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Article ; Online: Overview of major molecular alterations during progression from Barrett's esophagus to esophageal adenocarcinoma.

Kalatskaya, Irina

Annals of the New York Academy of Sciences

2016 Volume 1381, Issue 1, Page(s) 74–91

Abstract: Esophageal adenocarcinoma (EAC) develops in the sequential transformation of normal epithelium into metaplastic epithelium, called Barrett's esophagus (BE), then to dysplasia, and finally cancer. BE is a common condition in which normal stratified ... ...

Abstract	Esophageal adenocarcinoma (EAC) develops in the sequential transformation of normal epithelium into metaplastic epithelium, called Barrett's esophagus (BE), then to dysplasia, and finally cancer. BE is a common condition in which normal stratified squamous epithelium of the esophagus is replaced with an intestine-like columnar epithelium, and it is the most prominent risk factor for EAC. This review aims to impartially systemize the knowledge from a large number of publications that describe the molecular and biochemical alterations occurring over this progression sequence. In order to provide an unbiased extraction of the knowledge from the literature, a text-mining methodology was used to select genes that are involved in the BE progression, with the top candidate genes found to be TP53, CDKN2A, CTNNB1, CDH1, GPX3, and NOX5. In addition, sample frequencies across analyzed patient cohorts at each stage of disease progression are summarized. All six genes are altered in the majority of EAC patients, and accumulation of alterations correlates well with the sequential progression of BE to cancer, indicating that the text-mining method is a valid approach for gene prioritization. This review discusses how, besides being cancer drivers, these genes are functionally interconnected and might collectively be considered a central hub of BE progression.
MeSH term(s)	Adenocarcinoma/diagnosis ; Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Animals ; Barrett Esophagus/diagnosis ; Barrett Esophagus/genetics ; Barrett Esophagus/metabolism ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cyclin-Dependent Kinase Inhibitor p18/genetics ; Cyclin-Dependent Kinase Inhibitor p18/metabolism ; Disease Progression ; Esophageal Neoplasms/diagnosis ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; NADPH Oxidase 5 ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Biomarkers, Tumor ; CDKN2A protein, human ; Cyclin-Dependent Kinase Inhibitor p18 ; Membrane Proteins ; Reactive Oxygen Species ; TP53 protein, human ; Tumor Suppressor Protein p53 ; NADPH Oxidase 5 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; NOX5 protein, human (EC 1.6.3.-)
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.13134
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Article ; Online: Revealing the immune cell subtype reconstitution profile in patients from the CLARITY study using deconvolution algorithms after cladribine tablets treatment.

Kalatskaya, Irina / Giovannoni, Gavin / Leist, Thomas / Cerra, Joseph / Boschert, Ursula / Rolfe, P Alexander

Scientific reports

2023 Volume 13, Issue 1, Page(s) 8067

Abstract: Immune Cell Deconvolution methods utilizing gene expression profiling to quantify immune cells in tissues and blood are an appealing alternative to flow cytometry. Our objective was to investigate the applicability of deconvolution approaches in clinical ...

Abstract	Immune Cell Deconvolution methods utilizing gene expression profiling to quantify immune cells in tissues and blood are an appealing alternative to flow cytometry. Our objective was to investigate the applicability of deconvolution approaches in clinical trial settings to better investigate the mode of action of drugs for autoimmune diseases. Popular deconvolution methods CIBERSORT and xCell were validated using gene expression from the publicly available GSE93777 dataset that has comprehensive matching flow cytometry. As shown in the online tool, ~ 50% of signatures show strong correlation (r > 0.5) with the remainder showing moderate correlation, or in a few cases, no correlation. Deconvolution methods were then applied to gene expression data from the phase III CLARITY study (NCT00213135) to evaluate the immune cell profile of relapsing multiple sclerosis patients treated with cladribine tablets. At 96 weeks after treatment, deconvolution scores showed the following changes vs placebo: naïve, mature, memory CD4
MeSH term(s)	Humans ; Cladribine/therapeutic use ; Cladribine/pharmacology ; Immunosuppressive Agents/therapeutic use ; Immunosuppressive Agents/pharmacology ; CD8-Positive T-Lymphocytes ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Multiple Sclerosis/drug therapy ; Tablets/therapeutic use ; Algorithms
Chemical Substances	Cladribine (47M74X9YT5) ; Immunosuppressive Agents ; Tablets
Language	English
Publishing date	2023-05-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-34384-5
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Article ; Online: Identification of Distinct Prognostic Groups: Implications for Patient Selection to Targeted Therapies Among Anti-Endocrine Therapy-Resistant Early Breast Cancers.

