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Biliary malignancies include those arising from the intrahepatic and extrahepatic bile ducts as well as the gallbladder and hepatopancreatic ampulla of Vater. The majority of intrahepatic and extrahepatic malignancies are cholangiocarcinomas (CCAs). They arise owing to a complex interplay between the patient-specific genetic background and multiple risk factors and may occur in the liver (intrahepatic CCA), hilum (perihilar CCA), or extrahepatic bile ducts (distal CCA). Biliary-type adenocarcinoma constitutes the most common histologic type of ampullary and gallbladder malignancies. Its prognosis is poor and surgical resection is considered curative, so early detection is key, with multimodality imaging playing a central role in making the diagnosis. There are several risk factors for biliary malignancy as well as predisposing conditions that increase the risk; this review highlights the pertinent imaging features of these entities with histopathologic correlation. The predisposing factors are broken down into three major categories

Neoadjuvant therapy (NAT) is increasingly used to treat patients with pancreatic ductal adenocarcinoma (PDAC). Patients with PDAC often show heterogenous responses to NAT with variable clinical outcomes, and the clinicopathologic parameters associated with these variable outcomes remain unclear. In this study, we systematically examined the clinicopathologic characteristics of 60 short-term survivors (overall survival < 15 months) and 149 long-term survivors (overall survival > 60 months) and compared them to 352 intermediate-term survivors (overall survival: 15–60 months) of PDAC who received NAT and pancreatoduodenectomy. We found that the short-term survivor group was associated with male gender (p = 0.03), tumor resectability prior to NAT (p = 0.04), poorly differentiated tumor histology (p = 0.006), more positive lymph nodes (p = 0.04), higher ypN stage (p = 0.002), and higher positive lymph node ratio (p = 0.03). The long-term survivor group had smaller tumor size (p = 0.001), lower ypT stage (p = 0.001), fewer positive lymph nodes (p < 0.001), lower ypN stage (p < 0.001), lower positive lymph node ratio (p < 0.001), lower rate of lymphovascular invasion (p = 0.001) and perineural invasion (p < 0.001), better tumor response grading (p < 0.001), and less frequent recurrence/metastasis (p < 0.001). The ypN stage is an independent predictor of both short-term and long-term survivors by multivariate logistic regression analyses. In addition, tumor differentiation was also an independent predictor for short-term survivors, and tumor response grading and perineural invasion were independent predictors for long-term survivors. Our results may help to plan and select post-operative adjuvant therapy for patients with PDAC who received NAT and pancreatoduodenectomy based on the pathologic data.

Numerous cell states are known to comprise the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment (TME). However, the developmental stemness and co-occurrence of these cell states remain poorly defined. Here, we performed single-cell RNA sequencing (scRNA-seq) on a cohort of treatment-naive PDAC time-of-diagnosis endoscopic ultrasound-guided fine needle biopsy (EUS-FNB) samples (n=25) and surgical resections (n=6), which were then combined with publicly available samples to increase statistical power (n=80). Following annotation into 25 distinct cell states, cells were scored for developmental stemness and a customized version of the Ecotyper tool was used to identify communities of co-occurring cell states in bulk RNA-seq samples (n=268). We discovered a tumor microenvironmental community comprised of aggressive basal-like malignant cells, tumor-promoting SPP1+ macrophages, and myofibroblastic cancer-associated fibroblasts associated with especially poor prognosis. We also found a developmental stemness continuum with implications for survival that is present in both malignant cells and cancer-associated fibroblasts (CAFs). We further demonstrated that high-dimensional analyses predictive of survival are feasible using standard-of-care, time-of-diagnosis EUS-FNB specimens. In summary, we identified novel tumor microenvironmental and developmental stemness characteristics from a high-dimensional gene expression analysis of PDAC using human tissue specimens including time-of-diagnosis EUS-FNB samples. These reveal new connections between tumor microenvironmental composition, CAF and malignant cell stemness, and patient survival that could lead to better upfront risk stratification and more personalized upfront clinical decision-making.

