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Article ; Online: Corrigendum to 'True thymic hyperplasia causing pure red cell aplasia: a case report'.

Mohammad, Adam / Dawson, Alan G / Bajaj, Amrita / Rathinam, Sridhar

Interactive cardiovascular and thoracic surgery

2022 Volume 34, Issue 5, Page(s) 942

Language	English
Publishing date	2022-01-13
Publishing country	England
Document type	Published Erratum
ZDB-ID	2095298-3
ISSN	1569-9285 ; 1569-9293
ISSN (online)	1569-9285
ISSN	1569-9293
DOI	10.1093/icvts/ivab374
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Article ; Online: Metastatic renal cell carcinoma extending to the left atrium through the inferior pulmonary vein.

Dawson, Alan G / Richards, Cathy J / Hadjinikolaou, Leonidas / Nakas, Apostolos

Interactive cardiovascular and thoracic surgery

2021 Volume 32, Issue 6, Page(s) 991–992

Abstract: Metastatic renal cell carcinoma with involvement through the pulmonary veins to the left atrium is very rare. We report the case of a 70-year-old male with metastatic renal cell carcinoma to the right lower lobe of the lung abutting the inferior ... ...

Abstract	Metastatic renal cell carcinoma with involvement through the pulmonary veins to the left atrium is very rare. We report the case of a 70-year-old male with metastatic renal cell carcinoma to the right lower lobe of the lung abutting the inferior pulmonary vein with extension to the left atrium without pre-operative evidence. Surgical resection was achieved through a posterolateral thoracotomy. Lung masses that abut the pulmonary veins should prompt further investigation with a pre-operative transoesophageal echocardiogram to minimize unexpected intraoperative findings.
MeSH term(s)	Aged ; Carcinoma, Renal Cell/diagnostic imaging ; Carcinoma, Renal Cell/surgery ; Heart Atria/diagnostic imaging ; Heart Atria/surgery ; Humans ; Kidney Neoplasms/diagnostic imaging ; Kidney Neoplasms/surgery ; Lung ; Male ; Pulmonary Veins/diagnostic imaging ; Pulmonary Veins/surgery
Language	English
Publishing date	2021-01-27
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2095298-3
ISSN	1569-9285 ; 1569-9293
ISSN (online)	1569-9285
ISSN	1569-9293
DOI	10.1093/icvts/ivab018
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Article ; Online: True thymic hyperplasia causing pure red cell aplasia: a case report.

Mohammad, Adam / Dawson, Alan G / Bajaj, Amrita / Rathinam, Sridhar

Interactive cardiovascular and thoracic surgery

2021 Volume 34, Issue 4, Page(s) 697–699

Abstract: Pure red cell aplasia caused by true thymic hyperplasia is extremely rare. We report the case of a 25-year-old female diagnosed with pure red cell aplasia. Following a thymectomy confirming true thymic hyperplasia and corticosteroid therapy, complete ... ...

Abstract	Pure red cell aplasia caused by true thymic hyperplasia is extremely rare. We report the case of a 25-year-old female diagnosed with pure red cell aplasia. Following a thymectomy confirming true thymic hyperplasia and corticosteroid therapy, complete response was achieved. Patients diagnosed with pure red cell aplasia should be investigated with a computerized tomographic scan to assess for thymic pathology and if present, this should be resected. Follow-up is essential to monitor for recurrence.
MeSH term(s)	Adult ; Female ; Humans ; Red-Cell Aplasia, Pure/diagnosis ; Red-Cell Aplasia, Pure/etiology ; Thymectomy/adverse effects ; Thymoma/complications ; Thymoma/diagnostic imaging ; Thymoma/surgery ; Thymus Hyperplasia/complications ; Thymus Hyperplasia/diagnostic imaging ; Thymus Neoplasms/complications ; Thymus Neoplasms/diagnostic imaging ; Thymus Neoplasms/surgery
Language	English
Publishing date	2021-11-17
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2095298-3
ISSN	1569-9285 ; 1569-9293
ISSN (online)	1569-9285
ISSN	1569-9293
DOI	10.1093/icvts/ivab301
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Article ; Online: Cytoreductive surgery with hyperthermic intrathoracic chemotherapy for malignant pleural mesothelioma: a systematic review.