Bayani, Jane / Kornaga, Elizabeth N / Crozier, Cheryl / Jang, Gun Ho / Bathurst, Lauren / Kalatskaya, Irina / Trinh, Quang M / Yao, Cindy Q / Livingstone, Julie / Boutros, Paul C / Spears, Melanie / McPherson, John D / Stein, Lincoln D / Rea, Daniel / Bartlett, John M S

JCO precision oncology

2022 Volume 3, Page(s) 1–13

Abstract: Purpose: Hormone receptor-positive breast cancer remains an ongoing therapeutic challenge, despite optimal anti-endocrine therapies. In this study, we assessed the prognostic ability of genomic signatures to identify patients at risk for recurrence ... ...

Abstract	Purpose: Hormone receptor-positive breast cancer remains an ongoing therapeutic challenge, despite optimal anti-endocrine therapies. In this study, we assessed the prognostic ability of genomic signatures to identify patients at risk for recurrence after endocrine therapy. Analysis was performed on the basis of an a priori hypothesis related to molecular pathways, which might predict response to existing targeted therapies. Patients and methods: A subset of patients from the Tamoxifen Versus Exemestane Adjuvant Multinational trial (ClinicalTrials.gov identifiers: NCT00279448 and NCT00032136, and NCT00036270) pathology cohort were analyzed to determine the prognostic ability of mutational and copy number aberration biomarkers that represent the cyclin D/cyclin-dependent kinase (CCND/CDK), fibroblast growth factor receptor/fibroblast growth factor (FGFR/FGF), and phosphatidylinositol 3-kinase/protein kinase B (PI3K/ATK) pathways to inform the potential choice of additional therapies to standard endocrine treatment. Copy number analysis and targeted sequencing was performed. Pathways were identified as aberrant if there were copy number aberrations and/or mutations in any of the predetermined pathway genes: Results: The 390 of 420 samples that passed quality control were analyzed for distant metastasis-free survival between groups. Patients with no changes in the CCND/CDK pathway experienced a better distant metastasis-free survival (hazard ratio, 1.94; 95% CI, 1.45 to 2.61; Conclusion: We show that aberrations of genes in these pathways are independently linked to a higher risk of relapse after endocrine treatment. Improvement of the clinical management of early breast cancers could be made by identifying those for whom current endocrine therapies are sufficient, thus reducing unnecessary treatment, and secondly, by identifying those who are at high risk for recurrence and linking molecular features that drive these cancers to treatment with targeted therapies.
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article
ISSN	2473-4284
ISSN (online)	2473-4284
DOI	10.1200/PO.18.00373
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Book ; Online ; Thesis: Role of the tyrosine in the highly conserved NPxxY sequence of the human B2 bradykinin receptor

Kalatskaya, Irina [Verfasser]

2005

Author's details	Irina Kalatskaya
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article: Combined EsophaCap cytology and MUC2 immunohistochemistry for screening of intestinal metaplasia, dysplasia and carcinoma.

Zhou, Zhongren / Kalatskaya, Irina / Russell, Donna / Marcon, Norman / Cirocco, Maria / Krzyzanowski, Paul M / Streutker, Cathy / Liang, Hua / Litle, Virginia R / Godfrey, Tony E / Stein, Lincoln

Clinical and experimental gastroenterology

2019 Volume 12, Page(s) 219–229

Abstract: Purpose: ...

Abstract	Purpose:
Language	English
Publishing date	2019-05-15
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2520690-4
ISSN	1178-7023
ISSN	1178-7023
DOI	10.2147/CEG.S186958
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Article ; Online: ISOWN: accurate somatic mutation identification in the absence of normal tissue controls.

Kalatskaya, Irina / Trinh, Quang M / Spears, Melanie / McPherson, John D / Bartlett, John M S / Stein, Lincoln

Genome medicine

2017 Volume 9, Issue 1, Page(s) 59

Abstract: Background: A key step in cancer genome analysis is the identification of somatic mutations in the tumor. This is typically done by comparing the genome of the tumor to the reference genome sequence derived from a normal tissue taken from the same donor. ...