Risk stratification of gastrointestinal stromal tumors (GISTs) is based on experience with tumors of the stomach, small bowel, and rectum, which are far more common than GISTs of other sites. In this study from 47 institutions, we analyzed GISTs of the esophagus (n = 102), colon (n = 136), and appendix (n = 27) for their size, mitotic rate, morphology, and outcome to determine which criteria predict their behavior. Esophageal GISTs were small (median: 2.5 cm) with spindle cell morphology and a low mitotic rate (mean: 3.6/5 mm2). Twelve (12%) tumors progressed, including 11 with a mitotic rate >5/5 mm2 and one large (6.8 cm) GIST with a mitotic rate of 2/5 mm2. Colonic GISTs were smaller (median: 1.4 cm) and presented with abdominal pain or bleeding in 29% of cases. Most (92%) were composed of spindle cells with a mean mitotic rate of 4.6/5 mm2. Sixteen (12%) tumors progressed: 14 had mitotic rates >5/5 mm2, and two were >5.0 cm with a mitotic rate 5/5 mm2) and size >5.0 cm. These findings support the use of size and mitotic rate for prognostication of GISTs in these locations, similar to tumors of the stomach, small bowel, and rectum.

Multivariate Analysis of Factors Associated with Overall Survival, Recurrence-Free Survival, and Liver-Specific Recurrence-Free Survival.

Mathematical model simulation of low delta tumor growth (lambda = 0.2)

Purpose:Pancreatic ductal adenocarcinoma (PDAC) is a heterogeneous disease with variable presentations and natural histories of disease. We hypothesized that different morphologic characteristics of PDAC tumors on diagnostic computed tomography (CT) scans would reflect their underlying biology.Experimental Design:We developed a quantitative method to categorize the PDAC morphology on pretherapy CT scans from multiple datasets of patients with resectable and metastatic disease and correlated these patterns with clinical/pathologic measurements. We modeled macroscopic lesion growth computationally to test the effects of stroma on morphologic patterns, hypothesizing that the balance of proliferation and local migration rates of the cancer cells would determine tumor morphology.Results:In localized and metastatic PDAC, quantifying the change in enhancement on CT scans at the interface between tumor and parenchyma (delta) demonstrated that patients with conspicuous (high-delta) tumors had significantly less stroma, higher likelihood of multiple common pathway mutations, more mesenchymal features, higher likelihood of early distant metastasis, and shorter survival times compared with those with inconspicuous (low-delta) tumors. Pathologic measurements of stromal and mesenchymal features of the tumors supported the mathematical model's underlying theory for PDAC growth.Conclusions:At baseline diagnosis, a visually striking and quantifiable CT imaging feature reflects the molecular and pathological heterogeneity of PDAC, and may be used to stratify patients into distinct subtypes. Moreover, growth patterns of PDAC may be described using physical principles, enabling new insights into diagnosis and treatment of this deadly disease.

Vectra Image analysis workflow, Double IF staining of lumican and collagen I, and TGF-β secretion in HPSC.

Purpose: The most common genetic lesions in pancreatic ductal adenocarcinoma (PDAC) have been identified. However, significant gaps still exist in our understanding of how such genetic alterations act in concert to induce PDAC development. In this study, we investigated the mechanism of tumorigenic transformation in the immortalized human pancreatic ductal epithelial (HPDE) cell line by sequentially introducing PDAC signature alterations into this cell line.Experimental Design: The phenotype for stable expression of mutant K-ras, Her2, p16/p14shRNA, and Smad4shRNA in HPDE cells was examined by assays for cell proliferation, migration, invasion, soft agar, and orthotopic tumorigenesis. The mechanisms of tumorigenic transformation were further explored by gene expression profiling and pathway analyses.Results: The transformed cells exhibited enhanced proliferation, migration, and invasion, displayed anchorage-independent growth in soft agar, and grew orthotopic tumors with some histopathologic features of PDAC. We found that Smad4 played key roles in the tumorigenic transformation of HPDE cells. We further found that MDM2 and Bmi-1 were overexpressed in the tumorigenic HPDE cells and that Bmi-1 overexpression was regulated by Smad4. Ingenuity Pathway Analysis software analysis of microarray data revealed that dysregulation of integrin-linked kinase signaling and the cell cycle were the most significant changes involved in tumorigenic transformation. Altogether, this cell culture model closely recapitulated human pancreatic carcinogenesis from gene lesions, activation of specific signaling pathways, and some histopathologic features.Conclusion: The combination of activated K-ras and Her2 with inactivated p16/p14 and Smad4 was sufficient and essential to transform HPDE cells, thus revealing the potential tumorigenic mechanism. Clin Cancer Res; 19(3); 549–59. ©2012 AACR.

