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Article ; Online: LOXL2 in pancreatic tumourigenesis: the complexity of tumour-stromal crosstalk exemplified.

Coffelt, Seth B / Morton, Jennifer P

2022 Volume 72, Issue 2, Page(s) 221–222

MeSH term(s)	Humans ; Neoplasms ; Pancreas ; Carcinogenesis/genetics ; Amino Acid Oxidoreductases/genetics ; Pancreatic Neoplasms/genetics ; Tumor Microenvironment
Chemical Substances	Amino Acid Oxidoreductases (EC 1.4.-) ; LOXL2 protein, human (EC 1.4.3.-)
Language	English
Publishing date	2022-04-15
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2022-327430
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Article: Heterogeneity in Pancreatic Cancer Fibroblasts-TGFβ as a Master Regulator?

Watt, Dale M / Morton, Jennifer P

Cancers

2021 Volume 13, Issue 19

Abstract: Pancreatic ductal adenocarcinoma is an aggressive disease for which there are very few available therapies. It is notable for its high degree of tumour complexity, with the tumour microenvironment often accounting for the majority of the tumour volume. ... ...

Abstract	Pancreatic ductal adenocarcinoma is an aggressive disease for which there are very few available therapies. It is notable for its high degree of tumour complexity, with the tumour microenvironment often accounting for the majority of the tumour volume. Until recently, the biology of the stroma was poorly understood, particularly in terms of heterogeneity. Recent research, however, has shed light on the intricacy of signalling within the stroma and particularly the molecular and functional heterogeneity of the cancer associated fibroblasts. In this review, we summarise the recent improvements in our understanding of the different fibroblast populations within PDAC, with a focus on the role TGFβ plays to dictate their formation and function. These studies have highlighted some of the reasons for the failure of trials targeting the tumour stroma, however, there are still considerable gaps in our knowledge, and more work is needed to make effective fibroblast targeting a reality in the clinic.
Language	English
Publishing date	2021-10-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13194984
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Article ; Online: Environment Influences Tumor Progression and Transcriptional Subtype in a New Model of Pancreatic Cancer.

Pickering, Karen A / Morton, Jennifer P

Cancer discovery

2020 Volume 10, Issue 10, Page(s) 1448–1450

Abstract: In this issue, Miyabayashi and colleagues describe a novel intraductal model of pancreatic cancer that allows modeling of the transcriptional subtypes of pancreatic cancer. Using this model, they are able to observe subtype switching driven by the ... ...

Abstract	In this issue, Miyabayashi and colleagues describe a novel intraductal model of pancreatic cancer that allows modeling of the transcriptional subtypes of pancreatic cancer. Using this model, they are able to observe subtype switching driven by the microenvironment, a process at least partially mediated by RAS signaling.
MeSH term(s)	Carcinoma, Pancreatic Ductal/genetics ; Humans ; Pancreatic Neoplasms/genetics ; Signal Transduction ; Tumor Microenvironment/genetics
Language	English
Publishing date	2020-09-29
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-1090
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Zs.A 6916: Show issues

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Article ; Online: Therapeutic targeting of tumour myeloid cells.

Barry, Simon T / Gabrilovich, Dmitry I / Sansom, Owen J / Campbell, Andrew D / Morton, Jennifer P

Nature reviews. Cancer

2023 Volume 23, Issue 4, Page(s) 216–237

Abstract: Myeloid cells are pivotal within the immunosuppressive tumour microenvironment. The accumulation of tumour-modified myeloid cells derived from monocytes or neutrophils - termed 'myeloid-derived suppressor cells' - and tumour-associated macrophages is ... ...

