Calretinin, CD34, and α-smooth muscle actin in the identification of peritoneal invasive implants of serous borderline tumors of the ovary

Lee, Eung Seok; Leong, Anthony S.‐Y.; Kim, Young‐Sik; Lee, Ju Han; Kim, Insun; Ahn, Geung Hwan; Kim, Hye Sun; Chun, Yi Kyeong

doi:10.1038/modpathol.3800539

Cited by 23 publications

(8 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This process is commonly observed in peritoneal dialysis patients and leads to loss of the mesothelium, fibrosis, and peritoneal membrane failure [130, 131]. A similar transdifferentiation could explain the loss of mesothelial and fibroblast cells and the gain of αSMA-positive myofibroblasts at sites of invasive tumor implantation in the peritoneum [132]. Bone marrow-derived circulating cells and endothelial cells are also activated by TGF-β and contribute to the peritoneal myofibroblast population [131].…”

Section: Derivation Of Tumor-associated Myofibroblastsmentioning

confidence: 99%

Cell–cell and cell–matrix dynamics in intraperitoneal cancer metastasis

Sodek

Murphy

Brown

et al. 2012

Cancer Metastasis Rev

123

163

View full text Add to dashboard Cite

The peritoneal metastatic route of cancer dissemination is shared by cancers of the ovary and gastrointestinal tract. Once initiated, peritoneal metastasis typically proceeds rapidly in a feed-forward manner. Several factors contribute to this efficient progression. In peritoneal metastasis, cancer cells exfoliate into the peritoneal fluid and spread locally, transported by peritoneal fluid. Inflammatory cytokines released by tumor and immune cells compromise the protective, anti-adhesive mesothelial cell layer that lines the peritoneal cavity, exposing the underlying extracellular matrix to which cancer cells readily attach. The peritoneum is further rendered receptive to metastatic implantation and growth by myofibroblastic cell behaviors also stimulated by inflammatory cytokines. Individual cancer cells suspended in peritoneal fluid can aggregate to form multicellular spheroids. This cellular arrangement imparts resistance to anoikis, apoptosis, and chemotherapeutics. Emerging evidence indicates that compact spheroid formation is preferentially accomplished by cancer cells with high invasive capacity and contractile behaviors. This review focuses on the pathological alterations to the peritoneum and the properties of cancer cells that in combination drive peritoneal metastasis.

show abstract

Section: Derivation Of Tumor-associated Myofibroblastsmentioning

confidence: 99%

Cell–cell and cell–matrix dynamics in intraperitoneal cancer metastasis

Sodek

Murphy

Brown

et al. 2012

Cancer Metastasis Rev

123

163

View full text Add to dashboard Cite

show abstract

“…In a previous study, we have demonstrated the occurrence of a-SMA+ myofibroblasts around invasive nests. 10 The histogenesis of clefts, which are seen in the context of stromal desmoplasia, may well be related to the presence of myofibroblasts that contract to cause the cleft by separation of stroma from epithelium. In this study, all type II GI and invasive implants with clefts showed accompanying desmoplastic stromal reaction and occurrence of surrounding a-SMA+ myofibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Glomeruloid peritoneal implants in ovarian serous borderline tumours – distinction between invasive and non‐invasive implants and pathogenesis

Lee

Kim

et al. 2009

Histopathology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Because it appears that true destructive tissue invasion remains the most important and accepted determining feature of so‐called ‘invasive’ implants, methods to delineate the relationship between the implants and the native peritoneum could be of value. Recently, Lee and colleagues investigated a series of implants using immunohistochemistry for calretinin, CD34 and smooth muscle actin to demonstrate mesothelial cells, stromal fibrocytes and myofibroblasts, respectively 28 . They found that invasive implants lacked mesothelial cells or fibrocytes and were associated with myofibroblasts in the stroma.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Lee and colleagues investigated a series of implants using immunohistochemistry for calretinin, CD34 and smooth muscle actin to demonstrate mesothelial cells, stromal fibrocytes and myofibroblasts, respectively. 28 They found that invasive implants lacked mesothelial cells or fibrocytes and were associated with myofibroblasts in the stroma. In contrast, non-invasive implants often showed retained mesothelial cells and CD34+ fibrocytes and showed a more variable myofibroblastic reaction.…”

Section: Discussionmentioning

confidence: 99%

Value of elastin staining in the assessment of peritoneal implants associated with ovarian serous borderline tumours

et al. 2007

View full text Add to dashboard Cite

Demonstration of the PEL using elastin stains can be useful in the subclassification of implants associated with ovarian SBT and is of most value in confirming the superficial distribution of non-invasive lesions. However, evaluation is limited by the absence of a defined elastic layer in a proportion of biopsy specimens, possibly reflecting their superficial location, as well as absence of a distinct PEL in sites such as the omentum.

show abstract

Calretinin, CD34, and α-smooth muscle actin in the identification of peritoneal invasive implants of serous borderline tumors of the ovary

Cited by 23 publications

References 18 publications

Cell–cell and cell–matrix dynamics in intraperitoneal cancer metastasis

Cell–cell and cell–matrix dynamics in intraperitoneal cancer metastasis

Glomeruloid peritoneal implants in ovarian serous borderline tumours – distinction between invasive and non‐invasive implants and pathogenesis

Value of elastin staining in the assessment of peritoneal implants associated with ovarian serous borderline tumours

Contact Info

Product

Resources

About