Dawson, Alan G / Kutywayo, Kudzayi / Mohammed, Seid B / Fennell, Dean A / Nakas, Apostolos

Thorax

2022 Volume 78, Issue 4, Page(s) 409–417

Abstract: Introduction: Cytoreductive surgery has been used a part of multimodality treatment in patients with malignant pleural mesothelioma (MPM). The residual microscopic disease that remains will lead to disease progression in the majority of patients. ... ...

Abstract	Introduction: Cytoreductive surgery has been used a part of multimodality treatment in patients with malignant pleural mesothelioma (MPM). The residual microscopic disease that remains will lead to disease progression in the majority of patients. Delivery of hyperthermic intrathoracic chemotherapy at the time of surgery has been used to address this microscopic disease, however it's effect and place in the multimodality treatment sphere is unknown. The aim of this systematic review was to assess the effect of surgery and hyperthermic intrathoracic chemotherapy in patients with MPM on overall survival and disease-free interval. Methods: Ovid MEDLINE, Embase, Web of Science and the Cochrane Database of Systematic Reviews were searched from database inception through to June 2021. Studies reporting overall survival and/or disease-free interval in patients with MPM undergoing cytoreductive surgery with hyperthermic intrathoracic chemotherapy were considered. Study quality was assessed using the Newcastle-Ottawa Scale. A narrative review was performed. Results: Fifteen studies were eligible for inclusion comprising 598 patients. Surgery with hyperthermic intrathoracic chemotherapy was associated with a median overall survival and disease-free interval ranging from 11 to 75 months and 7.2 to 57 months, respectively. These appeared to be superior to patients not receiving hyperthermic intrathoracic chemotherapy (overall survival: 5-36 months and disease-free interval: 12.1-21 months). A higher dose of hyperthermic intrathoracic chemotherapy was associated with an improvement in overall survival compared with a lower dose: 18-31 months versus 6-18 months, respectively. The most common morbidity was atrial fibrillation followed by renal complications. Conclusion: Surgery with hyperthermic intrathoracic chemotherapy offers a safe and effective therapy with an improvement in disease-free interval and overall survival, particularly when hyperthermic intrathoracic chemotherapy is administered at a higher dose. Prospero registration number: CRD42019129002.
MeSH term(s)	Humans ; Mesothelioma, Malignant ; Mesothelioma/surgery ; Cisplatin/therapeutic use ; Cytoreduction Surgical Procedures ; Pleural Neoplasms/drug therapy ; Pleural Neoplasms/surgery ; Combined Modality Therapy
Chemical Substances	Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2022-04-11
Publishing country	England
Document type	Review ; Journal Article ; Systematic Review
ZDB-ID	204353-1
ISSN	1468-3296 ; 0040-6376
ISSN (online)	1468-3296
ISSN	0040-6376
DOI	10.1136/thoraxjnl-2021-218214
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Article: Randomized controlled trials in malignant pleural mesothelioma surgery-mistakes made and lessons learned.

Waller, David A / Dawson, Alan G

Annals of translational medicine

2017 Volume 5, Issue 11, Page(s) 240

Abstract: Randomized surgical trials are of the most difficult to design and recruit, however, they are the only robust method available to establish a new surgical procedure. Mesothelioma is a disease with a perceived poor prognosis for which surgical ... ...

Abstract	Randomized surgical trials are of the most difficult to design and recruit, however, they are the only robust method available to establish a new surgical procedure. Mesothelioma is a disease with a perceived poor prognosis for which surgical intervention has relatively high complications and not insignificant mortality. This review will consider the mesothelioma and radical surgery (MARS) 1 and 2 trials, SAKK 17/04 trial and the EORTC 1205 trial all aimed at assessing the potential benefit of radical surgery for malignant pleural mesothelioma. In addition, MesoVATS and MesoTRAP will be explored assessing the value of debulking surgery for malignant pleural mesothelioma. We also endeavour to identify the mistakes made and the lessons learned which will inform future randomized controlled clinical trials in the field of malignant pleural mesothelioma. Despite the insurmountable problems with randomized controlled clinical trials, we show that they are possible and continuing with uncontrolled experiments will perpetuate unproven and potentially harmful operations.
Language	English
Publishing date	2017-06-29
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2893931-1
ISSN	2305-5847 ; 2305-5839
ISSN (online)	2305-5847
ISSN	2305-5839
DOI	10.21037/atm.2017.04.05
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Article ; Online: Targeting FAK in anticancer combination therapies.