Abstract	Myeloid cells are pivotal within the immunosuppressive tumour microenvironment. The accumulation of tumour-modified myeloid cells derived from monocytes or neutrophils - termed 'myeloid-derived suppressor cells' - and tumour-associated macrophages is associated with poor outcome and resistance to treatments such as chemotherapy and immune checkpoint inhibitors. Unfortunately, there has been little success in large-scale clinical trials of myeloid cell modulators, and only a few distinct strategies have been used to target suppressive myeloid cells clinically so far. Preclinical and translational studies have now elucidated specific functions for different myeloid cell subpopulations within the tumour microenvironment, revealing context-specific roles of different myeloid cell populations in disease progression and influencing response to therapy. To improve the success of myeloid cell-targeted therapies, it will be important to target tumour types and patient subsets in which myeloid cells represent the dominant driver of therapy resistance, as well as to determine the most efficacious treatment regimens and combination partners. This Review discusses what we can learn from work with the first generation of myeloid modulators and highlights recent developments in modelling context-specific roles for different myeloid cell subtypes, which can ultimately inform how to drive more successful clinical trials.
MeSH term(s)	Humans ; Neoplasms/drug therapy ; Myeloid Cells ; Immunotherapy ; Myeloid-Derived Suppressor Cells ; Neutrophils ; Tumor Microenvironment
Language	English
Publishing date	2023-02-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-022-00546-2
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Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 24: Show issues

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Article: Neutrophils: Homing in on the myeloid mechanisms of metastasis

Leach, Joshua / Morton, Jennifer P / Sansom, Owen J

Molecular immunology. 2019 June, v. 110

2019

Abstract: The metastasis cascade is complex and comprises several stages including local invasion into surrounding tissue, intravasation and survival of tumour cells in the circulation, and extravasation and colonisation of a distant site. It is increasingly clear ...

Abstract	The metastasis cascade is complex and comprises several stages including local invasion into surrounding tissue, intravasation and survival of tumour cells in the circulation, and extravasation and colonisation of a distant site. It is increasingly clear that these processes are driven not only by signals within the tumour cells, but are also profoundly influenced by stromal cells and signals in the tumour microenvironment. Amongst the many cell types within the tumour microenvironment, immune cells such as lymphocytes, macrophages and neutrophils play a prominent role in tumour development and progression. Neutrophils, however, have only recently emerged as important players, particularly in metastasis. Here we review the current evidence suggesting a multi-faceted role for neutrophils in the metastatic cascade.
Keywords	lymphocytes ; macrophages ; metastasis ; neoplasm cells ; neoplasms ; neutrophils ; stromal cells
Language	English
Dates of publication	2019-06
Size	p. 69-76.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2017.12.013
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 166: Show issues

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Article ; Online: KRAS allelic imbalance drives tumour initiation yet suppresses metastasis in colorectal cancer in vivo.

Najumudeen, Arafath K / Fey, Sigrid K / Millett, Laura M / Ford, Catriona A / Gilroy, Kathryn / Gunduz, Nuray / Ridgway, Rachel A / Anderson, Eve / Strathdee, Douglas / Clark, William / Nixon, Colin / Morton, Jennifer P / Campbell, Andrew D / Sansom, Owen J

Nature communications

2024 Volume 15, Issue 1, Page(s) 100

Abstract: Oncogenic KRAS mutations are well-described functionally and are known to drive tumorigenesis. Recent reports describe a significant prevalence of KRAS allelic imbalances or gene dosage changes in human cancers, including loss of the wild-type allele in ... ...

Abstract	Oncogenic KRAS mutations are well-described functionally and are known to drive tumorigenesis. Recent reports describe a significant prevalence of KRAS allelic imbalances or gene dosage changes in human cancers, including loss of the wild-type allele in KRAS mutant cancers. However, the role of wild-type KRAS in tumorigenesis and therapeutic response remains elusive. We report an in vivo murine model of colorectal cancer featuring deletion of wild-type Kras in the context of oncogenic Kras. Deletion of wild-type Kras exacerbates oncogenic KRAS signalling through MAPK and thus drives tumour initiation. Absence of wild-type Kras potentiates the oncogenic effect of KRASG12D, while incidentally inducing sensitivity to inhibition of MEK1/2. Importantly, loss of the wild-type allele in aggressive models of KRASG12D-driven CRC significantly alters tumour progression, and suppresses metastasis through modulation of the immune microenvironment. This study highlights the critical role for wild-type Kras upon tumour initiation, progression and therapeutic response in Kras mutant CRC.
MeSH term(s)	Humans ; Mice ; Animals ; Proto-Oncogene Proteins p21(ras)/genetics ; Allelic Imbalance ; Genes, ras ; Cell Transformation, Neoplastic/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Mutation ; Tumor Microenvironment/genetics
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; KRAS protein, human
Language	English
Publishing date	2024-01-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44342-4
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Article ; Online: Targeted irradiation in an autochthonous mouse model of pancreatic cancer.

