Author: xuchen.zhang

Welcome to PBPS Challenging Cases (Case 1)

 Instructions for participation:

  1. Review this digital case as though it arrived to you in consultation. 
  2. Provide your diagnosis, differential diagnoses and suggested ancillary tests at the bottom of this page within 2 weeks of the post date*.
  3. All responses will be collated and compiled along with the final diagnosis.
  4. Please return to this page in the coming weeks to view the final diagnosis as well as others’ responses. 

PBPS Challenging Case 1 – July 11, 2022

Clinical history:
A 32-year-old male with a history of Hodgkin’s lymphoma and biliary atresia. He had undergone transplant and was found to have distal pancreas mass during surveillance.

Pathologic findings:

Distal pancreatectomy revealed a 4.3 cm, well circumscribed, predominantly solid mass abutting the splenic vein. 

Representative scanned H&E slides (select link to open images)

H&E 1

https://pathpresenter.net/public/display?token=f8789272

H&E 2

https://pathpresenter.net/public/display?token=ca3927d4

Select scanned immunohistochemical (IHC) stains (select link to open images):

Cam 5.2 IHC

https://pathpresenter.net/public/display?token=6e1b407d

Calretinin IHC

https://pathpresenter.net/public/display?token=b4d3bde0

Beta-catenin IHC

https://pathpresenter.net/public/display?token=cb61d7fb

Summary of all IHC stains performed:

– Express: CAM 5.2 (scanned), CK19, CK5, Ber-EP4, claudin-4 (focal), calretinin (scanned), SATB2 (patchy), CD99 (patchy, membranous), inhibin (rare cells), CD10 (focal) and a Ki67 stain reveals a
proliferative rate of 15%.

– Do NOT express: CK7, CK20, CDX2, trypsin, chymotrypsin, carboxyl ester lipase, chromogranin, synaptophysin, INSM1, insulin, glucagon, somatostatin, pancreatic polypeptide, p40, p63, monoclonal CEA, EMA, TTF1, HepPar-1, Glypican-3, GATA3, PAX8, NKX3.1, SF-1, WT1, D2-40, SALL4, CD117, DOG1, CD34, SMA, calponin, ERG, CD45, S100, SOX10, melanoma cocktail

– Other: aberrant beta-catenin (nuclear and cytoplasmic, scanned), E-cadherin (membranous), p53 wild-type, RB1 retained, ATRX retained, MMR retained, mucicarmine negative

Next generation sequencing (NGS) result: No mutations, deletions or fusion detected

Case was submitted by: Dr. Klaudia Nowak from Toronto General Hospital, and Dr. Olca Basturk from Memorial Sloan Kettering Cancer Center.

*NOTE: The submission of case discussion has been closed.

*Thank you all for your feedback on the Pancreatobiliary Pathology Society’s first challenging case. A panel of experts (Drs. Volkan Adsay, Michelle Reid, and Huamin Wang) has also reviewed the case and rendered their diagnoses. Please see the discussion summary now posted HERE for details. 

Abstract Award in USCAP 2022

Pancreatobiliary Pathology Society Abstract Award

Dear members of the PBPS,

The PBPS is now accepting applications for this year’s PBPS Abstract Award. This award will go to a pathology trainee with an abstract (poster/platform) in pancreatobiliary pathology presented at the 2022 annual USCAP meeting. Submitted abstracts will be evaluated for originality, scientific merit and presentation, and the winner will receive a $500 prize. At least one author should be a PBPS member. Trainees are strongly encouraged to apply.

The deadline for submission of Award applications is February 15, 2022.

Please email your completed abstract in Word format along with the information below to the education committee chair Dr. Michelle Reid (michelle.reid@emory.edu).

Name:
Training Institution:
Position:
PGY Year:
Date/Time of Presentation:
Abstract Name:
Poster Number (if applicable):

Case 4: Quarter 3, 2021

Clinical History

A 2-year-old-baby presented as a transfer from an outside hospital (OSH) due to concerns for possible acute cholecystitis. The patient has a history of abdominal pain for the last 2 weeks. The laboratory tests from the OSH were notable for leukocytosis. An abdominal CT scan showed a thickened gallbladder wall with numerous polypoid, non-mobile lesions. Eventually, the patient underwent laparoscopic cholecystectomy.

Macroscopic Description
On gross examination, the gallbladder measured 8.8 x 1.5 x 1.2 cm, with multiple, scattered polypoid mucosal lesions mainly in the body and fundus. The largest lesion measured 2 cm in the greatest dimension (arrows) (Figure 1). No cholelithiasis was present.