Dawson, John C / Serrels, Alan / Stupack, Dwayne G / Schlaepfer, David D / Frame, Margaret C

Nature reviews. Cancer

2021 Volume 21, Issue 5, Page(s) 313–324

Abstract: Focal adhesion kinase (FAK) is both a non-receptor tyrosine kinase and an adaptor protein that primarily regulates adhesion signalling and cell migration, but FAK can also promote cell survival in response to stress. FAK is commonly overexpressed in ... ...

Abstract	Focal adhesion kinase (FAK) is both a non-receptor tyrosine kinase and an adaptor protein that primarily regulates adhesion signalling and cell migration, but FAK can also promote cell survival in response to stress. FAK is commonly overexpressed in cancer and is considered a high-value druggable target, with multiple FAK inhibitors currently in development. Evidence suggests that in the clinical setting, FAK targeting will be most effective in combination with other agents so as to reverse failure of chemotherapies or targeted therapies and enhance efficacy of immune-based treatments of solid tumours. Here, we discuss the recent preclinical evidence that implicates FAK in anticancer therapeutic resistance, leading to the view that FAK inhibitors will have their greatest utility as combination therapies in selected patient populations.
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols ; Focal Adhesion Protein-Tyrosine Kinases/antagonists & inhibitors ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Neoplasms/pathology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Protein Kinase Inhibitors ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2)
Language	English
Publishing date	2021-03-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-021-00340-6
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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)
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Article ; Online: Pulmonary Valve Replacement: What Did We Learn?

Dawson, Alan G / Corno, Antonio F

The Annals of thoracic surgery

2015 Volume 100, Issue 6, Page(s) 2418–2419

MeSH term(s)	Female ; Heart Valve Prosthesis Implantation ; Humans ; Male ; Pulmonary Valve/surgery ; Tetralogy of Fallot/surgery ; Ventricular Remodeling
Language	English
Publishing date	2015-12
Publishing country	Netherlands
Document type	Comment ; Letter
ZDB-ID	211007-6
ISSN	1552-6259 ; 0003-4975
ISSN (online)	1552-6259
ISSN	0003-4975
DOI	10.1016/j.athoracsur.2015.06.076
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Article ; Online: 11β-HSD1 inhibition does not affect murine tumour angiogenesis but may exert a selective effect on tumour growth by modulating inflammation and fibrosis.

Davidson, Callam T / Miller, Eileen / Muir, Morwenna / Dawson, John C / Lee, Martin / Aitken, Stuart / Serrels, Alan / Webster, Scott P / Homer, Natalie Z M / Andrew, Ruth / Brunton, Valerie G / Hadoke, Patrick W F / Walker, Brian R

PloS one

2023 Volume 18, Issue 3, Page(s) e0255709

Abstract: Glucocorticoids inhibit angiogenesis by activating the glucocorticoid receptor. Inhibition of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) reduces tissue-specific glucocorticoid action and promotes angiogenesis ... ...

