005.7587216.bard.

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Gram-negative plant pathogenic bacteria employ specialized type-III secretion systems (TTSS) to deliver an arsenal of pathogenicity proteins directly into host cells. These secretion systems are encoded by hrp genes (for hypersensitive response and pathogenicity) and the effector proteins by so-called dsp or avr genes. The functions of effectors are to enable bacterial multiplication by damaging host cells and/or by blocking host defenses. We characterized essential hrp gene clusters in the Stewart's Wilt of maize pathogen, Pantoea stewartii subsp. stewartii (Pnss; formerly Erwinia stewartii) and the gall-forming bacterium, Pantoea agglomerans (formerly Erwinia herbicola) pvs. gypsophilae (Pag) and betae (Pab). We proposed that the virulence and host specificity of these pathogens is a function of a) the perception of specific host signals resulting in bacterial hrp gene expression and b) the action of specialized signal proteins (i.e. Hrp effectors) delivered into the plant cell. The specific objectives of the proposal were: 1) How is the expression of the hrp and effector genes regulated in response to host cell contact and the apoplastic environment? 2) What additional effector proteins are involved in pathogenicity? 3) Do the presently known Pantoea effector proteins enter host cells? 4) What host proteins interact with these effectors? We characterized the components of the hrp regulatory cascade (HrpXY ->7 HrpS ->7 HrpL ->7 hrp promoters), showed that they are conserved in both Pnss and Fag, and discovered that the regulation of the hrpS promoter (hrpSp) may be a key point in integrating apoplastic signals. We also analyzed the promoters recognized by HrpL and demonstrated the relationship between their composition and efficiency. Moreover, we showed that promoter strength can influence disease expression. In Pnss, we found that the HrpXY two-component signal system may sense the metabolic status of the bacterium and is required for full hrp gene expression in planta. In both species, acyl-homoserine lactone-mediated quorum sensing may also regulate epiphytic fitness and/or pathogenicity. A common Hrp effector protein, DspE/WtsE, is conserved and required for virulence of both species. When introduced into corn cells, Pnss WtsE protein caused water-soaked lesions. In other plants, it either caused cell death or acted as an Avr determinant. Using a yeast- two-hybrid system, WtsE was shown to interact with a number of maize signal transduction proteins that are likely to have roles in either programmed cell death or disease resistance. In Pag and Pab, we have characterized the effector proteins HsvG, HsvB and PthG. HsvG and HsvB are homologous proteins that determine host specificity of Pag and Pab on gypsophila and beet, respectively. Both possess a transcriptional activation domain that functions in yeast. PthG was found to act as an Avr determinant on multiple beet species, but was required for virulence on gypsophila. In addition, we demonstrated that PthG acts within the host cell. Additional effector genes have been characterized on the pathogenicity plasmid, pPATHₚₐg, in Pag. A screen for HrpL- regulated genes in Pnsspointed up 18 candidate effector proteins and four of these were required for full virulence. It is now well established that the virulence of Gram-negative plant pathogenic bacteria is governed by Hrp-dependent effector proteins. However; the mode of action of many effectors is still unresolved. This BARD supported research will significantly contribute to the understanding of how Hrp effectors operate in Pantoea spp. and how they control host specificity and affect symptom production. This may lead to novel approaches for genetically engineering plants resistant to a wide range of bacterial pathogens by inactivating the Hrp effectors with "plantabodies" or modifying their receptors, thereby blocking the induction of the susceptible response. Alternatively, innovative technologies could be used to interfere with the Hrp regulatory cascade by blocking a critical step or mimicking plant or quorum sensing signals.
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Hansen, Peter J., and Zvi Roth. Use of Oocyte and Embryo Survival Factors to Enhance Fertility of Heat-stressed Dairy Cattle. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697105.bard.

