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Article ; Online: Idiopathic granulomatous mastitis: experience at a New York hospital.

Bhattarai, P / Srinivasan, A / Valenzuela, C D / Sulzbach, C / Wallack, M K / Mariadason, J G

Annals of the Royal College of Surgeons of England

2021 Volume 104, Issue 7, Page(s) 543–547

Abstract: Introduction: Idiopathic granulomatous mastitis (IGM) often mimics breast cancer. Presentation includes pain, palpable mass, suppuration or suspicious imaging. Widely reported in Asia and the Middle East, IGM is diagnosed after excluding specific ... ...

Abstract	Introduction: Idiopathic granulomatous mastitis (IGM) often mimics breast cancer. Presentation includes pain, palpable mass, suppuration or suspicious imaging. Widely reported in Asia and the Middle East, IGM is diagnosed after excluding specific granulomatous mastitis (SGM). Aetiology remains unknown. Lactation, prolactinaemia, ethnicity, autoimmune disease and Corynebacteria are associated. Treatment is controversial and the prevalence rising. Surgery and non-operative treatments including antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs), steroids, methotrexate and observation have advocates. Methods: A retrospective chart review of 63 patients with IGM from 2008 to 2018 was undertaken focusing on birthplace, age, clinical presentation, wound cultures, imaging, treatments and outcomes. Results: Sixty-one of 63 patients were Hispanic; 53 were Mexican-born women aged 23-46. Clinical presentation included pain, painful mass, painless mass, suppuration and abnormal imaging. Some 31/61 ultrasound examinations and 17/33 mammograms were deemed Breast Imaging Reporting and Data System (BI-RADS) score 4 or 5. Management included antibiotics (43), incision and drainage (24), NSAIDs (29), steroids (8), lumpectomy (18) and observation (12). Some 12/20 patients with painless masses resolved with observation, 3 received NSAIDs, 2 received steroids and 3 underwent lumpectomies. Antibiotics resolved 8/43 cases, 5 needed incision and drainage, 26 received NSAIDs, 6 received steroids and 5 underwent lumpectomies. Nineteen patients had indolent disease or recurrence. Conclusions: Excluding malignancy is critical, treatment challenging and recurrence common in IGM. A preponderance of patients were Mexican-born, similar to other reports from the USA. Over 50% of IGM cases had suspicious BI-RADS scores. Best management remains a challenge and ranges from observation to lumpectomy.
MeSH term(s)	Anti-Bacterial Agents/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Breast Neoplasms/diagnosis ; Female ; Granulomatous Mastitis/diagnosis ; Granulomatous Mastitis/epidemiology ; Granulomatous Mastitis/therapy ; Hospitals ; Humans ; Immunoglobulin M/therapeutic use ; New York ; Pain ; Retrospective Studies ; Steroids/therapeutic use ; Suppuration/drug therapy
Chemical Substances	Anti-Bacterial Agents ; Anti-Inflammatory Agents, Non-Steroidal ; Immunoglobulin M ; Steroids
Language	English
Publishing date	2021-11-23
Publishing country	England
Document type	Journal Article
ZDB-ID	80044-2
ISSN	1478-7083 ; 0035-8843
ISSN (online)	1478-7083
ISSN	0035-8843
DOI	10.1308/rcsann.2021.0239
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Article ; Online: IL-36G promotes cancer-cell intrinsic hallmarks in human gastric cancer cells.

Le, Ngan / Luk, Ian / Chisanga, David / Shi, Wei / Pang, Lokman / Scholz, Glen / Mariadason, John / Ernst, Matthias / Huynh, Jennifer

Cytokine

2022 Volume 155, Page(s) 155887

Abstract: Interleukin-36 gamma (IL-36G) is a member of the IL-36 subfamily of cytokines and acts as a potent driver of inflammation. IL-36G has been extensively characterized in the pathogenesis of psoriasis and has been recently described to play roles in wound ... ...

