Katrina Collins

Indiana University School of Medicine

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Andrés Acosta

Indiana University School of Medicine

Muhammad T. Idrees

Indiana University – Purdue University Indianapolis

Thomas M. Ulbright

Indiana University School of Medicine

Michelle S. Hirsch

Brigham and Women's Hospital

Sean R. Williamson

Cleveland Clinic

Fiona Maclean

Douglass Hanly Moir Pathology

Liang Cheng

Indiana University – Purdue University Indianapolis

Lynette M. Sholl

Harvard University

Kristine M. Cornejo

Massachusetts General Hospital

Kiril Trpkov

University of Calgary

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Indiana University – Purdue University Indianapolis

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Indiana University School of Medicine

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John Wiley & Sons (United States)

The University of Texas MD Anderson Cancer Center

Indiana University

Brigham and Women's Hospital

Massachusetts General Hospital

Indiana University Health

Memorial Sloan Kettering Cancer Center

Harvard University

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Analysis of benign neoplasms of the rete testis formerly termed “Sertoliform cystadenomas” demonstrates that they are not Sertoli cell tumours with intra‐rete growth

Histopathology (2025)

Katrina Collins Květoslava Michalová Dario de Biase Costantino Ricci Giovanni Tallini

Aims Benign tumours of the rete testis include mostly cystadenomas and adenomas. A subset with tubular or tubulopapillary architecture shows morphological similarities to Sertoli cell tumours; these neoplasms were previously termed “Sertoliform cystadenomas of the rete testis”. In the most recent WHO classification, they have been interpreted as Sertoli cell tumours, not otherwise specified (NOS), with pure intra‐rete growth, and therefore excluded as an entity. The remaining cystadenomas of the rete testis vaguely resemble tumours of Mullerian origin arising in the ovaries. In this study we analyse benign tumours of the rete testis, including a subset with Sertoliform features. Methods and Results Benign neoplasms of the rete testis were identified through query of consultation and institutional files. Clinicopathologic data were collected, and available slides were reviewed. Cases were assessed using IHC and three separate DNA sequencing panels. Eleven tumours from patients 32–78 years old were evaluated. Four were classified as Sertoliform adenomas/cystadenomas, displaying tubulo‐papillary or tubular/trabecular architecture; all of them were PAX8‐positive and lacked nuclear beta‐catenin expression. The remaining seven tumours were benign cystadenomas NOS. Genomic analysis was performed successfully in 10/11 tumours (including all Sertoliform adenomas/cystadenomas) and revealed no pathogenic variants in CTNNB1 , KRAS , or BRAF. Conclusion Sertoliform cystadenomas of the rete testis differ from Sertoli cell tumours NOS, as evidenced by the absence of molecular markers characteristic of Sertoli cell tumours. The remaining benign cystadenomas lack molecular alterations seen in Mullerian tumors of the ovaries.

Rete testis

Mucinous cystadenoma

Cystadenoma

10.1111/his.15422

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Artificial Intelligence–Based Classification of Renal Oncocytic Neoplasms: Advancing From a 2-Class Model of Renal Oncocytoma and Low-Grade Oncocytic Tumor to a 3-Class Model Including Chromophobe Renal Cell Carcinoma

Archives of Pathology & Laboratory Medicine (2025)

Katrina Collins Shubham Innani Kingsley Ebare Mohammed Saad Stephanie Siegmund

Distinguishing between renal oncocytic tumors, such as renal oncocytoma (RO), and a subset of tumors with overlapping characteristics, including the recently identified low-grade oncocytic tumor (LOT), can present a diagnostic challenge for pathologists owing to shared histopathologic features. To develop an automatic computational classifier for stratifying whole slide images of biopsy and resection specimens into 2 distinct groups: RO and LOT. A total of 269 whole slide images from 125 cases across 6 institutions were collected. A weakly supervised attention-based multiple-instance-learning deep learning (DL) model was trained and initially evaluated through 5-fold cross validation with case-level stratification, followed by validation using an independent holdout data set. Quantitative performance evaluation was based on accuracy and the area under the receiver operating characteristic curve (AUC). The developed model data set yielded generalizable performance, with a 5-fold average testing accuracy of 84% (AUC = 0.78), and a closely aligning accuracy of 83% (AUC = 0.92) on the independent holdout data set. The proposed artificial intelligence approach contributes toward a comprehensive solution for addressing commonly encountered renal oncocytic neoplasms, encompassing well-established entities like RO along with the challenging "gray zone" LOT, thereby proving applicable in clinical practice.