Abstract	Glucocorticoids inhibit angiogenesis by activating the glucocorticoid receptor. Inhibition of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) reduces tissue-specific glucocorticoid action and promotes angiogenesis in murine models of myocardial infarction. Angiogenesis is important in the growth of some solid tumours. This study used murine models of squamous cell carcinoma (SCC) and pancreatic ductal adenocarcinoma (PDAC) to test the hypothesis that 11β-HSD1 inhibition promotes angiogenesis and subsequent tumour growth. SCC or PDAC cells were injected into female FVB/N or C57BL6/J mice fed either standard diet, or diet containing the 11β-HSD1 inhibitor UE2316. SCC tumours grew more rapidly in UE2316-treated mice, reaching a larger (P<0.01) final volume (0.158 ± 0.037 cm3) than in control mice (0.051 ± 0.007 cm3). However, PDAC tumour growth was unaffected. Immunofluorescent analysis of SCC tumours did not show differences in vessel density (CD31/alpha-smooth muscle actin) or cell proliferation (Ki67) after 11β-HSD1 inhibition, and immunohistochemistry of SCC tumours did not show changes in inflammatory cell (CD3- or F4/80-positive) infiltration. In culture, the growth/viability (assessed by live cell imaging) of SCC cells was not affected by UE2316 or corticosterone. Second Harmonic Generation microscopy showed that UE2316 reduced Type I collagen (P<0.001), whilst RNA-sequencing revealed that multiple factors involved in the innate immune/inflammatory response were reduced in UE2316-treated SCC tumours. 11β-HSD1 inhibition increases SCC tumour growth, likely via suppression of inflammatory/immune cell signalling and extracellular matrix deposition, but does not promote tumour angiogenesis or growth of all solid tumours.
MeSH term(s)	Mice ; Female ; Animals ; Glucocorticoids/metabolism ; 11-beta-Hydroxysteroid Dehydrogenase Type 1/metabolism ; Inflammation ; Neovascularization, Pathologic ; Neoplasms ; Fibrosis
Chemical Substances	Glucocorticoids ; (4-(2-chlorophenyl-4-fluoro-1-piperidinyl)(5-(1H-pyrazol-4-yl)-3-thienyl)methanone ; 11-beta-Hydroxysteroid Dehydrogenase Type 1 (EC 1.1.1.146)
Language	English
Publishing date	2023-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0255709
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Article ; Online: BAP1 loss induces mitotic defects in mesothelioma cells through BRCA1-dependent and independent mechanisms.

Singh, Anita / Busacca, Sara / Gaba, Aarti / Sheaff, Michael / Poile, Charlotte / Nakas, Apostolos / Dzialo, Joanna / Bzura, Aleksandra / Dawson, Alan G / Fennell, Dean A / Fry, Andrew M

Oncogene

2022 Volume 42, Issue 8, Page(s) 572–585

Abstract: The tumour suppressor BRCA1-associated protein 1 (BAP1) is the most frequently mutated cancer gene in mesothelioma. Here we report novel functions for BAP1 in mitotic progression highlighting the relationship between BAP1 and control of genome stability ... ...

Abstract	The tumour suppressor BRCA1-associated protein 1 (BAP1) is the most frequently mutated cancer gene in mesothelioma. Here we report novel functions for BAP1 in mitotic progression highlighting the relationship between BAP1 and control of genome stability in mesothelioma cells with therapeutic implications. Depletion of BAP1 protein induced proteasome-mediated degradation of BRCA1 in mesothelioma cells while loss of BAP1 correlated with BRCA1 loss in mesothelioma patient tumour samples. BAP1 loss also led to mitotic defects that phenocopied the loss of BRCA1 including spindle assembly checkpoint failure, centrosome amplification and chromosome segregation errors. However, loss of BAP1 also led to additional mitotic changes that were not observed upon BRCA1 loss, including an increase in spindle length and enhanced growth of astral microtubules. Intriguingly, these consequences could be explained by loss of expression of the KIF18A and KIF18B kinesin motors that occurred upon depletion of BAP1 but not BRCA1, as spindle and astral microtubule defects were rescued by re-expression of KIF18A and KIF18B, respectively. We therefore propose that BAP1 inactivation causes mitotic defects through BRCA1-dependent and independent mechanisms revealing novel routes by which mesothelioma cells lacking BAP1 may acquire genome instability and exhibit altered responses to microtubule-targeted agents.
MeSH term(s)	Humans ; BRCA1 Protein/genetics ; BRCA1 Protein/metabolism ; Chromosome Segregation ; Genes, Tumor Suppressor ; Kinesins/genetics ; Kinesins/metabolism ; Lung Neoplasms/pathology ; Mesothelioma/pathology ; Mesothelioma, Malignant/genetics ; Mesothelioma, Malignant/metabolism ; Microtubules/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	BAP1 protein, human ; BRCA1 Protein ; BRCA1 protein, human ; KIF18A protein, human (EC 3.6.1.-) ; KIF18B protein, human (EC 3.6.1.-) ; Kinesins (EC 3.6.4.4) ; Tumor Suppressor Proteins ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2022-12-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-022-02577-3
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Article ; Online: ATR Inhibitor AZD6738 (Ceralasertib) Exerts Antitumor Activity as a Monotherapy and in Combination with Chemotherapy and the PARP Inhibitor Olaparib.