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The overall goal was to identify survival factors that can improve pregnancy success following insemination or embryo transfer in lactating dairy cows exposed to heat stress. First, we demonstrated that oocytes are actually damaged by elevated temperature in the summer. Then we tested two thermoprotective molecules for their effect on oocyte damage caused by heat shock. One molecule, ceramide was not thermoprptective. Another, insulin-like growth factor-1 (IGF) reduced the effects of heat shock on oocyte apoptosis and oocyte cleavage when added during maturation. We also used lactating cows exposed to heat stress to determine whether bovine somatotropin (bST), which increases IGF1 levels in vivo, would improve fertility in summer. Cows treated with bST received a single injection at 3 days before insemination. Controls received no additional treatment. Treatment with bST did not significantly increase the proportion of inseminated cows diagnosed pregnant although it was numerically greater for the bST group (24.2% vs 17.8%, 124–132 cows per group). There was a tendency (p =0.10) for a smaller percent of control cows to have high plasma progesterone concentrations (≥ 1 ng/ml) at Day 7 after insemination than for bST-treated cows (72.6 vs 81.1%). When only cows that were successfully synchronized were considered, the magnitude of the absolute difference in the percentage of inseminated cows that were diagnosed pregnant between bST and control cows was reduced (24.8 vs 22.4% pregnant for bST and control). Results failed to indicate a beneficial effect of bST treatment on fertility of lactating dairy cows. In another experiment, we found a tendency for addition of IGF1 to embryo culture medium to improve embryonic survival after embryo transfer when the experiment was done during heat stress but not when the experiment was done in the absence of heat stress. Another molecule tested, granulocyte-macrophage colony-stimulating factor (GM-CSF; also called colony-stimulating factor-2), improved embryonic survival in the absence of heat stress. We also examined whether heat shock affects the sperm cell. There was no effect of heat shock on sperm apoptosis (programmed cell death) or on sperm fertilizing ability. Therefore, effects of heat shock on sperm function after ejaculation if minimal. However, there were seasonal changes in sperm characteristics that indicates that some of the decrease in dairy cow fertility during the summer in Israel is due to using semen of inferior quality. Semen was collected from five representative bulls throughout the summer (August and September) and winter (December and January). There were seasonal differences in ion concentration in seminal plasma and in the mRNA for various ion channels known to be involved in acrosome reactions. Furthermore, the proportion of sperm cells with damaged acrosomes was higher in post-thaw semen collected in the summer than in its counterpart collected in winter (54.2 ± 3.5% vs. 51.4 ± 1.9%, respectively; P < 0.08Further examination is required to determine whether such alterations are involved in the low summer fertility of dairy cows.
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Granot, David, Richard Amasino, and Avner Silber. Mutual effects of hexose phosphorylation enzymes and phosphorous on plant development. United States Department of Agriculture, January 2006. http://dx.doi.org/10.32747/2006.7587223.bard.

