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Article ; Online: Neoplastic Progression in Neuroendocrine Neoplasms of the Pancreas.

Luchini, Claudio / Scarpa, Aldo

Archives of pathology & laboratory medicine

2023

Abstract: Context.—: Pancreatic neuroendocrine neoplasms (PanNENs) represent a heterogeneous group of epithelial tumors of the pancreas showing neuroendocrine differentiation. These neoplasms are classified into well-differentiated pancreatic neuroendocrine ... ...

Abstract	Context.—: Pancreatic neuroendocrine neoplasms (PanNENs) represent a heterogeneous group of epithelial tumors of the pancreas showing neuroendocrine differentiation. These neoplasms are classified into well-differentiated pancreatic neuroendocrine tumors (PanNETs), which include G1, G2, and G3 tumors, and poorly differentiated pancreatic neuroendocrine carcinomas (PanNECs), which are G3 by definition. This classification mirrors clinical, histologic, and behavioral differences and is also supported by robust molecular evidence. Objective.—: To summarize and discuss the state of the art regarding neoplastic progression of PanNENs. A better comprehension of the mechanisms underpinning neoplastic evolution and progression of these neoplasms may open new horizons for expanding the biologic knowledge and ultimately for addressing new therapeutic strategies for patients with PanNEN. Data sources.—: Literature review of published studies and the authors' own work. Conclusions.—: PanNETs can be seen as a unique category, where G1-G2 tumors may progress to G3 tumors mainly driven by DAXX/ATRX mutations and alternative lengthening of telomeres. Conversely, PanNECs display totally different histomolecular features more closely related to pancreatic ductal adenocarcinoma, including TP53 and Rb alterations. They seem to derive from a nonneuroendocrine cell of origin. Even the study of PanNEN precursor lesions corroborates the rationale of considering PanNETs and PanNECs as separate and distinct entities. Improving the knowledge regarding this dichotomous distinction, which guides tumor evolution and progression, will represent a critical basis for PanNEN precision oncology.
Language	English
Publishing date	2023-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	194119-7
ISSN	1543-2165 ; 0363-0153 ; 0096-8528 ; 0003-9985
ISSN (online)	1543-2165
ISSN	0363-0153 ; 0096-8528 ; 0003-9985
DOI	10.5858/arpa.2022-0417-RA
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Article ; Online: The landscape of molecular alterations in pancreatic and small intestinal neuroendocrine tumours.

Scarpa, Aldo

Annales d'endocrinologie

2019 Volume 80, Issue 3, Page(s) 153–158

Abstract: Gastroenteropancreatic Neuroendocrine Neoplasms (GEP-NENs) arise throughout the gut and feature varying biological behaviour and malignant potential. GEP-NENs include two genetically different entities, well-differentiated neuroendocrine tumours (NETs) ... ...

Abstract	Gastroenteropancreatic Neuroendocrine Neoplasms (GEP-NENs) arise throughout the gut and feature varying biological behaviour and malignant potential. GEP-NENs include two genetically different entities, well-differentiated neuroendocrine tumours (NETs) and poorly differentiated neuroendocrine carcinomas (NEC). NECs are characterized by a dismal prognosis and by distinctive TP53 and RB1 inactivation which sets them apart from NETs. The latter, conversely, have a wide spectrum of aggressiveness and molecular alterations. Knowledge on their biology has recently expanded thanks to high-throughput studies focused on two important groups of well-differentiated neuroendocrine neoplasms: pancreatic (PanNETs) and small intestinal (SiNETs) tumours. PanNETs have been among the most studied also due to genetic syndromes featuring their onset. Research stemming from this observation has uncovered the inactivation of MEN1, VHL, TSC1/2, and the hyperactivation of the PI3K/mTOR pathway as distinctive biological features of these neoplasms. Next-Generation Sequencing added information on the role of telomere lengthening via ATRX/DAXX inactivation in a fraction of PanNETs, while other display shortened telomeres and recurrent chromosomal alterations. The data so far disclosed a heterogeneous combination of driver events, yet converging into four pathways including DNA damage repair, cell cycle regulation, PI3K/mTOR signalling and telomere maintenance. SiNETs showed a lesser relationship with mutational driver events, even in the case of familial cases. High throughput studies identified putative driver mutations in CDKN1 and APC which, however, were reported in a minor fraction (∼10%) of cases. Tumorigenesis of SiNETs seems to depend more on chromosomal alterations (loss of chromosome 8, gains at 4, 5 and 20) and epigenetic events, which converge to hyperactivate the PI3K/mTOR, MAPK and Wnt pathways. While calling for further integrative studies, these data lay previous and recent findings in a more defined frame and provide clinical research with several candidate markers for patient stratification and companion diagnostics.
MeSH term(s)	Cyclin-Dependent Kinase Inhibitor p21/genetics ; Epigenesis, Genetic ; Gene Amplification ; High-Throughput Nucleotide Sequencing ; Humans ; Intestinal Neoplasms/genetics ; Intestinal Neoplasms/physiopathology ; Intestine, Small ; Mitogen-Activated Protein Kinases/genetics ; Molecular Targeted Therapy ; Mutation ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/physiopathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/physiopathology ; Phosphatidylinositol 3-Kinases/genetics ; Signal Transduction ; Syndrome ; TOR Serine-Threonine Kinases/genetics ; Wnt Signaling Pathway/genetics
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p21 ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2019-04-11
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	299-9
ISSN	2213-3941 ; 0003-4266
ISSN (online)	2213-3941
ISSN	0003-4266
DOI	10.1016/j.ando.2019.04.010
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Article ; Online: Microsatellite instability in pancreatic and ampullary carcinomas: histology, molecular pathology, and clinical implications.