Abstract	Interleukin-36 gamma (IL-36G) is a member of the IL-36 subfamily of cytokines and acts as a potent driver of inflammation. IL-36G has been extensively characterized in the pathogenesis of psoriasis and has been recently described to play roles in wound healing particularly in the gastrointestinal tract. However, the effects of IL-36G during cancer development including gastric cancer remain unexplored. Here, we show that IL-36G induced ERK1/2 activation in AGS, MKN1 and MKN45 human gastric cancer cell lines. Moreover, IL-36G induced colony formation, migration and invasion of these gastric cancer cell lines that was inhibited by the natural antagonist, IL-36 receptor antagonist (RA). Interrogation of TCGA stomach adenocarcinoma patient datasets revealed highly elevated IL-36G gene expression in human gastric cancer compared to normal tissue independent of tumor stage, and high IL-36G expression corresponded with poorer patient survival. Collectively, our results indicate for the first time that IL-36G supports a neoplastic phenotype in human gastric cancer cells.
MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Cell Line, Tumor ; Cell Movement ; Gene Expression Regulation, Neoplastic ; Humans ; Signal Transduction ; Stomach Neoplasms/pathology
Language	English
Publishing date	2022-05-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2022.155887
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Zs.A 2840: Show issues

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Article ; Online: Role of the faecolith in modern-day appendicitis.

Singh, J P / Mariadason, J G

Annals of the Royal College of Surgeons of England

2012 Volume 95, Issue 1, Page(s) 48–51

Abstract: Introduction: The prevailing view on appendicitis is that the main aetiology is obstruction owing to faecoliths in adults and lymphoid hyperplasia in children. Faecoliths on imaging studies are believed to correlate well with appendicitis.: Methods: ... ...

Abstract	Introduction: The prevailing view on appendicitis is that the main aetiology is obstruction owing to faecoliths in adults and lymphoid hyperplasia in children. Faecoliths on imaging studies are believed to correlate well with appendicitis. Methods: A retrospective chart review was conducted of 1,014 emergency appendicectomy patients between 2001 and 2011. Faecolith prevalence in adult and paediatric appendicectomy specimens with and without perforation was studied. The sensitivity and positive predictive value (PPV) of computed tomography (CT) for identifying faecoliths in the pathology specimen were examined. Results: Overall, faecoliths were found in 18.1% (178/986) of appendicitis specimens and 28.6% (8/28) of negative appendicectomies. Faecolith prevalence for positive cases was 29.9% (79/264) in paediatric patients and 13.7% (99/722) in adults (p<0.05). Faecolith prevalence was 39.4% in perforated appendicitis but only 14.6% in non-perforated appendicitis (p<0.05). In adults, faecolith prevalence was 27.5% in perforated appendicitis and 12.0% in non-perforated appendicitis (p<0.05) while in paediatric patients, it was 56.1% in perforated appendicitis and 22.7% in non-perforated appendicitis (p=0.00). Sensitivity and PPV of preoperative CT in identifying faecoliths on pathology were 53.1% (86/162) and 44.8% (86/192) respectively. Conclusions: Faecolith prevalence is too low to consider the faecolith the most common cause of non-perforated appendicitis. Faecoliths are more prevalent in paediatric appendicitis than in adult appendicitis. Preoperative CT is an unreliable predictor of faecoliths in pathology specimens.
MeSH term(s)	Adolescent ; Adult ; Aged ; Appendectomy/statistics & numerical data ; Appendicitis/etiology ; Appendicitis/surgery ; Child ; Child, Preschool ; Fecal Impaction/complications ; Humans ; Infant ; Middle Aged ; Retrospective Studies ; Tomography, X-Ray Computed ; Young Adult
Language	English
Publishing date	2012-11-29
Publishing country	England
Document type	Journal Article
ZDB-ID	80044-2
ISSN	1478-7083 ; 0035-8843
ISSN (online)	1478-7083
ISSN	0035-8843
DOI	10.1308/003588413X13511609954851
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Article ; Online: Dual Antiangiogenesis Agents Bevacizumab Plus Trebananib, without Chemotherapy, in First-line Treatment of Metastatic Colorectal Cancer: Results of a Phase II Study.