Renal oncocytoma

Chromophobe cell

10.5858/arpa.2024-0374-oa

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Sarcomatoid Yolk Sac Tumor Harbors Somatic Mutations That Are Otherwise Rare in Testicular Germ Cell Tumors

The American Journal of Surgical Pathology (2022)

Andrés Acosta Khaleel I. Al‐Obaidy Lynette M. Sholl Brendan C. Dickson Neal I. Lindeman

In testicular germ cell tumors (TGCTs), components with nonspecific sarcomatous features that express keratins and glypican 3 are classified as sarcomatoid yolk sac tumor (SYST). SYST is most frequently seen in metastatic sites after chemotherapy. Like so-called "somatic-type" malignancies arising in TGCTs, SYST is markedly resistant to systemic therapy and has a more aggressive clinical course than conventional types of TGCT. However, the clinicopathologic and molecular features of SYST remain incompletely described. This study evaluated a multi-institutional series of 20 SYSTs using massively parallel sequencing and p53 immunohistochemistry. The histologic and clinical characteristics of the cases were also assessed, including analyses of disease-specific outcomes. DNA sequencing identified somatic mutations in 12/20 cases (60%), including recurrent TP53 and RIF1 mutations (present in 4/20 cases, 20% each). In 3 of the 4 SYST with TP53 mutations, there was molecular evidence of loss of heterozygosity. Immunohistochemistry demonstrated diffuse overexpression of p53 protein in 3/4 (75%) cases with TP53 mutations. The remaining TP53-mutant case demonstrated multifocal overexpression of p53, suggestive of subclonal inactivation of the gene. Overexpression of p53 protein was not seen in any of 15 TP53 wild-type cases evaluated by immunohistochemistry. A subset of 4 cases underwent RNA sequencing (fusion panel), which demonstrated the absence of oncogenic gene fusions. A 2-tiered grading system based on 3 histologic parameters (cellularity, number of mitoses, and necrosis) demonstrated that high-grade SYSTs have a higher risk of disease-specific death compared to low-grade tumors. The risk of disease-specific mortality was also higher in SYSTs with somatic mutations. In conclusion, this study demonstrated that 60% of SYSTs harbor somatic oncogenic mutations that are otherwise rare in TGCTs, and the presence of these mutations is associated with an aggressive clinical course. In addition, the results presented herein suggest that grading SYSTs may be clinically relevant.

Grading (engineering)

10.1097/pas.0000000000001865

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Reprint of: morphologic spectrum of treatment-related changes in prostate tissue and prostate cancer: an updated review

Human Pathology (2023)

Katrina Collins Liang Cheng

Hormonal Therapy

Hormone Therapy

10.1016/j.humpath.2023.02.007

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Comprehensive Clinicopathologic Features in Autoimmune Atrophic Gastritis: Insights from a European Cohort of 57 Patients

Pathology - Research and Practice (2024)

Luiz M. Nova‐Camacho Saul De Burgos Irune Ruiz Díaz Katrina Collins

Atrophic gastritis

Autoimmune Gastritis

10.1016/j.prp.2024.155631

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Genomic analysis of primary epithelial neoplasms of the seminal vesicle identifies a subset of mucinous cystic tumours driven by KRAS mutations

Histopathology (2024)

Katrina Collins Laurence A. Galea Forough Foroughi Stephanie Siegmund William J. Anderson