Luchini, Claudio / Scarpa, Aldo

Human pathology

2022 Volume 132, Page(s) 176–182

Abstract: Microsatellite instability (MSI)/defective DNA mismatch repair (dMMR) represents an important molecular alteration with diagnostic, prognostic, and predictive value. The increasing interest toward this genetic alteration is given to the high response ... ...

Abstract	Microsatellite instability (MSI)/defective DNA mismatch repair (dMMR) represents an important molecular alteration with diagnostic, prognostic, and predictive value. The increasing interest toward this genetic alteration is given to the high response rate of MSI/dMMR tumors to immunotherapy. There are different cancers in the periampullary region that can harbor MSI/dMMR, and significant morphological-molecular correlates should be acknowledged in this district: (1) pancreatic ductal adenocarcinoma (PDAC): in this tumor category, the prevalence of MSI/dMMR is about 1-2%, and medullary and colloid variants are the most typically involved; (2) ampullary adenocarcinoma: here the prevalence of MSI/dMMR is up to 18%, and in this neoplastic group, MSI/dMMR is more commonly found in the intestinal subtype; (3) pancreatic acinar cell carcinoma: here the prevalence of MSI/dMMR is up to 14%; and (4) pancreatic and ampullary neuroendocrine carcinoma: in this tumor category, the prevalence of MSI/dMMR is up to 5-8%, and this molecular alteration should be assessed also in cases of mixed neuroendocrine-non-neuroendocrine neoplasms. Given the clinical importance of MSI/dMMR and its not-negligible prevalence among the different carcinomas arising in this district, its assessment should become part of the routine diagnostic workflow at least for the most typical histotypes. The test of choice is represented by immunohistochemistry for PDAC and ampullary carcinomas, and by direct molecular analyses including MSI-based polymerase chain reaction and next-generation sequencing for acinar cell and neuroendocrine carcinomas.
MeSH term(s)	Humans ; Ampulla of Vater/pathology ; Microsatellite Instability ; Pathology, Molecular ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Carcinoma, Pancreatic Ductal/pathology ; DNA Mismatch Repair ; Colorectal Neoplasms/genetics ; Pancreatic Neoplasms
Language	English
Publishing date	2022-06-14
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2022.06.009
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Article ; Online: Co-occurring IPMN and pancreatic cancer: the same or different? An overview from histology to molecular pathology.

Omori, Yuko / Furukawa, Toru / Scarpa, Aldo / Luchini, Claudio

Journal of clinical pathology

2023 Volume 76, Issue 11, Page(s) 734–739

Abstract: Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is one of the most well-established precursors of pancreatic cancer. Its progression to acquire invasiveness is a complex process, based on the accumulation of morphological and genetic ... ...

