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Article ; Online: Beta cell regeneration in human pancreas.

Gianani, Roberto

2010 Volume 33, Issue 1, Page(s) 23–27

Abstract: The issue of beta cell regeneration in human pancreas is probably one of the most controversial aspects of type 1 diabetes research. In this review, we will first describe the known mechanisms underlying beta cell development and expansion in normal ... ...

Abstract	The issue of beta cell regeneration in human pancreas is probably one of the most controversial aspects of type 1 diabetes research. In this review, we will first describe the known mechanisms underlying beta cell development and expansion in normal human pancreatic development because it is likely that such mechanisms might also play a role in beta cell regeneration. The sensu strictiori definition of beta cells implies replacement of lost beta cell mass by new beta cells. In our discussion, however, we will use the term in a more general way, defining as regeneration the formation of new beta cells, whether or not a loss of beta cells has actually occurred. The potential mechanisms of beta cell regeneration in the human pancreas will be discussed in the second part of this review. In particular, we will analyze beta cell regeneration through proliferation of beta cells, neogenesis from non-beta cell precursors, and transdifferentiation from alpha cells. In the third part of this review, we will explore the arguments for and against the ability of the human pancreas to regenerate functional beta cells in the context of type 1 diabetes and in other pathological conditions.
MeSH term(s)	Cell Differentiation/physiology ; Diabetes Mellitus, Type 1/physiopathology ; Glucagon-Secreting Cells/cytology ; Glucagon-Secreting Cells/metabolism ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/metabolism ; Pancreas/cytology ; Pancreatic Ducts/cytology ; Regeneration/physiology
Language	English
Publishing date	2010-12-25
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-010-0235-7
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Article: The multiple endocrine neoplasia type-1 (MEN-1) syndrome and its effect on the pancreas.

Gianani, Roberto

The Journal of clinical endocrinology and metabolism

2007 Volume 92, Issue 3, Page(s) 811–812

MeSH term(s)	Adenoma/etiology ; Adenoma/genetics ; Humans ; Loss of Heterozygosity ; Multiple Endocrine Neoplasia Type 1/genetics ; Multiple Endocrine Neoplasia Type 1/pathology ; Pancreatic Neoplasms/etiology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Proto-Oncogene Proteins/genetics
Chemical Substances	MEN1 protein, human ; Proto-Oncogene Proteins
Language	English
Publishing date	2007-03
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/jc.2007-0104
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Article ; Online: A digital assay for programmed death-ligand 1 (22C3) quantification combined with immune cell recognition algorithms in non-small cell lung cancer.

Paces, Will / Ergon, Elliott / Bueche, Elizabeth / Young, G Dave / Adisetiyo, Vitria / Luengo, Cris / James, Meredith / Caldwell, Charles / Miller, Dannah / Wambaugh, Morgan / Metcalf, Geoffrey / Gianani, Roberto

Scientific reports

2022 Volume 12, Issue 1, Page(s) 9745

Abstract: PD-L1 (22C3) checkpoint inhibitor therapy represents a mainstay of modern cancer immunotherapy for non-small cell lung cancer (NSCLC). In vitro diagnostic (IVD) PD-L1 antibody staining is widely used to predict clinical intervention efficacy. However, ... ...

Abstract	PD-L1 (22C3) checkpoint inhibitor therapy represents a mainstay of modern cancer immunotherapy for non-small cell lung cancer (NSCLC). In vitro diagnostic (IVD) PD-L1 antibody staining is widely used to predict clinical intervention efficacy. However, pathologist interpretation of this assay is cumbersome and variable, resulting in poor positive predictive value concerning patient therapy response. To address this, we developed a digital assay (DA) termed Tissue Insight (TI) 22C3 NSCLC, for the quantification of PD-L1 in NSCLC tissues, including digital recognition of macrophages and lymphocytes. We completed clinical validation of this digital image analysis solution in 66 NSCLC patient samples, followed by concordance studies (comparison of PD-L1 manual and digital scores) in an additional 99 patient samples. We then combined this DA with three distinct immune cell recognition algorithms for detecting tissue macrophages, alveolar macrophages, and lymphocytes to aid in sample interpretation. Our PD-L1 (22C3) DA was successfully validated and had a scoring agreement (digital to manual) higher than the inter-pathologist scoring. Furthermore, the number of algorithm-identified immune cells showed significant correlation when compared with those identified by immunohistochemistry in serial sections stained by double immunofluorescence. Here, we demonstrated that TI 22C3 NSCLC DA yields comparable results to pathologist interpretation while eliminating the intra- and inter-pathologist variability associated with manual scoring while providing characterization of the immune microenvironment, which can aid in clinical treatment decisions.
MeSH term(s)	Algorithms ; B7-H1 Antigen ; Biomarkers, Tumor/analysis ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Humans ; Lung Neoplasms/drug therapy ; Tumor Microenvironment
Chemical Substances	B7-H1 Antigen ; Biomarkers, Tumor ; CD274 protein, human
Language	English
Publishing date	2022-06-13
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/s41598-022-12697-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Beta-cell regeneration in human pancreas: the lessons of pancreatic pathology.