Mooi, Jennifer / Chionh, Fiona / Savas, Peter / Da Gama Duarte, Jessica / Chong, Geoffrey / Brown, Stephen / Wong, Rachel / Price, Timothy J / Wann, Alysson / Skrinos, Effie / Mariadason, John M / Tebbutt, Niall C

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 27, Issue 8, Page(s) 2159–2167

Abstract: Purpose: To assess the efficacy and safety of dual antiangiogenesis agents, bevacizumab plus trebananib, without chemotherapy, in first-line treatment of metastatic colorectal cancer (mCRC).: Patients and methods: This open-label phase II study ... ...

Abstract	Purpose: To assess the efficacy and safety of dual antiangiogenesis agents, bevacizumab plus trebananib, without chemotherapy, in first-line treatment of metastatic colorectal cancer (mCRC). Patients and methods: This open-label phase II study enrolled patients with unresectable mCRC with no prior systemic treatment. All patients received bevacizumab 7.5 mg/kg 3-weekly and trebananib 15 mg/kg weekly. The primary endpoint was disease control [stable disease, partial response (PR), or complete response (CR)] at 6 months (DC6m). Secondary endpoints included toxicity, overall response rate (ORR), progression-free survival (PFS), and overall survival (OS). Exploratory biomarkers in plasma angiogenesis-related proteins, tumor gene expression, and plasma antibodies to tumor antigens were examined. Results: Forty-five patients were enrolled from four Australian sites. DC6m was 63% [95% confidence interval (CI), 47-77]. ORR was 17% (95% CI, 7-32), comprising of seven PRs. Median duration of response was 20 months (range, 10-48 months). Median PFS was 8.4 months and median OS 31.4 months. Grade 1-2 peripheral edema and joint-related symptoms were common. Overall incidence of grade 3-4 adverse events (AE) of any type was 33% ( Conclusions: In a first-line mCRC population, the dual antiangiogenic combination, bevacizumab plus trebananib, without chemotherapy, was efficacious with durable responses. The toxicity profile of the combination was manageable and did not exceed that expected with bevacizumab +/- chemotherapy. Exploratory biomarker results raise the hypothesis that the antiangiogenic combination may enable the antitumor immune response in immunotolerant colorectal cancer.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Angiogenesis Inhibitors/administration & dosage ; Angiogenesis Inhibitors/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Bevacizumab/administration & dosage ; Bevacizumab/adverse effects ; Biomarkers, Tumor/analysis ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Drug Administration Schedule ; Female ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Progression-Free Survival ; Recombinant Fusion Proteins/administration & dosage ; Recombinant Fusion Proteins/adverse effects ; Risk Assessment/methods
Chemical Substances	Angiogenesis Inhibitors ; Biomarkers, Tumor ; Recombinant Fusion Proteins ; Bevacizumab (2S9ZZM9Q9V) ; trebananib (X8Y5U6NC7E)
Language	English
Publishing date	2021-01-29
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-20-2714
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Zs.A 4223: Show issues

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Article ; Online: Genotype-Tailored ERK/MAPK Pathway and HDAC Inhibition Rewires the Apoptotic Rheostat to Trigger Colorectal Cancer Cell Death.

Molecular cancer therapeutics

2022 Volume 22, Issue 1, Page(s) 52–62

Abstract: The EGFR/RAS/MEK/ERK signaling pathway (ERK/MAPK) is hyperactivated in most colorectal cancers. A current limitation of inhibitors of this pathway is that they primarily induce cytostatic effects in colorectal cancer cells. Nevertheless, these drugs do ... ...

