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Precursor Lesions of Cholangiocarcinoma: A Clinicopathologic Review.

ABSTRACT: Cholangiocarcinoma (CCA) develops through multistep carcinogenesis. During the past decades, 2 precursors have been proved to evolve to CCA. The 2 main precursor lesions of CCA are biliary intraepithelial neoplasia and intraductal papillary neoplasm of the bile duct. It is an interesting and relatively novel entity for the hepatobiliary surgeons, radiologists, oncologists, and pathologists. It worth being familiar with these 2 entities for better communication between pathologists, oncologists, and surgeons to improve the treatment and follow-up of these lesions, which can definitely decrease their evolvement to CCA as an aggressive, poor prognostic, and life-threatening cancer. In this narrative review, I collected and discussed all published studies about these 2 precursor lesions of CCA including radiologic, clinical, and pathological manifestation.

SUBMITTER: Geramizadeh B

PROVIDER: S-EPMC7297471 | biostudies-literature | 2020 Jan-Dec

REPOSITORIES: biostudies-literature

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Precursor Lesions of Cholangiocarcinoma: A Clinicopathologic Review.

Geramizadeh Bita B Geramizadeh Bita B

Clinical pathology (Thousand Oaks, Ventura County, Calif.) 20200101

Cholangiocarcinoma (CCA) develops through multistep carcinogenesis. During the past decades, 2 precursors have been proved to evolve to CCA. The 2 main precursor lesions of CCA are biliary intraepithelial neoplasia and intraductal papillary neoplasm of the bile duct. It is an interesting and relatively novel entity for the hepatobiliary surgeons, radiologists, oncologists, and pathologists. It worth being familiar with these 2 entities for better communication between pathologists, oncologists, ...[more]

PMID: 32596664

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Project description:BackgroundThe present study reviewed the clinicopathological features and outcomes of bilateral lacrimal gland lesions.MethodsThe data of 113 patients who underwent lacrimal gland biopsy at the West China Hospital of Sichuan University, China, between January 1, 2010, and December 31, 2021, are presented in this case series. The patients all presented with bilateral lacrimal gland lesions. The collected data included patient demographics, clinical features, the results of laboratory examinations, imaging presentations, histopathological diagnoses, treatments, and outcomes.ResultsThe mean age of the 113 enrolled patients was 47.4 ± 14.9 years (range, 11-77 years) with a predominance of females (54.9%, n = 62). The lacrimal gland was the source of the majority of biopsy tissue (98.2%, n = 111). The most prevalent etiology was immunoglobulin G4-related ophthalmic disease (IgG4-ROD) (32.7%, n = 37), followed by idiopathic orbital inflammation (IOI) (28.3%, n = 32), mucosa-associated lymphoid tissue (MALT) lymphoma (17.7%, n = 20), reactive lymphoid hyperplasia (RLH) (10.6%, n = 12), and mantle cell lymphoma (4.4%, n = 5). Patients with IOI were significantly younger than those with IgG4-ROD and MALT lymphoma (t = 2.932, P = 0.005; t = 3.865, P<0.001, respectively). Systemic symptoms were more prevalent among patients with IgG4-ROD (χ2 = 7.916, P = 0.005). The majority of patients were treated with surgery (53.1%, n = 60), with surgery combined with corticosteroid therapy (21.2%, n = 24) being the second most common treatment. The majority of patients (91.2%, n = 103) attained complete resolution, stable disease, or significant improvement.ConclusionIn conclusion, there are several aetiologies associated with bilateral lacrimal gland lesions, the most prevalent being IgG4-ROD, IOI, and MALT lymphoma. Systemic symptoms were more common in patients with IgG4-ROD. The majority of patients who presented with bilateral lesions of the lacrimal glands responded satisfactorily to treatment, with favorable results.

Project description:PurposeThe current paradigm in the development of high-grade serous ovarian carcinoma (HGSC) proposes that the majority of HGSCs arise from precursor serous tubal intraepithelial carcinoma (STIC) lesions of the fallopian tube. Here we survey genome-wide methylation in HGSC precursor lesions to identify genomic regions that exhibit high-specificity differential hypermethylation for potential use as biomarkers for detecting STIC and HGSC at stages when curative intervention likely remains feasible.Experimental designWe first identified quality control criteria for performing reliable methylomic analysis of DNA-limited tubal precursor lesions with the Illumina Infinium MethylationEPIC array. We then used this platform to compare genome-wide methylation among 12 STICs with paired adjacent-normal epithelia, one p53 signature lesion and two samples of concurrent HGSC. The resulting methylomic data were analyzed by unsupervised hierarchical clustering and multidimensional analysis. Regions of high-confidence STIC-specific differential hypermethylation were identified using selective bioinformatic criteria and compared with published MethylationEPIC data from 23 HGSC tumors and 11 healthy fallopian tube mucosae.ResultsUnsupervised analysis showed that STICs largely clustered with HGSCs, but were clearly distinct from adjacent-normal fallopian tube epithelia. Forty-two genomic regions exhibited high-confidence STIC-specific differential hypermethylation, of which 17 (40.5%) directly overlapped with HGSC-specific differentially methylated regions. Methylation at these shared loci was able to completely distinguish STIC and HGSC samples from normal and adjacent-normal specimens.ConclusionsOur results suggest that most STICs are epigenetically similar to HGSCs and share regions of differential hypermethylation that warrant further evaluation for potential use as biomarkers for early detection of ovarian HGSC.See related commentary by Ishak and De Carvalho, p. 6083.