Figure 1. Gross photograph of the gallbladder showing polypoid exophytic lesions on the mucosa.

Histologic/Cytologic Features 

Microscopic pictures of the gallbladder lesions are shown in Figures 2-4. As shown in Figure 2, The lesions had an intraluminal exophytic (mass-forming) growth pattern and papillary architecture (black arrows). Adjacent mucosa (white arrows) is also involved by papillary overgrowth of epithelium. Figure 3 showed that the neoplastic epithelial lining is composed of a combination of biliary (black arrow), gastric foveolar-type (white arrow), and intestinal-type epithelium with goblet cells (blue arrow). No high grade cytologic atypia or architectural abnormalities were identified. A higher-power image is shown in Figure 4 and highlights a collection of the lamina propria macrophages (black arrows).

Figure 2. Low-power view of the exophytic lesion, H&E stain.
Figure 3. Medium-power view of the exophytic lesion, H&E stain.
Figure 4. High-power view of the lamina propria of the lesion, H&E stain.

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Please select your diagnosis in the poll, then see the answer and the discussion in the links below.

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What is the diagnosis of the lesion?

View Results

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Answer: Intracholecystic papillary neoplasm

Final diagnosis:  

Intracholecystic papillary neoplasm

Educational Objectives and Discussion:

Educational Objectives

  1. To understand the definition of intracholecystic papillary neoplasm
    (ICPN) of the gallbladder by 2019 WHO Digestive System Tumours.
  2. To recognize the gallbladder lesions associated with metachromatic
    leukodystrophy (MLD), an unusual neurologic disease in pediatric patients.
  3. To discuss the differential diagnosis of ICPN.

Discussion

Intracholecystic papillary neoplasm (ICPN) is a precancerous lesion of the gallbladder. Per the 2019 WHO Digestive System Tumours [1], ICPN encompasses/replaces the previous terminologies, including biliary
adenoma, tubulopapillary adenoma, intracystic papillary neoplasm, and papillomatosis. Grossly, these tumors form distinct polypoid/exophytic intraluminal masses that are grossly visible. Microscopically, these tumors show papillary and/or tubular configuration with varying degrees of epithelial dysplasia. There are four morphologic patterns recognized: biliary, intestinal, gastric, oncocytic, or combination of these. These morphologic patterns contrast with classifications of intraductal papillary mucinous neoplasms (IPMN) of the pancreas in which oncocytic lesions (intraductal oncocytic papillary neoplasms (IOPN)) have been separated from IPMN due to distinct molecular findings. Mucosa surrounding ICPN may demonstrate dysplasia as well. About 50% of ICPNs are associated with invasive adenocarcinoma, but they have a better clinical outcome than conventional gallbladder adenocarcinomas [1, 2].

Our case exhibited low-grade ICPN with combined biliary, gastric, and intestinal differentiation. Adjacent mucosa also showed diffuse low-grade dysplasia. No high-grade dysplasia or invasive carcinoma was identified in extensively submitted sections. The aforementioned unusual findings in the gallbladder from a 2-year-old baby triggered further work-up since there is a well-known association between ICPN (previously called gallbladder papillomatosis) and metachromatic leukodystrophy (MLD) [3-5]. Genetic analysis was performed and the results revealed homozygous deletion of pathogenic variant c.1283C>T (p.Pro428Leu) in ARSA gene, which is associated with MLD. Brain MRI findings were non-specific and she has no history of developmental delay, neurologic symptoms, or regression.

MLD is a lysosomal storage disease caused by a deficiency of arylsulfatase A (ASA) with autosomal recessive inheritance in most cases. The ASA deficiency leads to the accumulation of sulfatides in the central and peripheral nervous system, which results in the destruction of the myelin sheath and eventually leads to neurologic symptoms such as seizures, loss of motor functions, and peripheral neuropathy [6]. Sufatide accumulation is also detected in other organs, e.g., the gallbladder, kidney, lymph nodes, liver, and bone marrow. The gallbladder epithelial cells and macrophages contain cytoplasmic inclusions on electron microscopic examination, consistent with sulfatide accumulation [3, 7]. Almost all case reports described the presence of collections of the lamina propria macrophages in the gallbladder [3, 4, 7, 8], as seen in our case (Figure 4). This accumulation of macrophages could show histologic overlap with cholesterolosis, a more common finding in the gallbladder. In MLD, Giemsa and toluidine blue stains will show metachromasia of the cytoplasm of macrophages, consistent with the accumulation of sulfatide deposits. In contrast, the accumulation of cholesterol esters and triglycerides can be highlighted on frozen tissue with Oil red O or Sudan black stains.