Abstract	The EGFR/RAS/MEK/ERK signaling pathway (ERK/MAPK) is hyperactivated in most colorectal cancers. A current limitation of inhibitors of this pathway is that they primarily induce cytostatic effects in colorectal cancer cells. Nevertheless, these drugs do induce expression of proapoptotic factors, suggesting they may prime colorectal cancer cells to undergo apoptosis. As histone deacetylase inhibitors (HDACis) induce expression of multiple proapoptotic proteins, we examined whether they could synergize with ERK/MAPK inhibitors to trigger colorectal cancer cell apoptosis. Combined MEK/ERK and HDAC inhibition synergistically induced apoptosis in colorectal cancer cell lines and patient-derived tumor organoids in vitro, and attenuated Apc-initiated adenoma formation in vivo. Mechanistically, combined MAPK/HDAC inhibition enhanced expression of the BH3-only proapoptotic proteins BIM and BMF, and their knockdown significantly attenuated MAPK/HDAC inhibitor-induced apoptosis. Importantly, we demonstrate that the paradigm of combined MAPK/HDAC inhibitor treatment to induce apoptosis can be tailored to specific MAPK genotypes in colorectal cancers, by combining an HDAC inhibitor with either an EGFR, KRASG12C or BRAFV600 inhibitor in KRAS/BRAFWT; KRASG12C, BRAFV600E colorectal cancer cell lines, respectively. These findings identify a series of ERK/MAPK genotype-tailored treatment strategies that can readily undergo clinical testing for the treatment of colorectal cancer.
MeSH term(s)	Humans ; Apoptosis ; Apoptosis Regulatory Proteins ; Cell Death ; Cell Line, Tumor ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; ErbB Receptors ; Histone Deacetylase Inhibitors/pharmacology ; Mitogen-Activated Protein Kinase Kinases ; MAP Kinase Signaling System
Chemical Substances	Apoptosis Regulatory Proteins ; ErbB Receptors (EC 2.7.10.1) ; Histone Deacetylase Inhibitors ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2022-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-22-0101
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Zs.A 5750: Show issues

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Article ; Online: Telomere length is a novel predictive biomarker of sensitivity to anti-EGFR therapy in metastatic colorectal cancer.

Augustine, T A / Baig, M / Sood, A / Budagov, T / Atzmon, G / Mariadason, J M / Aparo, S / Maitra, R / Goel, S

British journal of cancer

2015 Volume 112, Issue 2, Page(s) 313–318

Abstract: Background: Telomeres are TTAGGG tandem repeats capping chromosomal ends and partially controlled by the telomerase enzyme. The EGFR pathway putatively regulates telomerase function, prompting an investigation of telomere length (TL) and its association ...

Abstract	Background: Telomeres are TTAGGG tandem repeats capping chromosomal ends and partially controlled by the telomerase enzyme. The EGFR pathway putatively regulates telomerase function, prompting an investigation of telomere length (TL) and its association with anti-epidermal growth factor receptor (EGFR) therapy in metastatic colorectal cancer (mCRC). Methods: Colorectal cancer cell lines were treated with multiple drugs and sensitivity determined. Clinical information was gathered from 75 patients who had received anti-EGFR drugs. Telomere length was measured using a validated qRT-PCR technique. Results: In CRC cell lines, TL independently predicted cetuximab sensitivity. Cells with shorter TL had growth inhibition of 18.6±3.41% as compared with 41.39±8.58% in longer TL (P=0.02). These in vitro findings were validated clinically, in a robust multivariate model. Among patients with KRas WT tumours, those with longer TL had a superior median progression-free survival (PFS) of 24.9 weeks than those with shorter TL; median 11.1 weeks, HR 0.31; P=0.048. Conclusion: Telomere length could be a potential unique biomarker predictive of clinical benefit (PFS) of mCRC patients treated with anti-EGFR therapy. This is the novel demonstration of a complex hitherto undescribed interaction, placing anti-EGFR therapy, EGFR pathway, and the telomerase complex within a clinical context.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized/pharmacology ; Antibodies, Monoclonal, Humanized/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/genetics ; Cell Line, Tumor ; Cetuximab ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Disease-Free Survival ; Drug Resistance, Neoplasm ; Female ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/mortality ; Liver Neoplasms/secondary ; Male ; Middle Aged ; Molecular Targeted Therapy ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Telomere ; Telomere Shortening
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; Biomarkers, Tumor ; panitumumab (6A901E312A) ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Cetuximab (PQX0D8J21J)
Language	English
Publishing date	2015-01-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/bjc.2014.561
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Article ; Online: Overexpression of TP53 protein is associated with the lack of adjuvant chemotherapy benefit in patients with stage III colorectal cancer.