Lumican expression and secretion in HPaSteC with or without TGF-β exposure at 8 and 24 hours.

Lumican secretion associated with cell matrix migration.

Supplementary Table 1. List of antibodies used for immunohistochemical staining of mouse pancreas.

PDF file - 169K, Supplementary Fig. 2. Cell migration and invasion abilities of HPDE cells with expression of mutant K-ras, Her2, p16/p14shRNA, and Smad4shRNA.

PDF file - 114K

Clinical Correlation Studies, Tissue Microarray and Statistical Analysis.

Additional methods

Purpose: To evaluate the relevance between lumican expression patterns and the clinical course of patients with pancreatic ductal adenocarcinoma (PDAC), and to investigate the role of lumican in PDAC progression.Experimental Design: One hundred thirty-one patient tumors were chosen for tissue microarray staining, and Cox regression analysis was used to test the associations between lumican expression and clinical, pathologic, and oncologic outcomes in all patients. Primary PDAC cells and recombinant human lumican protein were used to establish a working model to mimic the in vivo interactions between stromal lumican and PDAC cells. Using this model, we tested the effects of lumican on EGFR signaling via Akt and hypoxia-inducible factor-1α (HIF1α) and its subsequent influence on glucose consumption, lactate production, intracellular ATP, and apoptotic cell death.Results: Lumican was present in the stroma surrounding PDAC cells in roughly one-half of primary tumors and the direct xenografts. Patients with stromal lumican were associated with a profound reduction in metastatic recurrence after surgery and 3-fold longer survival than patients without stromal lumican. In PDAC cells, extracellular lumican reduced EGFR expression and phosphorylation through enhanced dimerization and internalization of EGFR and the resultant inhibition of Akt kinase activity. Lumican also reduced HIF1α expression and activity via Akt. PDAC cells with enhanced HIF1α activity were resistant to lumican-induced inhibition of glucose consumption, lactate production, intracellular ATP, and apoptosis.Conclusions: There is a positive association between stromal lumican in primary PDAC tumors and prolonged survival after tumor resection. Lumican plays a restrictive role in EGFR-expressing pancreatic cancer progression. Clin Cancer Res; 20(24); 6529–40. ©2014 AACR.

Lipocalin-2 (LCN2) promotes malignant development in many cancer types. LCN2 is upregulated in patients with pancreatic ductal adenocarcinoma (PDAC) and in obese individuals, but whether it contributes to PDAC development is unclear. In this study, we investigated the effects of Lcn2 depletion on diet-induced obesity, inflammation, and PDAC development. Mice with acinar cell–specific expression of KrasG12D were crossed with Lcn2-depleted animals and fed isocaloric diets with varying amounts of fat content. Pancreas were collected and analyzed for inflammation, pancreatic intraepithelial neoplasia (PanIN), and PDAC. We also used a syngeneic orthotopic PDAC mouse model to study tumor growth in the presence or absence of Lcn2 expression. In addition, to understand the mechanistic role of how LCN2 could be mediating PDAC, we studied LCN2 and its specific receptor solute carrier family 22 member 17 (SLC22A17) in human pancreatic cancer stellate cells (PSC), key mediators of the PDAC stroma. Depletion of Lcn2 diminished extracellular matrix deposition, immune cell infiltration, PanIN formation, and tumor growth. Notably, it also increased survival in both obesity-driven and syngeneic orthotopic PDAC mouse models. LCN2 modulated the secretion of proinflammatory cytokines in PSC of the PDAC tumor microenvironment, whereas downregulation of LCN2-specific receptor SLC22A17 blocked these effects. Our results reveal how LCN2 acts in the tumor microenvironment links obesity, inflammation, and PDAC development. Cancer Res; 77(10); 2647–60. ©2017 AACR

PDF file - 77K, Supplementary Table 1. Summary of cell proliferation, migration, and invasion; anchorageindependent growth; and tumor incidence in NOD/SCID mice in various HPDE cell lines.

PDF file - 74K, Supplementary Table 2. The most significant changes in gene expression for cell line HPDE/Kras/ Her2/p16p14shRNA/Smad4shRNA versus cell line HPDE/K-ras/Her2/p16p14shRNA in cDNA microarray analysis.

Clinicopathologic and oncologic outcome correlation of lumican expression subgroups.