Maulis, Matthew / Gianani, Roberto

Advances in experimental medicine and biology

2012 Volume 771, Page(s) 310–318

Abstract: Diabetes mellitus has been traditionally classified as Type 1 and Type 2 on the basis of several criteria that generally reflect either insulin deficiency or functional defects in insulin secretion. In this chapter, we propose a new classification ... ...

Abstract	Diabetes mellitus has been traditionally classified as Type 1 and Type 2 on the basis of several criteria that generally reflect either insulin deficiency or functional defects in insulin secretion. In this chapter, we propose a new classification diabetes based on age of onset, body mass index and biomarkers such as islet autoantibodies and DR HLA alleles. In the second part of this chapter, we briefly discuss some novel hypotheses on the possibility of beta-cell regeneration in diabetes in relation to the islet pathology of the disease.
MeSH term(s)	Amyloid/metabolism ; Amyloidosis/pathology ; Amyloidosis/physiopathology ; Animals ; Biomarkers/metabolism ; Diabetes Mellitus, Type 1/classification ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/physiopathology ; Diabetes Mellitus, Type 2/classification ; Diabetes Mellitus, Type 2/pathology ; Diabetes Mellitus, Type 2/physiopathology ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/physiology ; Regeneration/physiology
Chemical Substances	Amyloid ; Biomarkers
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
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Article ; Online: Validation of a DKK1 RNAscope chromogenic in situ hybridization assay for gastric and gastroesophageal junction adenocarcinoma tumors.

Caldwell, Charles / Rottman, James B / Paces, Will / Bueche, Elizabeth / Reitsma, Sofia / Gibb, Joseph / Adisetiyo, Vitria / Haas, Michael S / Heath, Heidi / Newman, Walter / Baum, Jason / Gianani, Roberto / Kagey, Michael H

Scientific reports

2021 Volume 11, Issue 1, Page(s) 9920

Abstract: Dickkopf-1 (DKK1) is a secreted modulator of Wnt signaling that is frequently overexpressed in tumors and associated with poor clinical outcomes. DKN-01 is a humanized monoclonal therapeutic antibody that binds DKK1 with high affinity and has ... ...

Abstract	Dickkopf-1 (DKK1) is a secreted modulator of Wnt signaling that is frequently overexpressed in tumors and associated with poor clinical outcomes. DKN-01 is a humanized monoclonal therapeutic antibody that binds DKK1 with high affinity and has demonstrated clinical activity in gastric/gastroesophageal junction (G/GEJ) patients with elevated tumoral expression of DKK1. Here we report on the validation of a DKK1 RNAscope chromogenic in situ hybridization assay to assess DKK1 expression in G/GEJ tumor tissue. To reduce pathologist time, potential pathologist variability from manual scoring and support pathologist decision making, a digital image analysis algorithm that identifies tumor cells and quantifies the DKK1 signal was developed. Following CLIA guidelines the DKK1 RNAscope chromogenic in situ hybridization assay and digital image analysis algorithm were successfully validated for sensitivity, specificity, accuracy, and precision. The DKK1 RNAscope assay in conjunction with the digital image analysis solution is acceptable for prospective screening of G/GEJ adenocarcinoma patients. The work described here will further advance the companion diagnostic development of our DKK1 RNAscope assay and could generally be used as a guide for the validation of RNAscope assays with digital image quantification.
MeSH term(s)	Adenocarcinoma/diagnosis ; Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Adult ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Biomarkers, Tumor/analysis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor ; Clinical Trials, Phase II as Topic ; Esophageal Neoplasms/diagnosis ; Esophageal Neoplasms/drug therapy ; Esophageal Neoplasms/genetics ; Esophageal Neoplasms/pathology ; Esophagogastric Junction/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Image Processing, Computer-Assisted/methods ; In Situ Hybridization/methods ; Intercellular Signaling Peptides and Proteins/analysis ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Male ; Middle Aged ; Multicenter Studies as Topic ; Prospective Studies ; RNA, Messenger/analysis ; RNA, Messenger/metabolism ; Retrospective Studies ; Stomach Neoplasms/diagnosis ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/genetics ; Stomach Neoplasms/pathology ; Wnt Signaling Pathway/drug effects ; Wnt Signaling Pathway/genetics
Chemical Substances	Biomarkers, Tumor ; DKK1 protein, human ; Intercellular Signaling Peptides and Proteins ; RNA, Messenger
Language	English
Publishing date	2021-05-10
Publishing country	England
Document type	Journal Article ; Validation Study
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-89060-3
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Article ; Online: A digital assay for programmed death-ligand 1 (22C3) quantification combined with immune cell recognition algorithms in non-small cell lung cancer