Williams, David S / Mouradov, Dmitri / Browne, Clare / Palmieri, Michelle / Elliott, Meg J / Nightingale, Rebecca / Fang, Catherine G / Li, Rita / Mariadason, John M / Faragher, Ian / Jones, Ian T / Churilov, Leonid / Tebbutt, Niall C / Gibbs, Peter / Sieber, Oliver M

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

2019 Volume 33, Issue 3, Page(s) 483–495

Abstract: TP53 mutations drive colorectal cancer development, with missense mutations frequently leading to accumulation of abnormal TP53 protein. TP53 alterations have been associated with poor prognosis and chemotherapy resistance, but data remain controversial. ...

Abstract	TP53 mutations drive colorectal cancer development, with missense mutations frequently leading to accumulation of abnormal TP53 protein. TP53 alterations have been associated with poor prognosis and chemotherapy resistance, but data remain controversial. Here, we examined the predictive utility of TP53 overexpression in the context of current adjuvant treatment practice for patients with stage III colorectal cancer. A prospective cohort of 264 stage III patients was tested for association of TP53 expression with 5-year disease-free survival, grouped by adjuvant treatment. Findings were validated in an independent retrospective cohort of 274 stage III patients. Overexpression of TP53 protein (TP53+) was found in 53% and 52% of cases from the prospective and retrospective cohorts, respectively. Among patients receiving adjuvant chemotherapy, TP53+ status was associated with shorter disease-free survival (p ≤ 0.026 for both cohorts), while no difference in outcomes between TP53+ and TP53- cases was observed for patients treated with surgery alone. Considering patients with TP53- tumors, those receiving adjuvant treatment had better outcomes compared with those treated with surgery alone (p ≤ 0.018 for both cohorts), while no treatment benefit was apparent for patients with TP53+ tumors. Combined cohort-stratified analysis adjusted for clinicopathological variables and DNA mismatch repair status confirmed a significant interaction between TP53 expression and adjuvant treatment for disease-free survival (p
MeSH term(s)	Adenocarcinoma/chemistry ; Adenocarcinoma/mortality ; Adenocarcinoma/pathology ; Adenocarcinoma/therapy ; Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor/analysis ; Chemotherapy, Adjuvant ; Clinical Decision-Making ; Colectomy/adverse effects ; Colectomy/mortality ; Colorectal Neoplasms/chemistry ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/therapy ; Disease-Free Survival ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neoplasm Staging ; Predictive Value of Tests ; Prospective Studies ; Retrospective Studies ; Risk Factors ; Time Factors ; Tumor Suppressor Protein p53/analysis ; Up-Regulation
Chemical Substances	Biomarkers, Tumor ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2019-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645073-8
ISSN	1530-0285 ; 0893-3952
ISSN (online)	1530-0285
ISSN	0893-3952
DOI	10.1038/s41379-019-0353-2
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Zs.A 2450: Show issues

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Article ; Online: Negative appendicectomy rate as a quality metric in the management of appendicitis: impact of computed tomography, Alvarado score and the definition of negative appendicectomy.

Mariadason, J G / Wang, W N / Wallack, M K / Belmonte, A / Matari, H

Annals of the Royal College of Surgeons of England

2012 Volume 94, Issue 6, Page(s) 395–401

Abstract: Introduction: The negative appendicectomy rate (NAR) is a quality metric in the management of appendicitis. While computed tomography (CT) has been associated with a low NAR, Alvarado scoring produces an acceptable NAR. The definition of negative ... ...