Purpose: Pancreatic ductal adenocarcinoma (PDAC) is lethal cancer whose primary tumor is characterized by dense composition of cancer cells, stromal cells, and extracellular matrix (ECM) composed largely of collagen. Within the PDAC tumor microenvironment, activated pancreatic stellate cells (PSC) are the dominant stromal cell type and responsible for collagen deposition. Lumican is a secreted proteoglycan that regulates collagen fibril assembly. We have previously identified that the presence of lumican in the ECM surrounding PDAC cells is associated with improved patient outcome after multimodal therapy and surgical removal of localized PDAC.Experimental Design: Lumican expression in PDAC from 27 patients was determined by IHC and quantitatively analyzed for colocalization with PSCs. In vitro studies examined the molecular mechanisms of lumican transcription and secretion from PSCs (HPSCs and HPaSteC), and cell adhesion and migration assays examined the effect of lumican on PSCs in a collagen-rich environment.Results: Here we identify PSCs as a significant source of extracellular lumican production through quantitative IHC analysis. We demonstrate that the cytokine, TGF-β, negatively regulates lumican gene transcription within HPSCs through its canonical signaling pathway and binding of SMAD4 to novel SBEs identified within the promoter region. In addition, we found that the ability of HPSCs to produce and secrete extracellular lumican significantly enhances HPSCs adhesion and mobility on collagen.Conclusions: Our results demonstrate that activated pancreatic stellate cells within PDAC secrete lumican under the negative control of TGF-β; once secreted, the extracellular lumican enhances stellate cell adhesion and mobility in a collagen-rich environment. Clin Cancer Res; 22(19); 4934–46. ©2016 AACR.

PDF file - 96K, Supplementary Fig. 3. Confirmation of gene expression change of BMP7 and GRB10 in cDNA microarray analysis.

Univariate analysis of factors associated with overall survival, recurrence-free survival, and liver-specific recurrence-free survival.

Supplementary Table 2. List of human (h) and mouse (m) primer sequences used in study.

Additional Experimental Methods

HPaSteC and Media: Western blot and ELISA assay: Vectra Automated Quantitative Pathology Imaging System (VAQPIS, PerkinElmer): Double Immunofluorescence staining (IF), and Vectra multispectral analysis: Supplementary figure legends

Supplementary Table 1. Wild type and mutant lumican SBE oligos for EMSA. Supplementary Table 2. Clinicopathologic and oncologic outcome correlation of stromal lumican expression in PDAC. Supplementary Table 3. Amount of Lumican Secretion in HPSC and PDACs Supernatant at 8 and 24 hours.

Mathematical model simulation of high delta tumor growth (lambda = 1.5)

Although immune checkpoint inhibitors (ICIs) have been a revolutionary milestone in immuno-oncology, immune-related adverse events (irAEs) may occur due to enhanced T cell activation and immune dysregulation. The irAEs can occur as early as within days to reportedly as late as up to 26 weeks. They may affect any organ system in the body, most commonly the luminal gastrointestinal tract, liver, skin, endocrine system, and lungs. The mechanisms of irAEs are complex and have not been fully understood. A breach of self-tolerance, which leads to autoantigen reactivity due to the enhanced activation and infiltration of T cells or the production of autoantibodies, and a non-specific autoinflammatory mechanism have been proposed. Limited data is available on the clinical and pathologic features of ICI-induced liver injury. This review presents an overview of the clinical and common histopathologic features and patterns of ICI-induced liver injury, the differential diagnoses, and the clinical management. Available data suggest that the histopathologic findings of ICI-induced hepatic injury are often non-specific and overlap with other challenging differential diagnoses. Therefore, a good knowledge of the histopathologic spectrum of ICI-induced hepatic injury and their differential diagnoses combined with the serological test results, clinical correlation, and communication with the clinical team is necessary to make an accurate and timely diagnosis.

Pancreatic neuroendocrine neoplasms (PaNENs) are a unique group of pancreatic neoplasms with a wide range of clinical presentations and behaviors. Given their heterogeneous appearance and increasing detection on cross-sectional imaging, it is essential that radiologists understand the variable presentation and distinctions PaNENs display compared to other pancreatic neoplasms. Additionally, some of these neoplasms may be hormonally functional, and it is imperative that radiologists be aware of the common clinical presentations of hormonally active PaNENs. Knowledge of PaNEN pathology and treatments may influence which imaging modality is optimal for each patient. Each imaging modality used for PaNENs has distinct advantages and disadvantages, particularly in different treatment settings. Thus, the focus of this manuscript is to provide an update for the radiologist on PaNEN pathology, imaging, and treatments.