Project description:CD155, an immunoglobulin-like adhesion molecule, plays an important role in carcinoma such as cells migration, proliferation, metastasis, and tumor immune. The upregulation of CD155 has been found in several human malignancies, but its expression in cholangiocarcinoma (CCA) still remains unclear. The aim of this study is to investigate CD155 expression and its correlations with clinicopathologic data, angiogenesis, and prognosis in the patients with CCA.CD155 expression was investigated in 20 paired CCA tissues and corresponding paracancerous tissues by Western blotting and quantitative real-time polymerase chain reaction assays at protein and mRNA levels. Besides, this study evaluated the correlation between the tumor CD155 expression and the level of both vascular endothelial growth factor and intratumoral microvessel density by immunohistochemistry in 90 cases of CCA. Moreover, the clinical and prognostic significance of CD155 in CCA was assessed by immunohistochemistry.The protein and mRNA levels of CD155 were higher in CCA tumor tissues compared with corresponding paracancerous tissues (P<0.05). Immunohistochemical staining showed that CD155 was located in the cytoplasm of carcinoma cells and overexpressed in 61.2% (55/90) CCA tissues. Obviously, CD155 expression level was significantly correlated with tumor histological grade (P=0.002), lymph node metastasis (P<0.001), and tumor-node-metastasis (P=0.03). Additionally, Spearman rank correlation test demonstrated that CD155 expression was positively associated with vascular endothelial growth factor (r=0.481, P<0.001) and microvessel density (r=0.442, P<0.001) in CCA tissues. More importantly, CCA patients with high CD155 expression had a markedly shorter overall survival (P<0.001) and disease-free survival (P<0.001) after surgical resection, and multivariate analysis showed that high CD155 expression was an independent poor prognostic predictor of overall survival and disease-free survival (P<0.001).Our results revealed that upregulated CD155 correlated with aggressive clinicopathologic characteristics, angiogenesis, and poor prognosis in CCA and may be a promising prognostic biomarker for the CCA patients.

Project description:BackgroundWith less than a 5% survival rate pancreatic adenocarcinoma (PDAC) is almost uniformly lethal. In order to make a significant impact on survival of patients with this malignancy, it is necessary to diagnose the disease early, when curative surgery is still possible. Detailed knowledge of the natural history of the disease and molecular events leading to its progression is therefore critical.Methods and findingsWe have analysed the precursor lesions, PanINs, from prophylactic pancreatectomy specimens of patients from four different kindreds with high risk of familial pancreatic cancer who were treated for histologically proven PanIN-2/3. Thus, the material was procured before pancreatic cancer has developed, rather than from PanINs in a tissue field that already contains cancer. Genome-wide transcriptional profiling using such unique specimens was performed. Bulk frozen sections displaying the most extensive but not microdissected PanIN-2/3 lesions were used in order to obtain the holistic view of both the precursor lesions and their microenvironment. A panel of 76 commonly dysregulated genes that underlie neoplastic progression from normal pancreas to PanINs and PDAC were identified. In addition to shared genes some differences between the PanINs of individual families as well as between the PanINs and PDACs were also seen. This was particularly pronounced in the stromal and immune responses.ConclusionsOur comprehensive analysis of precursor lesions without the invasive component provides the definitive molecular proof that PanIN lesions beget cancer from a molecular standpoint. We demonstrate the need for accumulation of transcriptomic changes during the progression of PanIN to PDAC, both in the epithelium and in the surrounding stroma. An identified 76-gene signature of PDAC progression presents a rich candidate pool for the development of early diagnostic and/or surveillance markers as well as potential novel preventive/therapeutic targets for both familial and sporadic pancreatic adenocarcinoma.

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Precursor Lesions of Cholangiocarcinoma: A Clinicopathologic Review.

Publications

Precursor Lesions of Cholangiocarcinoma: A Clinicopathologic Review.

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