Abstract	Introduction: The negative appendicectomy rate (NAR) is a quality metric in the management of appendicitis. While computed tomography (CT) has been associated with a low NAR, Alvarado scoring produces an acceptable NAR. The definition of negative appendicectomy may affect the NAR. This study examined the impact of CT, Alvarado score and definition on the NAR. Methods: The charts of 1,306 emergency appendicectomy patients from 1996 to 2010 were reviewed. Three five-year cohorts were created (Cohort A: 1996-2000, Cohort B: 2001-2005, Cohort C: 2006-2010) and the NAR was calculated for each cohort using two definitions of negative appendicectomy: absence of inflammation (NAR-STD) and absence of intramural neutrophils (NAR-STR). NAR-STD was correlated to the CT rate for Cohorts B and C and also to Alvarado score for Cohort C. Results: When the definition of negative appendicectomy was changed, the NAR rose from 9.2% to 15.8% (p=0.0097) for Cohort A, from 2.8% to 8.6% (p=0.0180) for Cohort B (CT rate: 80.6%) and from 3.0% to 6.7% (p=0.0255) for Cohort C (CT rate: 92.4%). The introduction of CT lowered NAR-STD from 1996-2000 (9.2%) to 2001-2010 (2.9%) but increasing the CT rate from 2001-2010 had no impact on the NAR. The positive predictive value for Alvarado score (98.60%) and CT (99.03%) were similar. Conclusions: The definition of a negative appendicectomy determines the NAR. CT reduces the NAR regardless of definition but routine CT is unnecessary for male patients with positive Alvarado scores. Early/mild appendicitis may resolve without surgery and CT may contribute to unnecessary surgery. Alvarado scoring allows selective use of CT in suspected appendicitis.
MeSH term(s)	Adolescent ; Adult ; Aged ; Appendectomy/standards ; Appendectomy/statistics & numerical data ; Appendicitis/diagnostic imaging ; Appendicitis/surgery ; Child ; Child, Preschool ; Cohort Studies ; Diagnosis, Differential ; Female ; Humans ; Infant ; Male ; Middle Aged ; Quality of Health Care ; Severity of Illness Index ; Tomography, X-Ray Computed/statistics & numerical data ; Young Adult
Language	English
Publishing date	2012-09-03
Publishing country	England
Document type	Journal Article
ZDB-ID	80044-2
ISSN	1478-7083 ; 0035-8843
ISSN (online)	1478-7083
ISSN	0035-8843
DOI	10.1308/003588412X13171221592131
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Article ; Online: CSK-homologous kinase (CHK/MATK) is a potential colorectal cancer tumour suppressor gene epigenetically silenced by promoter methylation.

Oncogene

2021 Volume 40, Issue 17, Page(s) 3015–3029

Abstract: Hyperactivation of SRC-family protein kinases (SFKs) contributes to the initiation and progression of human colorectal cancer (CRC). Since oncogenic mutations of SFK genes are rare in human CRC, we investigated if SFK hyperactivation is linked to ... ...