The rate of syphilis in the United States has been increasing steadily in the past decade, but it remains an uncommon diagnosis in tissue biopsies. Most of the pathology literature on hepatic syphilis consists of older series or case reports. This study aimed to systematically characterize the histologic spectrum of hepatic syphilis in a contemporary cohort. Clinicopathologic features of 14 hepatic syphilis cases between 2012 and 2018 were analyzed to characterize the broad spectrum of histologic changes. Thirteen patients were men (age range: 19 to 59 y); 6 had known human immunodeficiency virus, 7 were men known to have sex with men, and no patient had known prior syphilis. Hepatic syphilis was the primary clinical suspicion in only 1 patient. Common symptoms included jaundice, rash, and abdominal pain. Thirteen had elevated transaminases, and 12 had elevated alkaline phosphatase. Pathologic changes were grouped into 5 histologic patterns: biliary-pattern injury (n=5), acute hepatitis (n=4), autoimmune hepatitis-like (n=1), fibroinflammatory mass-forming lesion (n=2), and no particular pattern (n=2). Nearly all showed portal and lobular lymphocytes and plasma cells; 12 had prominent histiocytes/Kupffer cells, 9 had ductular reaction, and 7 had duct inflammation. Occasional focal findings included dropout (n=7), phlebitis (n=7), and loose granulomata (n=5). Treponeme immunohistochemistry was positive in 10 and negative in 4, though treatment was given before biopsy in 3 of those 4. Thirteen patients had rapid plasma reagin testing either before or after biopsy, with 1:64 or higher titer. All patients who received treatment recovered. Hepatic syphilis is rare but likely underrecognized. It exhibits a variety of histologic appearances and therefore should be considered in several hepatic differential diagnoses, especially in men who have sex with men. Kupffer cells, granulomata, and phlebitis may suggest the diagnosis regardless of predominant histologic pattern. Negative treponeme immunohistochemical staining does not exclude the diagnosis, including in untreated patients.

Context.— Hypergastrinemia states such as achlorhydria from gastric mucosal atrophy or a gastrin-producing tumor in humans have been associated with the development of enterochromaffin-like (ECL) cell hyperplasia and gastric neuroendocrine tumors (GNETs). Whether drugs that can elevate serum gastrin levels, such as proton pump inhibitors (PPIs), can produce the same tissue effect is not known, and there is no concrete evidence linking the use of PPIs to GNETs outside animal models and case reports. Objective.— To explore the clinicopathologic association for GNETs of presumed ECL cell origin that cannot be reliably placed into any of the 3 established categories currently recognized by the World Health Organization. Design.— This is a retrospective clinicopathologic study of GNETs in the body/fundus during a period of 15 years (2005–2019). Results.— Of a total of 87 cases, 57 (65.5%) were associated with atrophic gastritis, 2 (2.3%) were associated with Zollinger-Ellison syndrome, and 28 (32.2%) were unclassified. Of the latter, 11 were consistent with true sporadic/type 3 GNETs, while 17 had background mucosal changes of parietal cell and ECL cell hyperplasia but without underlying detectable gastrinoma, and 88.2% (15 of 17) of patients from this group had documented long-term PPI use. This subtype of GNETs was more commonly multifocal and of higher grade (P = .03) than “true” sporadic GNETs. Conclusions.— A subset of GNETs arises in the background of gastric mucosal changes suggestive of hypergastrinemia, but without underlying gastrinoma, and could be linked to long-term PPI use.

The timing of cholecystectomy during acute cholecystitis (AC) is controversial, especially whether it is advisable to perform in patients with duration of symptoms between 3 and 10 days. The purpose of this study is to define clearly the sequential evolution of histological changes following symptoms onset to guide recommendations regarding timing of cholecystectomy.We identified patients with AC (2005-2018) who had cholecystectomy within 10 days of symptom onset of a first attack of AC. Histologic features of gallbladder injury including cellular and exudative inflammatory response to injury were determined on blinded pathologic slides.One hundred and forty-nine patients were divided into three groups; early-who underwent cholecystectomy 1-3 days after symptom-onset, intermediate-4-6 days, and late-7-10 days. Key features of injury were necrosis and hemorrhage. A subgroup of patients in the early phase developed severe necrosis and hemorrhage of an extent associated with difficult cholecystectomy. Large spikes in extent of necrosis and hemorrhage occurred at 7-10 days. Major inflammatory responses to injury were eosinophilic and lymphocytic infiltration and early fibrosis.Severe necrosis may develop rapidly and be present in the early period after symptom onset of AC. Cholecystectomy may be reasonable in some patients but by day 7-10, severe necrosis and hemorrhage may be expected to be present in most patients.