According to the age of disease onset, there are three clinical subtypes of MLD, including late infantile-onset, juvenile-onset, and adult-onset. Our patient showed no neurologic symptoms but was homozygous for mutation of the ARSA gene, which encodes ASA. Numerous mutations in the ARSA gene have been identified, and c.1283C_T mutation in our case is usually seen in juvenile or adult-onset phenotype [6]. That may explain the neurologic symptom-free status of our patient. A possible treatment for MLD so far is hematopoietic stem cell transplantation for selected cases [4]. MLD-associated gallbladder abnormalities occasionally appear before the onset of neurologic symptoms or an MLD diagnosis [3]. One case series with 34 patients reported that 76% of MLD patients showed gallbladder involvement [4]. The gallbladder abnormalities consist of benign and malignant conditions, e.g., cholecystitis, cholelithiasis, mucosal hyperplasia, polypoid lesions (now most lesions are under the category of ICPN), and adenocarcinoma [3-5]. In conclusion, gallbladder abnormalities, in particular polypoid lesions, are rare during childhood. This condition can be seen in cases with MLD, Peutz-Jeghers’ syndrome, and pancreaticobiliary malunion [8]. Pathologists should pay close attention to unusual gallbladder abnormalities in pediatric and adolescent patients to consider the above-mentioned possibilities and associated risk of malignancy.

Differential diagnosis:

Pyloric gland adenoma is composed of lobules of small, tightly packed, bland-looking glands that are morphologically similar to pyloric or Brunner glands. The uninvolved gallbladder mucosa is mostly devoid of dysplasia or pyloric gland metaplasia. Of note, pyloric gland nodules <0.5 cm arising in a background of pyloric gland metaplasia should not be designated as pyloric gland adenoma [9].
Reactive epithelial hyperplasia, commonly due to secondary causes (e.g., cholelithiasis, chronic cholecystitis, inflammatory bowel disease, primary sclerosing cholangitis), shows focal or diffuse papillary-shaped and elongated mucosal folds lined by bland epithelial cells with or without metaplastic changes. The presence of significant inflammation and no discrete, grossly visible mass-forming lesion, may help distinguish reactive hyperplasia from ICPN [1,10].
Invasive adenocarcinoma is present in about 50% of the ICPN cases at the time of diagnosis [2]. Gallbladder adenocarcinoma arising in ICPN is more commonly associated with papillary growth patterns, biliary epithelial lineage, and high-grade dysplasia. The invasive component is often a tubular adenocarcinoma, although other types, such as mucinous, adenosquamous, or neuroendocrine carcinoma, have also been reported. Extensive sampling is warranted because approximately 60% of ICPN with carcinoma showed ≤ 5mm of invasive focus, and the carcinoma may also occur away from the main ICPN lesion. Some patients with non-invasive ICPN can also die of new primary carcinoma in the biliary tract, typically long after the diagnosis of ICPN, possibly due to the field cancerization phenomenon. This observation supports long-term surveillance of these patients with ICPN even after resection [1, 2].

References:

  1. Basturk O, Aishima S, Esoposito I. World Health Organization Classification of Tumours. Intracholecystic papillary neoplasm. In: Digestive System Tumours. 2019, IARC, Lyon.
  2. Adsay V, Jang KT, Roa JC, Dursun N, Ohike N, Bagci P, Basturk O, Bandyopadhyay S, Cheng JD, Sarmiento JM, Escalona OT, Goodman M, Kong SY, Terry P. Intracholecystic papillary-tubular neoplasms (ICPN) of
    the gallbladder (neoplastic polyps, adenomas, and papillary neoplasms that are ≥1.0 cm): clinicopathologic and immunohistochemical analysis of 123 cases. Am J Surg Pathol. 2012 Sep;36(9):1279-301.
  3. McFadden K, Ranganathan S. Pathology of the gallbladder in a child with metachromatic leukodystrophy. Pediatr Dev Pathol. 2015 May-Jun;18(3):228-30.
  4. van Rappard DF, Bugiani M, Boelens JJ, van der Steeg AF, Daams F, de Meij TG, van Doorn MM, van Hasselt PM, Gouma DJ, Verbeke JI, Hollak CE, van Hecke W, Salomons GS, van der Knaap MS, Wolf NI. Gallbladder
    and the risk of polyps and carcinoma in metachromatic leukodystrophy. Neurology. 2016 Jul 5;87(1):103-11.
  5. Kim J, Sun Z, Ezekian B, Schooler GR, Prasad VK, Kurtzberg J, Rice HE, Tracy ET. Gallbladder abnormalities in children with metachromatic leukodystrophy. J Surg Res. 2017 Feb;208:187-191.
  6. Cesani M, Lorioli L, Grossi S, Amico G, Fumagalli F, Spiga I, Filocamo M, Biffi A. Mutation Update of ARSA and PSAP Genes Causing Metachromatic Leukodystrophy. Hum Mutat. 2016 Jan;37(1):16-27.
  7. Rodriguez-Waitkus PM, Byrd R, Hicks J. Metachromatic leukodystrophy and its effects on the gallbladder: a case report. Ultrastruct Pathol. 2011 Dec;35(6):271-6.
  8. Garavelli L, Rosato S, Mele A, Wischmeijer A, Rivieri F, Gelmini C, Sandonà F, Sassatelli R, Carlinfante G, Giovanardi F, Gemmi M, Della Giustina E, Amarri S, Banchini G, Bedogni G. Massive hemobilia and
    papillomatosis of the gallbladder in metachromatic leukodystrophy: a life-threatening condition. Neuropediatrics. 2009 Dec;40(6):284-6.
  9.  Basturk O, Aishima S, Esoposito I. World Health Organization Classification of Tumours. Pyloric gland adenoma of the gallbladder. In: Digestive System Tumours. 2019, IARC, Lyon.
  10. Umudum H, Gunbatili E, Sanal M, Ceyhan K. Primary diffuse papillary hyperplasia of the gallbladder. Pathology. 2006 Dec;38(6):591-2.

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Case contributed by:

Goo Lee, MD, PhD. University of Alabama at Birmingham

Rong Li, MD, PhD. Children’s of Alabama Benjamin Russell Hospital For Children

Conflict of Interest: NO

2021 PBPath Business Meeting agenda/minutes

Pancreatobiliary Pathology Society Members,

Alas, we will not be able to meet in person this year, therefore please find attached the 2021 Pancreatobiliary Pathology Society (PBPS) Annual Business meeting agenda/minutes for your review to learn what PBPS has accomplished: PBPath Business Meeting 2021

Two requests:
1. Listen to our PBPS Companion meeting speakers, submit your questions and attend the LIVE Question and Answer on Tuesday March 16, 2021 11-11:30 AM PST
2. Vote for our new member before March 20, 2021 (will only take 1 minute) https://www.surveymonkey.com/r/7PWVKV5

Can’t wait to see all of you in person next year!

Most appreciatively,
Grace E. Kim
Pancreatobiliary Pathology Society Secretary/Treasurer

USCAP 2021 Companion Society Program

Pancreatobiliary Pathology Society Companion Meeting USCAP 2021

Rondell Graham, MBBS, Mayo Clinic (Moderator)
Michelle D. Reid, MD, MSc, Emory University Hospital (Moderator)
Barbara A. Centeno, MD, H. Lee Moffitt Cancer Center & Research Institute
Vikram Deshpande, MBBS, MD, Massachusetts General Hospital, Harvard Medical School
Günter Klöppel, MD, PhD, Technical University of Munich
Giuseppe Zamboni, MD, University of Verona

Inflammatory Conditions of the Pancreatobiliary Tree 

This session includes 1.5 hours of on-demand educational content. This content can be viewed starting March 1. There will also be a live 30-minute Q&A session with the faculty on Tuesday, March 16, from 11:00 AM – 11:30 AM Pacific Time.