Abstract	Background: A key step in cancer genome analysis is the identification of somatic mutations in the tumor. This is typically done by comparing the genome of the tumor to the reference genome sequence derived from a normal tissue taken from the same donor. However, there are a variety of common scenarios in which matched normal tissue is not available for comparison. Results: In this work, we describe an algorithm to distinguish somatic single nucleotide variants (SNVs) in next-generation sequencing data from germline polymorphisms in the absence of normal samples using a machine learning approach. Our algorithm was evaluated using a family of supervised learning classifications across six different cancer types and ~1600 samples, including cell lines, fresh frozen tissues, and formalin-fixed paraffin-embedded tissues; we tested our algorithm with both deep targeted and whole-exome sequencing data. Our algorithm correctly classified between 95 and 98% of somatic mutations with F1-measure ranges from 75.9 to 98.6% depending on the tumor type. We have released the algorithm as a software package called ISOWN (Identification of SOmatic mutations Without matching Normal tissues). Conclusions: In this work, we describe the development, implementation, and validation of ISOWN, an accurate algorithm for predicting somatic mutations in cancer tissues in the absence of matching normal tissues. ISOWN is available as Open Source under Apache License 2.0 from https://github.com/ikalatskaya/ISOWN .
MeSH term(s)	DNA Mutational Analysis/methods ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Mutation ; Neoplasms/genetics ; Supervised Machine Learning
Language	English
Publishing date	2017-06-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-017-0446-9
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Article ; Online: ISOWN

Irina Kalatskaya / Quang M. Trinh / Melanie Spears / John D. McPherson / John M. S. Bartlett / Lincoln Stein

Genome Medicine, Vol 9, Iss 1, Pp 1-

accurate somatic mutation identification in the absence of normal tissue controls

2017 Volume 18

Abstract: Abstract Background A key step in cancer genome analysis is the identification of somatic mutations in the tumor. This is typically done by comparing the genome of the tumor to the reference genome sequence derived from a normal tissue taken from the ... ...

Abstract	Abstract Background A key step in cancer genome analysis is the identification of somatic mutations in the tumor. This is typically done by comparing the genome of the tumor to the reference genome sequence derived from a normal tissue taken from the same donor. However, there are a variety of common scenarios in which matched normal tissue is not available for comparison. Results In this work, we describe an algorithm to distinguish somatic single nucleotide variants (SNVs) in next-generation sequencing data from germline polymorphisms in the absence of normal samples using a machine learning approach. Our algorithm was evaluated using a family of supervised learning classifications across six different cancer types and ~1600 samples, including cell lines, fresh frozen tissues, and formalin-fixed paraffin-embedded tissues; we tested our algorithm with both deep targeted and whole-exome sequencing data. Our algorithm correctly classified between 95 and 98% of somatic mutations with F1-measure ranges from 75.9 to 98.6% depending on the tumor type. We have released the algorithm as a software package called ISOWN (Identification of SOmatic mutations Without matching Normal tissues). Conclusions In this work, we describe the development, implementation, and validation of ISOWN, an accurate algorithm for predicting somatic mutations in cancer tissues in the absence of matching normal tissues. ISOWN is available as Open Source under Apache License 2.0 from https://github.com/ikalatskaya/ISOWN .
Keywords	Next-generation sequencing ; Somatic mutation ; Matching normal tissue ; Variant classification ; Medicine ; R ; Genetics ; QH426-470
Subject code	616
Language	English
Publishing date	2017-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Plasma circulating tumor DNA as a potential tool for disease monitoring in head and neck cancer.

Egyud, Matthew / Sridhar, Praveen / Devaiah, Anand / Yamada, Emiko / Saunders, Stefanie / Ståhlberg, Anders / Filges, Stefan / Krzyzanowski, Paul M / Kalatskaya, Irina / Jiao, Wei / Stein, Lincoln D / Jalisi, Scharukh / Godfrey, Tony E

Head & neck

2018 Volume 41, Issue 5, Page(s) 1351–1358

Abstract: Background: Recommendations for perioperative therapy in head and neck cancer are not explicit and recurrence occurs frequently. Circulating tumor DNA is an emerging cancer biomarker, but has not been extensively explored for detection of recurrence in ... ...