Abstract	Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is one of the most well-established precursors of pancreatic cancer. Its progression to acquire invasiveness is a complex process, based on the accumulation of morphological and genetic alterations. Recent advances in DNA sequencing also showed that co-occurring IPMNs and pancreatic cancers could be totally independent, further complicating our understanding of this complex scenario. The distinction between IPMN and related pancreatic cancer vs IPMN and co-occurring-but not related-pancreatic cancer is a challenging task in routine diagnostic activity, but may have important implications for precision oncology. Of note, recent multiregional sequencing-based studies focused not only on IPMN multi-step tumourigenesis, but also on the divergent intratumoural heterogeneity of this neoplasm. Globally considered, there are three different situations in which co-occurring IPMNs and invasive carcinomas can be found in the same pancreata, indicated with different terminologies: (1) IPMN-associated carcinoma: this definition indicates a carcinoma arising from an IPMN and can be also defined as IPMN-derived carcinoma, sequential or likely related; (2) independent IPMN and invasive carcinoma: the two lesions are not related, and this situation is defined as concomitant, de novo or likely independent; (3) branch-off pathway, where an invasive carcinoma and an adjacent IPMN develop divergently in a forked fashion from a common ancestral clone. In this review, we aim at clarifying the most important nomenclature/definitions of these different situations, also providing an overview of the molecular state-of-the-art and of the clinical implications of this complex landscape.
MeSH term(s)	Humans ; Carcinoma, Pancreatic Ductal/diagnosis ; Carcinoma, Pancreatic Ductal/genetics ; Pancreatic Intraductal Neoplasms/diagnosis ; Pancreatic Intraductal Neoplasms/genetics ; Pathology, Molecular ; Adenocarcinoma, Mucinous/diagnosis ; Adenocarcinoma, Mucinous/genetics ; Adenocarcinoma, Mucinous/pathology ; Precision Medicine ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Retrospective Studies ; Pancreatic Neoplasms
Language	English
Publishing date	2023-07-27
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80261-x
ISSN	1472-4146 ; 0021-9746
ISSN (online)	1472-4146
ISSN	0021-9746
DOI	10.1136/jcp-2023-209012
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Article ; Online: Impact of a centralized archive for pathology laboratories on the health system.

Eccher, Albino / Scarpa, Aldo / Dei Tos, Angelo Paolo

Pathology, research and practice

2023 Volume 245, Page(s) 154488

Abstract: The pathology archive of any hospital is likely to contain tens of thousands of slides and formalin-fixed and paraffin-embedded (FFPE) blocks, with their number constantly increasing. As a result, serious space and management issues are created. There ... ...

Abstract	The pathology archive of any hospital is likely to contain tens of thousands of slides and formalin-fixed and paraffin-embedded (FFPE) blocks, with their number constantly increasing. As a result, serious space and management issues are created. There has always been a favorable location for the pathology laboratory to rapidly and efficiently collect specimens and to meet the different service requirements of clinicians and patients. However, archiving may be one of the most neglected issues in the planning of spaces and activities, so much so that many laboratories are currently in trouble and looking for space inside and outside their hospitals. Another crucial issue is related to the environmental conditions of the identified preservation place, which, based on their characteristics, probably provide suboptimal habitats in most cases. For FFPE blocks, controlled temperature (<27 °C) and humidity (>30% and <70%) are recommended, with control systems for parasite infestation. For glass slides, systems suitable for guaranteeing their safety, traceability and conservation suitable for possible revision are recommended. The aim of this position paper is to outline the issues that currently exist in archives and to suggest a rational health policy solution to overcome the problems raised.
MeSH term(s)	Humans ; Laboratories ; Paraffin Embedding ; Tissue Fixation ; Formaldehyde
Chemical Substances	Formaldehyde (1HG84L3525)
Language	English
Publishing date	2023-04-25
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	391889-0
ISSN	1618-0631 ; 0344-0338
ISSN (online)	1618-0631
ISSN	0344-0338
DOI	10.1016/j.prp.2023.154488
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Article ; Online: Fusion genes in pancreatic tumors.

Gkountakos, Anastasios / Singhi, Aatur D / Westphalen, C Benedikt / Scarpa, Aldo / Luchini, Claudio

Trends in cancer

2024

Abstract: Gene fusions and rearrangements play a crucial role in tumor biology. They are rare events typically detected in KRAS wild-type (WT) pancreatic tumors. Their identification can inform clinical management by enabling precision oncology, as fusions ... ...