Chronic pancreatitis is a complex inflammatory process with rising incidence and prevalence, and no curative treatment for frequently intractable chronic pain. Despite advances in the field, challenges remain in the radiologic, endoscopic and histologic diagnosis, and the distinction of pancreatitis from cancer. Although some specific pathologic subtypes of pancreatitis have been described and characterized in the past decade, many pathologists are still unaware of their existence, clinicopathologic characteristics, management and genetic implications. Pathologists also struggle with formulating diagnoses, reporting terminology, and determining etiology, particularly on small biopsies, fine needle aspirations and bile duct brushings. In the past year alone numerous multidisciplinary international, consensus guideline manuscripts have made new recommendations regarding risk factors, etiology, management (endoscopic, surgical/non-surgical), and histopathology of chronic pancreatitis. The latter was aimed at clarifying the pathologist’s role in diagnosis, histopathologic criteria, standardizing reports, and limiting confusion in reporting and the literature. The Pancreatobiliary Pathology Society executive committee determined the theme, titles, content and speakers for this year’s companion meeting, with a mission to educate surgical and Cytopathologists on recent advances in inflammatory conditions of the pancreatobiliary tree. This year’s meeting will provide a 360-degree expert analysis and update on acute and chronic inflammatory conditions of pancreatobiliary tree, including specific entities acute/alcoholic pancreatitis (Dr. Günter Klöppel), paraduodenal pancreatitis (Dr. Giuseppe Zamboni), IgG4-related (autoimmune) pancreatitis (Dr. Vikram Deshpande), and the cytopathology of inflammatory lesions of the pancreatobiliary tree (Dr. Barbara Centeno).

 The program can be accessed by USCAP attendees here:

USCAP 2021 Annual Meeting

 Continuing Medical Education

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of The United States and Canadian Academy of Pathology and the Pancreatobiliary Pathology Society. The United States and Canadian Academy of Pathology is accredited by the ACCME to provide continuing medical education for physicians.

The United States and Canadian Academy of Pathology designates this Other activity (enduring materials and internet live activity) for a maximum of 2 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Live Q&A Session: Tue, March 16, 11:00 AM – 11:30 AM PT

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Message from the President

Message from the President

 

Pancreatobiliary Pathology Society (PBPS) Members,

We will all remember 2020 as a year filled with challenges and new ways of doing things, and many of our modified processes are spilling into 2021 as well.  With the upcoming USCAP meeting being virtual, we have been working to prepare a compelling agenda for our PBPS Companion Meeting, and I am pleased to report that we have a very fine program devoted to the topic of pancreatitis.  Our speakers will include Dr. Barbara Centeno (Cytopathology of inflammatory lesions of the pancreatobiliary tree), Dr. Vikram Deshpande (IgG4-related (autoimmune) pancreatitis), Dr. Günter Klöppel (Acute/alcoholic pancreatitis) and Dr. Giuseppe Zamboni (Paraduodenal pancreatitis).  The lectures will be prerecorded, so you can listen to them any time after they go live on March 1.  Because of the modified format, the session will only be 90 minutes this year.  Please access the talks via the USCAP website.  There will be a 30 minute live question and answer session, hosted by Michelle Reid, PBPS Education Committee Chair, on Tuesday, March 16 at 2:00 PM Eastern time.  You can enter your questions on-line as well, and Michelle will review them with the speakers.  We hope this will be a highly interactive Q&A session, and that the virtual format will allow even more participants to hear these lectures.

I also want to remind everyone about the PBPS Abstract Award competition. Our PBPS Education Committee will select the winning abstract for 2021, and the first author will receive a $500 prize.  All applications should be submitted no later than 2/15/2021.  Please see the PBPS website for details.

In other news, we have recently revamped our Journal Watch feature, kindly edited by Daniela Allende, PBPS Chair of Journal Watch Subcommittee – please keep an eye on our website for updates about excellent publications related to pancreatobiliary pathology.

We truly regret that we cannot gather in person this year – one of the hardest things about the pandemic of course is the restriction on seeing family, friends, and colleagues – but there is a light at the end of the tunnel, and we will look forward to future meetings when we can gather again to share our interests and catch up on our professional lives!

David Klimstra,  Pancreatobiliary Pathology Society President

 

 

Abstract Award in USCAP 2021

Pancreatobiliary Pathology Society Abstract Award

Dear members of the PBPS,

Happy new year! 

The PBPS is now accepting applications for this year’s PBPS Abstract Award. This award will go to a pathology trainee with an abstract (poster/platform) in pancreatobiliary pathology presented at the 2021 annual USCAP meeting. Submitted abstracts will be evaluated for originality, scientific merit and presentation, and the winner will receive a $500 prize. At least one author should be a PBPS member. Trainees are strongly encouraged to apply.

The deadline for submission of Award applications is February 15, 2021.

Please email your completed abstract in Word format along with the information below to the education committee chair Dr. Michelle Reid (michelle.reid@emory.edu).