Abstract	Background: Recommendations for perioperative therapy in head and neck cancer are not explicit and recurrence occurs frequently. Circulating tumor DNA is an emerging cancer biomarker, but has not been extensively explored for detection of recurrence in head and neck cancer. Methods: Patients diagnosed with head and neck squamous cell carcinoma were recruited into the study protocol. Tumors were sequenced to identify patient-specific mutations. Mutations were then identified in plasma circulating tumor DNA from pre-treatment blood samples and longitudinally during standard follow-up. Circulating tumor DNA status during follow-up was correlated to disease recurrence. Results: Samples were taken from eight patients. Tumor mutations were verified in seven patients. Baseline circulating tumor DNA was positive in six patients. Recurrence occurred in four patients, two of whom had detectable circulating tumor DNA prior to recurrence. Conclusion: Circulating tumor DNA is a potential tool for disease and recurrence monitoring following curative therapy in head and neck cancer, allowing for better prognostication, and/or modification of treatment strategies.
MeSH term(s)	Aged ; Biomarkers, Tumor/blood ; Circulating Tumor DNA/blood ; DNA, Neoplasm/blood ; Disease-Free Survival ; Female ; Head and Neck Neoplasms/blood ; Head and Neck Neoplasms/mortality ; Head and Neck Neoplasms/pathology ; Head and Neck Neoplasms/therapy ; Humans ; Liquid Biopsy/methods ; Male ; Middle Aged ; Monitoring, Physiologic/methods ; Neoplasm Invasiveness ; Neoplasm Recurrence, Local/blood ; Neoplasm Recurrence, Local/mortality ; Neoplasm Recurrence, Local/physiopathology ; Neoplasm Staging ; Predictive Value of Tests ; Prognosis ; Prospective Studies ; Risk Assessment ; Sampling Studies ; Squamous Cell Carcinoma of Head and Neck/blood ; Squamous Cell Carcinoma of Head and Neck/mortality ; Squamous Cell Carcinoma of Head and Neck/pathology ; Squamous Cell Carcinoma of Head and Neck/therapy ; Survival Analysis ; United States
Chemical Substances	Biomarkers, Tumor ; Circulating Tumor DNA ; DNA, Neoplasm
Language	English
Publishing date	2018-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	645165-2
ISSN	1097-0347 ; 0148-6403 ; 1043-3074
ISSN (online)	1097-0347
ISSN	0148-6403 ; 1043-3074
DOI	10.1002/hed.25563
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Article ; Online: Detection of Circulating Tumor DNA in Plasma: A Potential Biomarker for Esophageal Adenocarcinoma.

Egyud, Matthew / Tejani, Mohamedtaki / Pennathur, Arjun / Luketich, James / Sridhar, Praveen / Yamada, Emiko / Ståhlberg, Anders / Filges, Stefan / Krzyzanowski, Paul / Jackson, Jennifer / Kalatskaya, Irina / Jiao, Wei / Nielsen, Gradon / Zhou, Zhongren / Litle, Virginia / Stein, Lincoln / Godfrey, Tony

The Annals of thoracic surgery

2019 Volume 108, Issue 2, Page(s) 343–349

Abstract: Background: Recent literature has demonstrated the potential of "liquid biopsy" and detection of circulating tumor (ct)DNA as a cancer biomarker. However, to date there is a lack of data specific to esophageal adenocarcinoma (EAC). This study was ... ...

Abstract	Background: Recent literature has demonstrated the potential of "liquid biopsy" and detection of circulating tumor (ct)DNA as a cancer biomarker. However, to date there is a lack of data specific to esophageal adenocarcinoma (EAC). This study was conducted to determine how detection and quantification of ctDNA changes with disease burden in patients with EAC and evaluate its potential as a biomarker in this population. Methods: Blood samples were obtained from patients with stage I to IV EAC. Longitudinal blood samples were collected from a subset of patients. Imaging studies and pathology reports were reviewed to determine disease course. Tumor samples were sequenced to identify mutations. Mutations in plasma DNA were detected using custom, barcoded, patient-specific sequencing libraries. Mutations in plasma were quantified, and associations with disease stage and response to therapy were explored. Results: Plasma samples from a final cohort of 38 patients were evaluated. Baseline plasma samples were ctDNA positive for 18 patients (47%) overall, with tumor allele frequencies ranging from 0.05% to 5.30%. Detection frequency of ctDNA and quantity of ctDNA increased with stage. Data from longitudinal samples indicate that ctDNA levels correlate with and precede evidence of response to therapy or recurrence. Conclusions: ctDNA can be detected in plasma of EAC patients and correlates with disease burden. Detection of ctDNA in early-stage EAC is challenging and may limit diagnostic applications. However, our data demonstrate the potential of ctDNA as a dynamic biomarker to monitor treatment response and disease recurrence in patients with EAC.
MeSH term(s)	Adenocarcinoma/blood ; Adenocarcinoma/diagnosis ; Adenocarcinoma/genetics ; Biomarkers, Tumor/blood ; Biomarkers, Tumor/genetics ; Circulating Tumor DNA/blood ; Circulating Tumor DNA/genetics ; DNA, Neoplasm/genetics ; Disease Progression ; Esophageal Neoplasms/blood ; Esophageal Neoplasms/diagnosis ; Esophageal Neoplasms/genetics ; Female ; Humans ; Liquid Biopsy ; Male ; Mutation ; Neoplasm Staging/methods
Chemical Substances	Biomarkers, Tumor ; Circulating Tumor DNA ; DNA, Neoplasm
Language	English
Publishing date	2019-05-03
Publishing country	Netherlands
Document type	Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural
ZDB-ID	211007-6
ISSN	1552-6259 ; 0003-4975
ISSN (online)	1552-6259
ISSN	0003-4975
DOI	10.1016/j.athoracsur.2019.04.004
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Article ; Online: Interruption of the ionic lock in the bradykinin B2 receptor results in constitutive internalization and turns several antagonists into strong agonists.