Will Paces / Elliott Ergon / Elizabeth Bueche / G. Dave Young / Vitria Adisetiyo / Cris Luengo / Meredith James / Charles Caldwell / Dannah Miller / Morgan Wambaugh / Geoffrey Metcalf / Roberto Gianani

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 11

Abstract: Abstract PD-L1 (22C3) checkpoint inhibitor therapy represents a mainstay of modern cancer immunotherapy for non-small cell lung cancer (NSCLC). In vitro diagnostic (IVD) PD-L1 antibody staining is widely used to predict clinical intervention efficacy. ... ...

Abstract	Abstract PD-L1 (22C3) checkpoint inhibitor therapy represents a mainstay of modern cancer immunotherapy for non-small cell lung cancer (NSCLC). In vitro diagnostic (IVD) PD-L1 antibody staining is widely used to predict clinical intervention efficacy. However, pathologist interpretation of this assay is cumbersome and variable, resulting in poor positive predictive value concerning patient therapy response. To address this, we developed a digital assay (DA) termed Tissue Insight (TI) 22C3 NSCLC, for the quantification of PD-L1 in NSCLC tissues, including digital recognition of macrophages and lymphocytes. We completed clinical validation of this digital image analysis solution in 66 NSCLC patient samples, followed by concordance studies (comparison of PD-L1 manual and digital scores) in an additional 99 patient samples. We then combined this DA with three distinct immune cell recognition algorithms for detecting tissue macrophages, alveolar macrophages, and lymphocytes to aid in sample interpretation. Our PD-L1 (22C3) DA was successfully validated and had a scoring agreement (digital to manual) higher than the inter-pathologist scoring. Furthermore, the number of algorithm-identified immune cells showed significant correlation when compared with those identified by immunohistochemistry in serial sections stained by double immunofluorescence. Here, we demonstrated that TI 22C3 NSCLC DA yields comparable results to pathologist interpretation while eliminating the intra- and inter-pathologist variability associated with manual scoring while providing characterization of the immune microenvironment, which can aid in clinical treatment decisions.
Keywords	Medicine ; R ; Science ; Q
Subject code	616 ; 610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The pancreas in human type 1 diabetes: providing new answers to age-old questions.

Atkinson, Mark A / Gianani, Roberto

Current opinion in endocrinology, diabetes, and obesity

2009 Volume 16, Issue 4, Page(s) 279–285

Abstract: Purpose of review: Although studies of pancreata from type 1 diabetes (T1D) patients largely fell dormant for a period of decades, research efforts have recently been 'rekindled' in this area to address, using modern techniques, many unanswered ... ...

Abstract	Purpose of review: Although studies of pancreata from type 1 diabetes (T1D) patients largely fell dormant for a period of decades, research efforts have recently been 'rekindled' in this area to address, using modern techniques, many unanswered questions related to the pathogenesis of this disease. Recent findings: As historically noted, a pancreatic infiltrate commonly referred to as 'insulitis' is present at the symptomatic onset of T1D. Recent studies have further characterized this infiltrate both in terms of its cellular composition as well as the mechanisms that likely underlie beta cell death in T1D. In addition, the notion that the pancreas from T1D patients is completely devoid of insulin producing cells years after the onset of disease has been challenged, whereas the concepts of whether beta cell regeneration or replication are present have also been subject to much debate. Novel concepts regarding the rate and degree of beta cell loss throughout the natural history of the disease have also been put forward to aid in explaining the disorder's pathogenesis. Summary: Although answers to many long-standing questions in T1D have recently been addressed, perhaps the main finding has been one supporting a disease of remarkable heterogeneity. However, additional lessons remain to be learned from the pancreas in T1D. Hence, attempts aimed at organizing the scientific community to address these issues are ongoing, particularly those from collaborative efforts, including the Belgium Organ Donor Consortium and the Network for Pancreatic Organ Donors with Diabetes (nPOD).
MeSH term(s)	Blood Glucose/metabolism ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/prevention & control ; Diabetes Mellitus, Type 1/therapy ; Humans ; Models, Biological ; Pancreas/pathology
Chemical Substances	Blood Glucose
Language	English
Publishing date	2009-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2272017-0
ISSN	1752-2978 ; 1752-296X
ISSN (online)	1752-2978
ISSN	1752-296X
DOI	10.1097/MED.0b013e32832e06ba
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Article ; Online: Kilham Rat Virus-induced type 1 diabetes involves beta cell infection and intra-islet JAK-STAT activation prior to insulitis.