Abstract	Hyperactivation of SRC-family protein kinases (SFKs) contributes to the initiation and progression of human colorectal cancer (CRC). Since oncogenic mutations of SFK genes are rare in human CRC, we investigated if SFK hyperactivation is linked to dysregulation of their upstream inhibitors, C-terminal SRC kinase (CSK) and its homolog CSK-homologous kinase (CHK/MATK). We demonstrate that expression of CHK/MATK but not CSK was significantly downregulated in CRC cell lines and primary tumours compared to normal colonic tissue. Investigation of the mechanism by which CHK/MATK expression is down-regulated in CRC cells uncovered hypermethylation of the CHK/MATK promoter in CRC cell lines and primary tumours. Promoter methylation of CHK/MATK was also observed in several other tumour types. Consistent with epigenetic silencing of CHK/MATK, genetic deletion or pharmacological inhibition of DNA methyltransferases increased CHK/MATK mRNA expression in CHK/MATK-methylated colon cancer cell lines. SFKs were hyperactivated in CHK/MATK-methylated CRC cells despite expressing enzymatically active CSK, suggesting loss of CHK/MATK contributes to SFK hyperactivation. Re-expression of CHK/MATK in CRC cell lines led to reduction in SFK activity via a non-catalytic mechanism, a reduction in anchorage-independent growth, cell proliferation and migration in vitro, and a reduction in tumour growth and metastasis in a zebrafish embryo xenotransplantation model in vivo, collectively identifying CHK/MATK as a novel putative tumour suppressor gene in CRC. Furthermore, our discovery that CHK/MATK hypermethylation occurs in the majority of tumours warrants its further investigation as a diagnostic marker of CRC.
MeSH term(s)	CSK Tyrosine-Protein Kinase ; Methylation ; Phosphorylation ; Protein Binding ; Protein Processing, Post-Translational ; src-Family Kinases
Chemical Substances	CSK Tyrosine-Protein Kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2021-03-25
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/s41388-021-01755-z
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Zs.A 2218: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: BCL-XL and MCL-1 are the key BCL-2 family proteins in melanoma cell survival.

Cell death & disease

2019 Volume 10, Issue 5, Page(s) 342

Abstract: Malignant melanoma is one of the most difficult cancers to treat due to its resistance to chemotherapy. Despite recent successes with BRAF inhibitors and immune checkpoint inhibitors, many patients do not respond or become resistant to these drugs. Hence, ...

Abstract	Malignant melanoma is one of the most difficult cancers to treat due to its resistance to chemotherapy. Despite recent successes with BRAF inhibitors and immune checkpoint inhibitors, many patients do not respond or become resistant to these drugs. Hence, alternative treatments are still required. Due to the importance of the BCL-2-regulated apoptosis pathway in cancer development and drug resistance, it is of interest to establish which proteins are most important for melanoma cell survival, though the outcomes of previous studies have been conflicting. To conclusively address this question, we tested a panel of established and early passage patient-derived cell lines against several BH3-mimetic drugs designed to target individual or subsets of pro-survival BCL-2 proteins, alone and in combination, in both 2D and 3D cell cultures. None of the drugs demonstrated significant activity as single agents, though combinations targeting MCL-1 plus BCL-XL, and to a lesser extent BCL-2, showed considerable synergistic killing activity that was elicited via both BAX and BAK. Genetic deletion of BFL-1 in cell lines that express it at relatively high levels only had minor impact on BH3-mimetic drug sensitivity, suggesting it is not a critical pro-survival protein in melanoma. Combinations of MCL-1 inhibitors with BRAF inhibitors also caused only minimal additional melanoma cell killing over each drug alone, whilst combinations with the proteasome inhibitor bortezomib was more effective in multiple cell lines. Our data show for the first time that therapies targeting specific combinations of BCL-2 pro-survival proteins, namely MCL-1 plus BCL-XL and MCL-1 plus BCL-2, could have significant benefit for the treatment of melanoma.
MeSH term(s)	Aniline Compounds/pharmacology ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Bortezomib/pharmacology ; Cell Line, Tumor ; Cell Survival/drug effects ; Humans ; Melanoma/metabolism ; Melanoma/pathology ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Pyrimidines/pharmacology ; Sulfonamides/pharmacology ; Thiophenes/pharmacology ; bcl-X Protein/metabolism
Chemical Substances	Aniline Compounds ; Antineoplastic Agents ; Myeloid Cell Leukemia Sequence 1 Protein ; Pyrimidines ; S63845 ; Sulfonamides ; Thiophenes ; bcl-X Protein ; Bortezomib (69G8BD63PP) ; navitoclax (XKJ5VVK2WD)
Language	English
Publishing date	2019-04-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-019-1568-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

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