Clinicopathological characteristics of pancreatic ductal adenocarcinoma with invasive micropapillary carcinoma component with emphasis on the usefulness of PKCζ immunostaining for detection of reverse polarity

We herein present a case of uterine cervical invasive micropapillary carcinoma (IMPC) in a 35-year-old woman. She had neither specific symptoms nor any previous gynecological history. A cervical punch biopsy revealed a high-grade squamous intraepithelial lesion and concurrent intestinal-type mucinous carcinoma. Based on the preoperative diagnosis of endocervical adenocarcinoma, she underwent radical hysterectomy with bilateral salpingo-oophorectomy and bilateral pelvic lymph node dissection. Grossly, there was an ovoid, slightly elevated mass with surface nodularity in the lower endocervix, measuring 10 × 8 mm. Histologically, the tumor consisted predominantly of tufts of tumor cells arranged in micropapillary structures devoid of fibrovascular cores and surrounded by clear, empty, lacunar spaces between tumor cell nests and stroma. The IMPC component comprised 90% of the entire tumor volume. The greatest dimension and stromal invasion depth of the IMPC were 8 and 3 mm, respectively (FIGO stage IA2). Immunostaining revealed that mucin 1 (MUC1) surrounded each micropapillary structure, indicating the reverse epithelial polarity of the glandular cells. MUC1 was localized predominantly in the stroma-facing surface of the cell clusters, accentuating the outlines of the micropapillary structures by forming a distinct, characteristic band on this surface. In addition, targeted sequencing analysis of the IMPC revealed a missense <i>PIK3CA</i> mutation (c.1633G>A). In summary, we present the clinicopathological characteristics of cervical IMPC. We demonstrate for the first time that IMPC of the uterine cervix harbors a pathogenic missense mutation in <i>PIK3CA</i>. Further investigations using larger cohorts of patients are necessary to confirm these findings.

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Upregulated CD58 is associated with clinicopathological characteristics and poor prognosis of patients with pancreatic ductal adenocarcinoma

Cancer Cell International ◽

10.1186/s12935-021-02037-0 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Yalu Zhang ◽

Qiaofei Liu ◽

Jingkai Liu ◽

Quan Liao

Keyword(s):

Pancreatic Ductal Adenocarcinoma ◽

Epithelial Mesenchymal Transition ◽

Histological Grade ◽

Disease Free Survival ◽

Enrichment Analysis ◽

Functional Enrichment Analysis ◽

Clinicopathological Characteristics ◽

Functional Enrichment ◽

Ductal Adenocarcinoma ◽

Mesenchymal Transition

Abstract Background CD58 has been demonstrated to be abnormally expressed in multiple hematopoietic malignancies and solid tumors and plays an essential role in tumorigenesis and progression; however, its clinical significance and prognostic value in pancreatic ductal adenocarcinoma (PDAC) remain unknown. Methods Based on diverse online public databases and 81 PDAC samples of tissue microarray-based immunohistochemistry (IHC), we evaluated CD58 expression in PDAC patients and analyzed its association with clinicopathological characteristics, clinical outcomes, and infiltration of immune cells in PDAC. Furthermore, the correlation between CD58 and the cancer stem cell (CSC)-related, epithelial–mesenchymal transition (EMT)-related, and immune-related markers were detected. Besides, the functional enrichment analysis and related pathways were analyzed and visualized. Results CD58 expression was elevated in pancreatitis and PDAC tissues than normal pancreas or adjacent nontumor tissues. The positive cases of CD58 (e.g. more than 50% positive cells) in PDAC account for 95.06% (77/81). Upregulated CD58 in cancer tissues was associated with worse histological grade, larger tumor size, and poorer overall survival and disease-free survival in PDAC patients. Furthermore, Cox multivariate regression analysis revealed that CD58 was an independent prognostic factor in PDAC. CD58 expression was correlated with infiltrations of neutrophils, CD8+ T cells, and dendritic cells (DCs). In addition, correlation gene analysis indicated that CD58 expression was strongly correlated with immune-related, EMT-related, and CSC-related markers. Functional enrichment analysis and KEGG pathway manifested that CD58 might be involved in PDAC initiation and progression. Conclusions CD58 expression is upregulated in PDAC tissues and its high expression is notably related to poor survival of PDAC. Therefore, CD58 may serve as a novel and effective marker for predicting the prognosis of PDAC patients.

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