Alkanani, Aimon K / Hara, Naoko / Gianani, Roberto / Zipris, Danny

Virology

2014 Volume 468-470, Page(s) 19–27

Abstract: We used the LEW1.WR1 rat model of Kilham Rat Virus (KRV)-induced type 1 diabetes (T1D) to test the hypothesis that disease mechanisms are linked with beta cell infection and intra-islet immune activation prior to insulitis. KRV induces genes involved in ... ...

Abstract	We used the LEW1.WR1 rat model of Kilham Rat Virus (KRV)-induced type 1 diabetes (T1D) to test the hypothesis that disease mechanisms are linked with beta cell infection and intra-islet immune activation prior to insulitis. KRV induces genes involved in type I and type II interferon pathways in islet cell lines in vitro and in islets from day-5-infected animals in vivo via mechanisms that do not involve insulitis, beta cell apoptosis, or impaired insulin expression. Immunohistochemistry studies indicated that KRV protein is expressed in beta cells 5 days following infection. KRV induces the phosphorylation of Janus Kinase 1/2 (JAK1/2) and signal transducer and activator of transcription 1 (STAT-1) in islet cells via a mechanism that could involve TLR9 and NF-κB pathways. These data demonstrate for the first time that KRV-induced islet destruction is associated with beta cell infection and intra-islet innate immune upregulation early in the disease process.
MeSH term(s)	Animals ; Cell Line ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/virology ; Inflammation/metabolism ; Islets of Langerhans/cytology ; Islets of Langerhans/physiology ; Islets of Langerhans/virology ; Janus Kinase 1/genetics ; Janus Kinase 1/metabolism ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Parvovirus/physiology ; Rats ; Rats, Inbred Strains ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; Signal Transduction ; Specific Pathogen-Free Organisms
Chemical Substances	STAT1 Transcription Factor ; Stat1 protein, rat ; Jak1 protein, rat (EC 2.7.10.2) ; Jak2 protein, rat (EC 2.7.10.2) ; Janus Kinase 1 (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2014-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2014.07.041
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Article ; Online: CD19+IgM+ cells demonstrate enhanced therapeutic efficacy in type 1 diabetes mellitus.

Vonberg, Andrew D / Acevedo-Calado, Maria / Cox, Aaron R / Pietropaolo, Susan L / Gianani, Roberto / Lundy, Steven K / Pietropaolo, Massimo

JCI insight

2018 Volume 3, Issue 23

Abstract: We describe a protective effect on autoimmune diabetes and reduced destructive insulitis in NOD.scid recipients following splenocyte injections from diabetic NOD donors and sorted CD19+ cells compared with NOD.scid recipients receiving splenocytes alone. ...

Abstract	We describe a protective effect on autoimmune diabetes and reduced destructive insulitis in NOD.scid recipients following splenocyte injections from diabetic NOD donors and sorted CD19+ cells compared with NOD.scid recipients receiving splenocytes alone. This protective effect was age specific (only CD19+ cells from young NOD donors exerted this effect; P < 0.001). We found that the CD19+IgM+ cell is the primary subpopulation of B cells that delayed transfer of diabetes mediated by diabetogenic T cells from NOD mice (P = 0.002). Removal of IgM+ cells from the CD19+ pool did not result in protection. Notably, protection conferred by CD19+IgM+ cotransfers were not dependent on the presence of Tregs, as their depletion did not affect their ability to delay onset of diabetes. Blockade of IL-10 with neutralizing antibodies at the time of CD19+ cell cotransfers also abrogated the therapeutic effect, suggesting that IL-10 secretion was an important component of protection. These results were strengthened by ex vivo incubation of CD19+ cells with IL-5, resulting in enhanced proliferation and IL-10 production and equivalently delayed diabetes progression (P = 0.0005). The potential to expand CD19+IgM+ cells, especially in response to IL-5 stimulation or by pharmacologic agents, may be a new therapeutic option for type 1 diabetes.
MeSH term(s)	Animals ; Antibodies, Neutralizing ; Antigens, CD19/therapeutic use ; B-Lymphocytes ; Cell Proliferation ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/therapy ; Female ; Histocompatibility Antigens Class I ; Immunoglobulin M/therapeutic use ; Interleukin-10/metabolism ; Interleukin-5/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID
Chemical Substances	Antibodies, Neutralizing ; Antigens, CD19 ; CD19 antigen, mouse ; Histocompatibility Antigens Class I ; Immunoglobulin M ; Interleukin-5 ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2018-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.99860
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Carcinosarcoma of the uterus metastasizing to the scalp

Gianani Roberto / Gandhi Sumul / Bero Jennifer

Scripta Medica, Vol 44, Iss 2, Pp 95-

2013 Volume 95

Keywords	Medicine ; R
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Medical Society of the Republic of Srpska, Banja Luka, University of Banja Luka. Faculty of Medicine
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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