Name:
Training Institution:
Position:
PGY Year:
Date/Time of Presentation:
Abstract Name:
Poster Number (if applicable):

Comments:

Pancreatic Cancer Awareness Month

 

This month, with so many global issues in front of us, I want to remind everyone that November is Pancreatic Cancer Awareness Month.  Pancreatic cancer has been in the national consciousness this year, in part due to well-known figures who have been affected, but we also draw greater awareness to the disease through Pancreatic Cancer Awareness Month, to urge private and public agencies to extend more funding to study this disease and help researchers search for a cure and improve the lives of those affected.  This year, over 56,000 people in the United States will be diagnosed with pancreatic cancer, and many more around the world will be affected.  Recognition of the growing prevalence of pancreatic cancer, with the help of foundations and organizations like the Pancreatobiliary Pathology Society, can help direct resources towards research and clinical care efforts.  Thursday, November 19 is World Pancreatic Cancer Day – an even more focused opportunity to recognize this disease and the numerous efforts to improve the care of those affected.  Please remember to “wear purple” and spread the word that we are redoubling our efforts, so that the impetus to address pancreatic cancer is also felt throughout the year and reflected in renewed energy and enthusiasm for research collaboration and knowledge sharing.  Pancreatobiliary pathologists are charged with establishing the diagnosis of pancreatic cancer, and surely we should be leading advocacy efforts as well!

David Klimstra, President 

Pancreatobiliary Pathology Society

 

Message from the President

Message from the President

Dear Colleagues, 

I am sad to share news of the death on July 7 in Milan, Italy of Dr. Juan Rosai. 

Dr. Rosai was clearly one of the most influential figures in surgical pathology in the last 50 years, whose broad diagnostic expertise was recognized worldwide.  For much of his career, he served as a consultant to the international pathology community, providing expert second opinions and making enormous contributions to direct patient care.  As a researcher, Dr. Rosai was best known for his work on neoplasms of the thyroid, thymus, and vascular system, but essentially there is no subspecialty area that did not receive his investigative attention.  In fact, he wrote many papers on pancreatic neoplasms, and it was his encouragement of me to pursue a case of pancreatic acinar cell carcinoma that led me to the field of pancreatic pathology.  Dr. Rosai was among the first to embrace technologies like electron microscopy, immunohistochemistry, and molecular biology to enhance pathologic diagnosis. He was also one of the first pathology leaders to promote digital pathology and predicted the field’s evolution from microscopic to digital pathology many years before it occurred, and he pushed for subspecialization of academic pathology years before it became commonplace – ironic, given that he himself was the quintessential generalist.  But perhaps his most lasting contributions were made as a mentor and teacher, roles he took on with great enthusiasm. He fostered the careers of countless trainees, many of whom are now in leadership positions around the world.   Recitation of his numerous achievements, awards, and honors can await more formal tributes that will appear in time, but no one can doubt that Juan Rosai achieved as much as any individual can in our field, and his influence has been felt across all subspecialties.  A world-renowned surgical pathologist, as well as a treasured friend to many, Dr. Rosai’s generous spirit and ability to build consensus are as much a part of his legacy as his unparalleled expertise. Our thoughts are with his wife, Dr. Maria Luisa Carcangiu, and his children.

David Klimstra

President, Pancreatobiliary Pathology Society

 

Pancreatobiliary Pathology Society’s Special Section in Archives of Pathology and Laboratory Medicine

Pancreatobiliary Pathology Society’s Special Section in Archives of Pathology and Laboratory Medicine

Dear Pancreatobiliary Pathology Society Members

I am writing to draw your attention to the newly released Archives of Pathology and Laboratory Medicine (https://archivesofpathology.org/toc/arpa/144/7) which includes a Special Section containing review articles on the topics we presented at our 2019 USCAP Companion Meeting session.

You will find comprehensive and authoritative reviews written by our speakers, Drs. Laura Wood, Laura Tang, Stefano La Rosa, and Huamin Wang, along with selected collaborators.  We are particularly pleased and grateful to the Editors of Archives, Drs. Philip Cagle and Donna Hansel, for agreeing to publish a Special Section based on our meeting, and to Managing Editor Katie Giesen, whose assistance was tremendously helpful during the process.

I am also happy to report that we will be publishing a second installment based on the presentations at the 2020 USCAP Companion Meeting, so stayed tuned.  Thanks to all who participated in authoring, reviewing, and publishing these reviews, and I hope you all enjoy reading them.

Best wishes, and Stay Safe!

David Klimstra

On behalf of the Executive and Education Committees

Pancreatobiliary Pathology Society