Tesson, Mathias / Stevenson, Katrina / Karim, Saadia A / Nixon, Colin / Chalmers, Anthony J / Sansom, Owen J / O'Neill, Eric / Jones, Keaton / Morton, Jennifer P

Disease models & mechanisms

2024 Volume 17, Issue 3

Abstract: The value of radiotherapy in the treatment of pancreatic cancer has been the subject of much debate but limited preclinical research. We hypothesise that the poor translation of radiation research into clinical trials of radiotherapy in pancreatic cancer ...

Abstract	The value of radiotherapy in the treatment of pancreatic cancer has been the subject of much debate but limited preclinical research. We hypothesise that the poor translation of radiation research into clinical trials of radiotherapy in pancreatic cancer is due, in part, to inadequate preclinical study models. Here, we developed and refined methods for targeted irradiation in autochthonous mouse models of pancreatic cancer, using a small animal radiotherapy research platform. We tested and optimised strategies for administration of contrast agents, iohexol and the liver imaging agent Fenestra LC, to enable the use of computed tomography imaging in tumour localisation. We demonstrate accurate tumour targeting, negligible off-target effects and therapeutic efficacy, depending on dose, number of fractions and tumour size, and provide a proof of concept that precise radiation can be delivered effectively to mouse pancreatic tumours with a clinically relevant microenvironment. This advance will allow investigation of the radiation response in murine pancreatic cancer, discovery of mechanisms and biomarkers of radiosensitivity or resistance, and development of radiosensitising strategies to inform clinical trials for precision radiotherapy in this disease.
MeSH term(s)	Animals ; Mice ; Radiotherapy Dosage ; Radiotherapy Planning, Computer-Assisted/methods ; Pancreatic Neoplasms/radiotherapy ; Disease Models, Animal ; Tomography, X-Ray Computed/methods ; Tumor Microenvironment
Language	English
Publishing date	2024-03-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.050463
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Article ; Online: CXCR2 inhibition in pancreatic cancer: opportunities for immunotherapy?

Morton, Jennifer P / Sansom, Owen J

Immunotherapy

2016 Volume 9, Issue 1, Page(s) 9–12

MeSH term(s)	Animals ; Anti-Inflammatory Agents/therapeutic use ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Agents/therapeutic use ; B7-H1 Antigen/immunology ; Carcinoma, Ductal/immunology ; Carcinoma, Ductal/therapy ; Clinical Trials as Topic ; Disease Models, Animal ; Humans ; Immunotherapy/methods ; Inflammation/immunology ; Inflammation/therapy ; Myeloid-Derived Suppressor Cells/immunology ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/therapy ; Receptors, Interleukin-8B/antagonists & inhibitors ; Signal Transduction
Chemical Substances	Anti-Inflammatory Agents ; Antibodies, Monoclonal ; Antineoplastic Agents ; B7-H1 Antigen ; Receptors, Interleukin-8B
Language	English
Publishing date	2016-12-21
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2495964-9
ISSN	1750-7448 ; 1750-743X
ISSN (online)	1750-7448
ISSN	1750-743X
DOI	10.2217/imt-2016-0115
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Article ; Online: Translating complexity and heterogeneity of pancreatic tumor: 3D in vitro to in vivo models.