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Research objectives 1) Analyze the combined effects of hexose phosphorylation and P level in tomato and Arabidopsis plants 2) Analyze the combined effects of hexose phosphorylation and P level in pho1 and pho2 Arabidopsis mutants 3) Clone and analyze the PHO2 gene 4) Select Arabidopsis mutants resistant to high and low P 5) Analyze the Arabidopsis mutants and clone the corresponding genes 6) Survey wild tomato species for growth characteristics at various P levels Background to the topic Hexose phosphorylating enzymes, the first enzymes of sugar metabolism, regulate key processes in plants such as photosynthesis, growth, senescence and vascular transport. We have previously discovered that hexose phosphorylating enzymes might regulate these processes as a function of phosphorous (P) concentration, and might accelerate acquisition of P, one of the most limiting nutrients in the soil. These discoveries have opened new avenues to gain fundamental knowledge about the relationship between P, sugar phosphorylation and plant development. Since both hexose phosphorylating enzymes and P levels affect plant development, their interaction is of major importance for agriculture. Due to the acceleration of senescence caused by the combined effects of hexose phosphorylation and P concentration, traits affecting P uptake may have been lost in the course of cultivation in which fertilization with relatively high P (30 mg/L) are commonly used. We therefore intended to survey wild tomato species for high P-acquisition at low P soil levels. Genetic resources with high P-acquisition will serve not only to generate a segregating population to map the trait and clone the gene, but will also provide a means to follow the trait in classical breeding programs. This approach could potentially be applicable for other crops as well. Major conclusions, solutions, achievements Our results confirm the mutual effect of hexose phosphorylating enzymes and P level on plant development. Two major aspects of this mutual effect arose. One is related to P toxicity in which HXK seems to play a major role, and the second is related to the effect of HXK on P concentration in the plant. Using tomato plants we demonstrated that high HXK activity increased leaf P concentration, and induced P toxicity when leaf P concentration increases above a certain high level. These results further support our prediction that the desired trait of high-P acquisition might have been lost in the course of cultivation and might exist in wild species. Indeed, in a survey of wild species we identified tomato species that acquired P and performed better at low P (in the irrigation water) compared to the cultivated Lycopersicon esculentum species. The connection between hexose phosphorylation and P toxicity has also been shown with the P sensitive species VerticordiaplumosaL . in which P toxicity is manifested by accelerated senescence (Silber et al., 2003). In a previous work we uncovered the phenomenon of sugar induced cell death (SICD) in yeast cells. Subsequently we showed that SICD is dependent on the rate of hexose phosphorylation as determined by Arabidopsis thaliana hexokinase. In this study we have shown that hexokinase dependent SICD has many characteristics of programmed cell death (PCD) (Granot et al., 2003). High hexokinase activity accelerates senescence (a PCD process) of tomato plants, which is further enhanced by high P. Hence, hexokinase mediated PCD might be a general phenomena. Botrytis cinerea is a non-specific, necrotrophic pathogen that attacks many plant species, including tomato. Senescing leaves are particularly susceptible to B. cinerea infection and delaying leaf senescence might reduce this susceptibility. It has been suggested that B. cinerea’s mode of action may be based on induction of precocious senescence. Using tomato plants developed in the course of the preceding BARD grant (IS 2894-97) and characterized throughout this research (Swartzberg et al., 2006), we have shown that B. cinerea indeed induces senescence and is inhibited by autoregulated production of cytokinin (Swartzberg et al., submitted). To further determine how hexokinase mediates sugar effects we have analyzed tomato plants that express Arabidopsis HXK1 (AtHXK1) grown at different P levels in the irrigation water. We found that Arabidopsis hexokinase mediates sugar signalling in tomato plants independently of hexose phosphate (Kandel-Kfir et al., submitted). To study which hexokinase is involved in sugar sensing we searched and identified two additional HXK genes in tomato plants (Kandel-Kfir et al., 2006). Tomato plants have two different hexose phosphorylating enzymes; hexokinases (HXKs) that can phosphorylate either glucose or fructose, and fructokinases (FRKs) that specifically phosphorylate fructose. To complete the search for genes encoding hexose phosphorylating enzymes we identified a forth fructokinase gene (FRK) (German et al., 2004). The intracellular localization of the four tomato HXK and four FRK enzymes has been determined using GFP fusion analysis in tobacco protoplasts (Kandel-Kfir et al., 2006; Hilla-Weissler et al., 2006). One of the HXK isozymes and one of the FRK isozymes are located within plastids. The other three HXK isozymes are associated with the mitochondria while the other three FRK isozymes are dispersed in the cytosol. We concluded that HXK and FRK are spatially separated in plant cytoplasm and accordingly might play different metabolic and perhaps signalling roles. We have started to analyze the role of the various HXK and FRK genes in plant development. So far we found that LeFRK2 is required for xylem development (German et al., 2003). Irrigation with different P levels had no effect on the phenotype of LeFRK2 antisense plants. In the course of this research we developed a rapid method for the analysis of zygosity in transgenic plants (German et al., 2003).
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