Leschner, Jasmin / Wennerberg, Goeran / Feierler, Jens / Bermudez, Marcel / Welte, Benjamin / Kalatskaya, Irina / Wolber, Gerhard / Faussner, Alexander

The Journal of pharmacology and experimental therapeutics

2013 Volume 344, Issue 1, Page(s) 85–95

Abstract: The DRY motif with the highly conserved R3.50 is a hallmark of family A G protein-coupled receptors (GPCRs). The crystal structure of rhodopsin revealed a salt bridge between R135(3.50) and another conserved residue, E247(6.30), in helix 6. This ionic ... ...

Abstract	The DRY motif with the highly conserved R3.50 is a hallmark of family A G protein-coupled receptors (GPCRs). The crystal structure of rhodopsin revealed a salt bridge between R135(3.50) and another conserved residue, E247(6.30), in helix 6. This ionic lock was shown to maintain rhodopsin in its inactive state. Thus far, little information is available on how interruption of this ionic bond affects signaling properties of nonrhodopsin GPCRs, because the focus has been on mutations of R3.50, although this residue is indispensable for G protein activation. To investigate the importance of an ionic lock for overall receptor activity in a nonrhodopsin GPCR, we mutated R128(3.50) and E238(6.30) in the bradykinin (BK) B(2) receptor (B(2)R) and stably expressed the constructs in HEK293 cells. As expected, mutation of R3.50 resulted in lack of G protein activation. In addition, this mutation led to considerable constitutive receptor internalization. Mutation of E6.30 (mutants E6.30A and E6.30R) also caused strong constitutive internalization. Most intriguingly, however, although the two E6.30 mutants displayed no increased basal phosphatidylinositol hydrolysis, they gave a response to three different B(2)R antagonists that was almost comparable to that obtained with BK. In contrast, swapping of R3.50 and E6.30, thus allowing the formation of an inverse ionic bond, resulted in rescue of the wild type phenotype. These findings demonstrate for the first time, to our knowledge, that interruption of the ionic lock in a family A GPCR can have distinctly different effects on receptor internalization and G protein stimulation, shedding new light on its role in the activation process.
MeSH term(s)	Amino Acids/metabolism ; Biotinylation ; Bradykinin/metabolism ; Bradykinin B2 Receptor Antagonists ; GTP-Binding Proteins/metabolism ; Gene Expression ; HEK293 Cells ; Humans ; Hydrolysis ; Inositol Phosphates/metabolism ; Ions/metabolism ; Phosphorylation ; Point Mutation ; Pyridones/pharmacology ; Quinolines/pharmacology ; Receptor, Bradykinin B2/agonists ; Receptor, Bradykinin B2/drug effects ; Receptors, G-Protein-Coupled/drug effects ; Receptors, G-Protein-Coupled/metabolism ; Temperature
Chemical Substances	1-(4-methyl-3-(2-methyl-4-(4-methyl-2H-pyrazol-3-yl)-quinolin-8-yloxymethyl)pyridin-2-ylmethyl)-3-trifluoromethyl-1H-pyridin-2-one ; Amino Acids ; Bradykinin B2 Receptor Antagonists ; Inositol Phosphates ; Ions ; Pyridones ; Quinolines ; Receptor, Bradykinin B2 ; Receptors, G-Protein-Coupled ; GTP-Binding Proteins (EC 3.6.1.-) ; Bradykinin (S8TIM42R2W)
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.112.199190
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