Heinrich, Marcel A / Mostafa, Ahmed M R H / Morton, Jennifer P / Hawinkels, Lukas J A C / Prakash, Jai

Advanced drug delivery reviews

2021 Volume 174, Page(s) 265–293

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive type of cancer with an overall survival rate of less than 7-8%, emphasizing the need for novel effective therapeutics against PDAC. However only a fraction of therapeutics which seemed ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive type of cancer with an overall survival rate of less than 7-8%, emphasizing the need for novel effective therapeutics against PDAC. However only a fraction of therapeutics which seemed promising in the laboratory environment will eventually reach the clinic. One of the main reasons behind this low success rate is the complex tumor microenvironment (TME) of PDAC, a highly fibrotic and dense stroma surrounding tumor cells, which supports tumor progression as well as increases the resistance against the treatment. In particular, the growing understanding of the PDAC TME points out a different challenge in the development of efficient therapeutics - a lack of biologically relevant in vitro and in vivo models that resemble the complexity and heterogeneity of PDAC observed in patients. The purpose and scope of this review is to provide an overview of the recent developments in different in vitro and in vivo models, which aim to recapitulate the complexity of PDAC in a laboratory environment, as well to describe how 3D in vitro models can be integrated into drug development pipelines that are already including sophisticated in vivo models. Hereby a special focus will be given on the complexity of in vivo models and the challenges in vitro models face to reach the same levels of complexity in a controllable manner. First, a brief introduction of novel developments in two dimensional (2D) models and ex vivo models is provided. Next, recent developments in three dimensional (3D) in vitro models are described ranging from spheroids, organoids, scaffold models, bioprinted models to organ-on-chip models including a discussion on advantages and limitations for each model. Furthermore, we will provide a detailed overview on the current PDAC in vivo models including chemically-induced models, syngeneic and xenogeneic models, highlighting hetero- and orthotopic, patient-derived tissues (PDX) models, and genetically engineered mouse models. Finally, we will provide a discussion on overall limitations of both, in vitro and in vivo models, and discuss necessary steps to overcome these limitations to reach an efficient drug development pipeline, as well as discuss possibilities to include novel in silico models in the process.
MeSH term(s)	Animals ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/pathology ; Disease Models, Animal ; Disease Progression ; Drug Development/methods ; Humans ; Mice ; Mice, Transgenic ; Models, Biological ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/pathology ; Tumor Microenvironment
Language	English
Publishing date	2021-04-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639113-8
ISSN	1872-8294 ; 0169-409X
ISSN (online)	1872-8294
ISSN	0169-409X
DOI	10.1016/j.addr.2021.04.018
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Zs.A 2241: Show issues

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Article ; Online: Efferocytosis reprograms the tumor microenvironment to promote pancreatic cancer liver metastasis.

Astuti, Yuliana / Raymant, Meirion / Quaranta, Valeria / Clarke, Kim / Abudula, Maidinaimu / Smith, Olivia / Bellomo, Gaia / Chandran-Gorner, Vatshala / Nourse, Craig / Halloran, Christopher / Ghaneh, Paula / Palmer, Daniel / Jones, Robert P / Campbell, Fiona / Pollard, Jeffrey W / Morton, Jennifer P / Mielgo, Ainhoa / Schmid, Michael C

Nature cancer

2024

Abstract: Pancreatic ductal adenocarcinoma is a highly metastatic disease and macrophages support liver metastases. Efferocytosis, or engulfment of apoptotic cells by macrophages, is an essential process in tissue homeostasis and wound healing, but its role in ... ...

Abstract	Pancreatic ductal adenocarcinoma is a highly metastatic disease and macrophages support liver metastases. Efferocytosis, or engulfment of apoptotic cells by macrophages, is an essential process in tissue homeostasis and wound healing, but its role in metastasis is less well understood. Here, we found that the colonization of the hepatic metastatic site is accompanied by low-grade tissue injury and that efferocytosis-mediated clearance of parenchymal dead cells promotes macrophage reprogramming and liver metastasis. Mechanistically, progranulin expression in macrophages is necessary for efficient efferocytosis by controlling lysosomal acidification via cystic fibrosis transmembrane conductance regulator and the degradation of lysosomal cargo, resulting in LXRα/RXRα-mediated macrophage conversion and upregulation of arginase 1. Pharmacological blockade of efferocytosis or macrophage-specific genetic depletion of progranulin impairs macrophage conversion, improves CD8
Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Journal Article
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-024-00731-2
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