Intracholecystic papillary-tubular neoplasm denotes a discrete mucosal-based neoplastic proliferation into the gallbladder lumen. It is diagnosed incidentally during cholecystectomy or radiologically during a workup for abdominal pain. The majority of polypoid lesions in the gallbladder are non-neoplastic; therefore, pathologic examination is the gold standard to establish this diagnosis. Intracholecystic papillary-tubular neoplasm is considered as premalignant, although associated invasive carcinomas may be present in the specimen. Invasive carcinoma arising from intracholecystic papillary-tubular neoplasm have a better prognosis than de novo gallbladder carcinomas. The pathology of intracholecystic papillary-tubular neoplasm, including the challenges involved in the diagnosis of this entity, is discussed.

Introduction: CLDN18.2 is an isoform of CLDN18, a member of the Claudin family of proteins with expression that is highly restricted to the gastric epithelium of normal gastric tissue. In tumor tissue from patients with gastric (G) and gastroesophageal junction (GEJ) adenocarcinoma, CLDN18.2 expression has been found to be frequently expressed as determined by gene expression and immunohistochemistry (IHC). Based on its expression pattern in malignant tissues and past clinical studies, CLDN18.2 has emerged as a target of interest for new therapeutics. The goal of this study was to obtain a deeper understanding of CLDN18.2 expression, prevalence, as well as its prognostic implications, clinical characteristics, and relationship with select biomarkers in G and GEJ adenocarcinoma patient samples. Methods: Formalin-Fixed Paraffin-Embedded tissue samples of G and GEJ adenocarcinoma patients (n=304) from a tissue biorepository at MD Anderson Cancer Center were retrospectively studied for CLDN18.2 expression by IHC (antibody clone 43-14A). Tissue samples included primary G and GEJ adenocarcinoma tissues, matched pre- and post- metastatic samples and matched naïve versus chemotherapy treated patients. Interpretation of CLDN18.2 expression was conducted by clinical pathologists to score samples based on staining intensity (≥2+) as well as the percentage of positively stained CLDN18.2 tumor cells (≥75% and ≥50%). CLDN18.2 expression was analyzed for its association with prognosis, clinical and demographic data and its relationship with other variables (e.g. sex, age, histology, HER2, PD-L1, EBV). Results: Prevalence of CLDN18.2 expression at the >75% cutoff was observed in 51% and 35% of samples from G and GEJ adenocarcinoma patients, respectively, with a combined prevalence of 44%. At the >50% cutoff, CLDN18.2 was expressed in 64% and 45% of G and GEJ adenocarcinoma samples, respectively, with a combined prevalence of 56%. CLDN18.2 expression did not appear to associate with prognosis at either CLDN18.2 expression cutoff. Associations between CLDN18.2 expression based upon sex, tumor grade, histology, peritoneal metastasis and signet ring morphology were observed. When evaluating the relationship between CLDN18.2 expression (at either cutoff) and other select biomarkers (MSI, PD-L1, HER2 and EBV), data suggests there is limited overlap. Conclusion: Based upon the data from this study, CLDN18.2 appears to be a highly prevalent, but not prognostically associated biomarker in G and GEJ adenocarcinoma patients. Additionally, CLDN18.2 expression appears independent of other biomarkers, however further research is warranted. These data are consistent with prior reports and support CLDN18.2 as a promising molecular target for therapeutics to treat G and GEJ adenocarcinoma patients. Citation Format: Matheus Sewastjanow, Kohei Yamashita, Kenneth K. Iwata, Diarmuid Moran, Dina Elsouda, Melissa Pizzi, Ernesto Rosa Vicentini, Namita Shanbhag, Anh Ta, Rebecca Waters, Deyali Chatterjee, Jaffer Ajani. Claudin 18.2 (CLDN18.2) expression prevalence, prognostication and clinical variables in gastric and gastroesophageal junction adenocarcinoma patient samples [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2141.