Wilson, Zena / Odedra, Rajesh / Wallez, Yann / Wijnhoven, Paul W G / Hughes, Adina M / Gerrard, Joe / Jones, Gemma N / Bargh-Dawson, Hannah / Brown, Elaine / Young, Lucy A / O'Connor, Mark J / Lau, Alan

Cancer research

2022 Volume 82, Issue 6, Page(s) 1140–1152

Abstract: AZD6738 (ceralasertib) is a potent and selective orally bioavailable inhibitor of ataxia telangiectasia and Rad3-related (ATR) kinase. ATR is activated in response to stalled DNA replication forks to promote G2-M cell-cycle checkpoints and fork restart. ... ...

Abstract	AZD6738 (ceralasertib) is a potent and selective orally bioavailable inhibitor of ataxia telangiectasia and Rad3-related (ATR) kinase. ATR is activated in response to stalled DNA replication forks to promote G2-M cell-cycle checkpoints and fork restart. Here, we found AZD6738 modulated CHK1 phosphorylation and induced ATM-dependent signaling (pRAD50) and the DNA damage marker γH2AX. AZD6738 inhibited break-induced replication and homologous recombination repair. In vitro sensitivity to AZD6738 was elevated in, but not exclusive to, cells with defects in the ATM pathway or that harbor putative drivers of replication stress such as CCNE1 amplification. This translated to in vivo antitumor activity, with tumor control requiring continuous dosing and free plasma exposures, which correlated with induction of pCHK1, pRAD50, and γH2AX. AZD6738 showed combinatorial efficacy with agents associated with replication fork stalling and collapse such as carboplatin and irinotecan and the PARP inhibitor olaparib. These combinations required optimization of dose and schedules in vivo and showed superior antitumor activity at lower doses compared with that required for monotherapy. Tumor regressions required at least 2 days of daily dosing of AZD6738 concurrent with carboplatin, while twice daily dosing was required following irinotecan. In a BRCA2-mutant patient-derived triple-negative breast cancer (TNBC) xenograft model, complete tumor regression was achieved with 3 to5 days of daily AZD6738 per week concurrent with olaparib. Increasing olaparib dosage or AZD6738 dosing to twice daily allowed complete tumor regression even in a BRCA wild-type TNBC xenograft model. These preclinical data provide rationale for clinical evaluation of AZD6738 as a monotherapy or combinatorial agent. Significance: This detailed preclinical investigation, including pharmacokinetics/pharmacodynamics and dose-schedule optimizations, of AZD6738/ceralasertib alone and in combination with chemotherapy or PARP inhibitors can inform ongoing clinical efforts to treat cancer with ATR inhibitors.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Carboplatin ; Humans ; Indoles ; Irinotecan ; Morpholines/pharmacology ; Phthalazines ; Piperazines ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Pyrimidines/pharmacology ; Sulfonamides/pharmacology ; Sulfoxides/pharmacology ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics
Chemical Substances	Antineoplastic Agents ; Indoles ; Morpholines ; Phthalazines ; Piperazines ; Poly(ADP-ribose) Polymerase Inhibitors ; Protein Kinase Inhibitors ; Pyrimidines ; Sulfonamides ; Sulfoxides ; Irinotecan (7673326042) ; ceralasertib (85RE35306Z) ; Carboplatin (BG3F62OND5) ; ATR protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; olaparib (WOH1JD9AR8)
Language	English
Publishing date	2022-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-21-2997
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