Abstract	Gene fusions and rearrangements play a crucial role in tumor biology. They are rare events typically detected in KRAS wild-type (WT) pancreatic tumors. Their identification can inform clinical management by enabling precision oncology, as fusions involving BRAF, FGFR2, RET, NTRK, NRG1, and ALK represent actionable targets in KRAS-WT cancers, and serve diagnostic purposes since fusions involving PRKACA/B represent the diagnostic hallmark of intraductal oncocytic papillary neoplasms (IOPNs). Although they are rare, the therapeutic and diagnostic importance of these genomic events should not be underestimated, highlighting the need for quality-ensured molecular diagnostics in the management of cancer. Herein we review the existing literature on the role of fusion genes in pancreatic tumors and their clinical potential as effective biomarkers and therapeutic targets.
Language	English
Publishing date	2024-02-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2024.01.009
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Article: Digital pathology all stars.

Eccher, Albino / Girolami, Ilaria / Scarpa, Aldo

Journal of pathology informatics

2022 Volume 13, Page(s) 100125

Abstract: Digital pathology plays an important role in accelerating the progression of healthcare and the potential benefits of adopting digital technologies have been solidly ... ...

Abstract	Digital pathology plays an important role in accelerating the progression of healthcare and the potential benefits of adopting digital technologies have been solidly established
Language	English
Publishing date	2022-07-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2579241-6
ISSN	2153-3539 ; 2229-5089
ISSN (online)	2153-3539
ISSN	2229-5089
DOI	10.1016/j.jpi.2022.100125
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Article ; Online: Hepatoid tumors of the gastrointestinal/pancreatobiliary district: morphology, immunohistochemistry, and molecular profiles.

Mattiolo, Paola / Scarpa, Aldo / Luchini, Claudio

Human pathology

2022 Volume 132, Page(s) 169–175

Abstract: Hepatoid tumors (HTs) histologically resemble hepatocellular carcinoma (HCC) but manifest outside the liver. Regarding immunohistochemistry (IHC), the classical markers of hepatoid differentiation are Hep Par-1, CD10, and arginase-1. This study provides ... ...

Abstract	Hepatoid tumors (HTs) histologically resemble hepatocellular carcinoma (HCC) but manifest outside the liver. Regarding immunohistochemistry (IHC), the classical markers of hepatoid differentiation are Hep Par-1, CD10, and arginase-1. This study provides a critical overview of HT in the gastrointestinal/biliopancreatic system, which is the most common site of origin. Gastric HTs are malignant neoplasms recognized by the current WHO classification as a variant of adenocarcinoma. In addition to the classic IHC markers, SALL4 and claudin-6 can help exclude a metastatic HCC at this site. Next-generation sequencing revealed the most common alterations, including TP53 mutation, microsatellite instability (MSI), and Her2 amplification. Esophageal HTs are exceptionally rare and usually arise in the context of Barrett's esophagus. In the intestine, HTs are classified within the adenocarcinoma spectrum and manifest more often in the background of inflammatory bowel disease. Regarding their molecular profile, recurrent alterations included MSI and NCOA4-RET fusions. In the pancreas, the current WHO classification acknowledges HT only as a possible variant of ductal adenocarcinoma, characterized by a poor prognosis. However, at this site, neuroendocrine tumors (NETs) and solid pseudopapillary neoplasms (SPNs) may also show hepatoid differentiation. Hepatoid NETs show aggressive behavior, whereas hepatoid SPNs harbor CTNNB1 mutations and are characterized by an indolent clinical course. Lastly, biliary HTs belong to the adenocarcinoma category and usually show a poor prognosis. In conclusion, gastrointestinal/pancreatobiliary HTs show specific histomolecular features, which should be considered for improving routine diagnostic activity and clinical management.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/pathology ; Liver Neoplasms/pathology ; Immunohistochemistry ; Biomarkers, Tumor/genetics ; Adenocarcinoma/pathology ; Gastrointestinal Neoplasms/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2022-06-14
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2022.06.011
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Article ; Online: Undifferentiated Sarcomatoid Carcinoma of the Pancreas: From Histology and Molecular Pathology to Precision Oncology.