Background Carcinomas of the seminal vesicle are exceedingly rare, with a limited number of cases described in the literature. Reported cases span a relatively wide morphological spectrum, and their genomic features remain unexplored. Design In this study, we interrogated five primary epithelial neoplasms of the seminal vesicle using a targeted DNA sequencing platform (OncoPanel, 447 genes). Results The tumours included one adenocarcinoma with intestinal phenotype presenting after external beam radiation (for prostatic adenocarcinoma), one carcinoma with Müllerian‐type clear cell phenotype, two mucinous tumours resembling low‐grade mucinous neoplasms of the appendix (LAMN) and one mucinous cystadenoma. The post‐radiation mucinous adenocarcinoma had genomic findings consistent with bi‐allelic inactivation of TP53 , as well as multiple copy‐number changes with regional and chromosomal arm‐level copy‐number losses. The Müllerian‐type clear cell carcinoma exhibited a complex copy‐number profile with numerous regional and arm‐level copy‐number changes, as well as focal amplification events, including copy‐number gain of 8q and amplification of a region within 20q13. Both low‐grade mucinous tumours resembling LAMN harboured hot‐spot gain‐of‐function KRAS variants (p.G12V and p.G13D) as the only genomic alteration. No genomic alterations were detected inthe lesion diagnosed as mucinous cystadenoma. Conclusion Our results suggest that primary low‐grade mucinous neoplasms of the seminal vesicle may represent a distinct entity equivalent to appendiceal counterparts, driven by gain‐of‐function variants of RAS GTPases. The remaining tumours showed genomic features that closely resembled those of neoplasms with comparable phenotypes and/or biological characteristics arising in other sites, suggesting that they could be managed similarly, with special considerations related to their anatomical location.

Mucinous cystadenoma

Comparative genomic hybridization

10.1111/his.15167

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Molecular correlates of male germ cell tumors with overgrowth of components resembling somatic malignancies

Modern Pathology (2022)

Nicolas Wyvekens Lynette M. Sholl Yiying Yang Ivy Tran Varshini Vasudevaraja

Isochromosome

Primitive neuroectodermal tumor

10.1038/s41379-022-01136-1

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Citations (14)

Assessing extra-prostatic extension for surgical guidance in prostate cancer: Comparing two PSMA-PET tracers with the standard-of-care

Urologic Oncology Seminars and Original Investigations (2022)

Clinton D. Bahler Mark A. Green Mark Tann Jordan Swensson Katrina Collins

Glutamate carboxypeptidase II

Standard of care

10.1016/j.urolonc.2022.10.003

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TFE3‐rearranged nonmelanotic renal PEComa: a case series expanding their phenotypic and fusion landscape

Histopathology (2024)

Abbas Agaimy Andrés Acosta Liang Cheng Katrina Collins Eddie Fridman

A subset of exceptionally rare primary renal perivascular epithelioid cell tumours (PEComas) that harbour Xp11.2 translocation have been reported, but no larger series devoted to this topic have been published.

TFE3

PAX8

Gene rearrangement

10.1111/his.15304

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Myoid gonadal stromal tumours are characterised by recurrent chromosome‐level copy number gains: molecular assessment of a multi‐institutional series

Histopathology (2022)

Katrina Collins Lynette M. Sholl Stephanie Siegmund Brendan C. Dickson Maurizio Colecchia

Myoid gonadal stromal tumours (MGST) represent a rare type of testicular sex cord-stromal tumour that has recently been recognised as a distinct entity by the World Health Organization (WHO) classification of genitourinary tumours. MGSTs affect adult men and have been reported to behave in an indolent fashion. Histologically, MGSTs are pure spindle cell neoplasms that coexpress SMA and S100 protein. Given that the molecular features of these neoplasms remain largely undescribed, we evaluated a multi-institutional series of MGSTs using DNA and RNA sequencing. This study included 12 tumours from 12 patients aged 28 to 57 years. Tumour sizes ranged from 0.6 to 4.3 cm. Aggressive histologic features, such as vascular invasion, necrosis, invasive growth, and atypical mitoses were invariably absent. Mitotic activity was low, with a median of less than 1 mitosis per 10 high power fields (HPF; maximum: 3 mitoses per 10 HPF). Molecular analyses did not identify recurrent mutations or gene fusions. All cases with interpretable copy number variant data (9/10 cases sequenced successfully) demonstrated a consistent pattern of chromosome arm-level and whole-chromosome-level copy number gains indicative of ploidy shifts, with recurrent gains involving chromosomes 3, 6, 7, 8, 9, 11, 12, 14q, 15q, 17, 18q, 20, and 21q. Similar findings have also been recognised in pure spindle cell and spindle-cell predominant sex cord-stromal tumours without S100 protein expression. MGSTs are characterised by ploidy shifts and may be part of a larger spectrum of spindle cell-predominant sex cord-stromal tumours, including cases without S100 protein expression.

10.1111/his.14825

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Citations (9)