Gkountakos, Anastasios / Simbolo, Michele / Bariani, Elena / Scarpa, Aldo / Luchini, Claudio

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Undifferentiated sarcomatoid carcinoma of the pancreas (SCP) is a rare and aggressive subtype of pancreatic cancer. Histologically, SCP is a poorly differentiated tumor characterized by the lack of glandular differentiation and the presence of ... ...

Abstract	Undifferentiated sarcomatoid carcinoma of the pancreas (SCP) is a rare and aggressive subtype of pancreatic cancer. Histologically, SCP is a poorly differentiated tumor characterized by the lack of glandular differentiation and the presence of mesenchymal-like, spindle-shaped tumor cells. Due to its rarity, only sporadic cases have been reported, while its molecular characterization has not been sufficiently described. Surgical resection with curative intent is the gold-standard of SCP management, but this strategy is possible only in a small proportion of cases due to SCP early metastasization. Although SCP is generally associated with a poor prognosis, some clinical cases amenable to surgical resection and followed by adjuvant chemotherapy have demonstrated a remarkably long survival. Preliminary molecular insights on the SCP molecular landscape have demonstrated the recurrent presence of
MeSH term(s)	Chemotherapy, Adjuvant/methods ; Humans ; Immunotherapy/methods ; Immunotherapy/trends ; Medical Oncology/methods ; Mutation ; Pancreas/pathology ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/pathology ; Precision Medicine/methods ; Proto-Oncogene Proteins p21(ras)/genetics ; Sarcoma/physiopathology ; Tumor Suppressor Protein p53/genetics ; Pancreatic Neoplasms
Chemical Substances	KRAS protein, human ; Tumor Suppressor Protein p53 ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2022-01-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031283
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Article ; Online: Atypical meningiomas with an immunohistochemical profile consistent with hypermetabolic or proliferative molecular groups show high mitotic index, chromosomal instability, and higher recurrence risk.

Barresi, Valeria / Ammendola, Serena / Simbolo, Michele / Pedron, Serena / Caffo, Maria / Scarpa, Aldo

Virchows Archiv : an international journal of pathology

2023 Volume 483, Issue 1, Page(s) 97–104

Abstract: The use of adjuvant radiotherapy is controversial for atypical meningiomas undergoing gross total resection. It has recently been proposed that meningiomas may be classified into four molecular groups (MG): immunogenic (MG1), benign NF2-wildtype (MG2), ... ...

Abstract	The use of adjuvant radiotherapy is controversial for atypical meningiomas undergoing gross total resection. It has recently been proposed that meningiomas may be classified into four molecular groups (MG): immunogenic (MG1), benign NF2-wildtype (MG2), hypermetabolic (MG3), and proliferative (MG4). The two latter have the worst prognosis, and it has been suggested that they can be identified using ACADL and MCM2 immunostainings. We studied 55 primary atypical meningiomas, treated with gross total resection and no adjuvant therapies, to assess whether ACADL and MCM2 immuno-expression may identify patients at higher recurrence risk, thus requiring adjuvant treatments. Twelve cases resulted ACADL-/MCM2-, 9 ACADL + /MCM2-, 17 ACADL + /MCM2 + , and 17 ACADL-/MCM2 + . MCM2 + meningiomas displayed more frequent atypical features (prominent nucleoli, small cells with high nuclear-to-cytoplasmic ratio) and CDKN2A hemizygous deletion (HeDe) (P = 0.011). The immunoexpression of ACADL and/or MCM2 was significantly associated with higher mitotic index, 1p and 18q deletions, increased recurrence rate (P = 0.0006), and shorter recurrence-free survival (RFS) (P = 0.032). At multivariate analysis, carried out including ACADL/MCM2 immuno-expression, mitotic index, and CDKN2A HeDe as covariates, this latter resulted a significant and independent prognosticator of shorter RFS (P = 0.0003).
MeSH term(s)	Humans ; Meningioma/genetics ; Meningeal Neoplasms/genetics ; Meningeal Neoplasms/surgery ; Mitotic Index ; Radiotherapy, Adjuvant ; Chromosomal Instability ; Neoplasm Recurrence, Local ; Retrospective Studies
Language	English
Publishing date	2023-04-04
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1184867-4
ISSN	1432-2307 ; 0945-6317
ISSN (online)	1432-2307
ISSN	0945-6317
DOI	10.1007/s00428-023-03537-2
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