Mucin histochemistry of stomach in metaplasia and adenocarcinoma: An observation

Mandal, Prakas Kumar; Chakrabarti, Sudipta; Ray, Amit; Chattopadhyay, Brajadulal; S, Das

doi:10.4103/0971-5851.125232

Cited by 8 publications

(3 citation statements)

References 15 publications

(20 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, we wanted to test the hypothesis that ABPAS may distinguish primary pulmonary mucinous AC from metastases to the lungs, as a limited occurrence of acid mucins has been demonstrated in e.g. gastric cancer 19 . Although there were no metastases to the lungs of gastric origin in our material, our data show that acid mucins are present in metastases of various origin, also previously known for e.g.…”

Section: Discussionmentioning

confidence: 99%

Mucin staining is of limited value in addition to basic immunohistochemical analyses in the diagnostics of non-small cell lung cancer

Micke

Botling

Mattsson

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Accurate diagnosis of histological type is important for therapy selection in lung cancer. Immunohistochemical (IHC) and histochemical stains are often used to complement morphology for definite diagnosis and are incorporated in the WHO classification. Our main aim was to compare different mucin stains and assess their value in relation to common IHC analyses in lung cancer diagnostics. Using tissue microarrays from 657 surgically treated primary lung cancers, we evaluated the mucin stains periodic acid-Schiff with diastase (PASD), alcian blue–periodic acid-Schiff (ABPAS) and mucicarmine, and compared with the IHC markers p40, p63, cytokeratin 5, thyroid transcription factor 1 (TTF-1), napsin A and cytokeratin 7. Ten or more cytoplasmic mucin inclusions in a tissue microarray core were seen in 51%, 48% and 31% of the 416 adenocarcinomas and 3%, 4% and 0.5% of the 194 squamous cell carcinomas with PASD, ABPAS and mucicarmine, respectively. Diagnostic pitfalls, such as entrapped benign epithelium, apoptotic/necrotic cells and glycogen, partly differed for the mucin stains. TTF-1 and napsin A IHC stainings had similar specificity but better sensitivity for adenocarcinoma than the mucin stains, but addition of PASD or ABPAS identified more tumors as adenocarcinomas (n = 8 and n = 10, respectively) than napsin A (n = 1) in cases with solid growth that were negative for TTF-1 and p40. We conclude that PASD and ABPAS have similar diagnostic performance and that these markers are of value in poorly differentiated cases. However, morphology and TTF-1 and p40 IHC staining is sufficient for correct diagnosis in most non-small cell lung cancers.

show abstract

Section: Discussionmentioning

confidence: 99%

Mucin staining is of limited value in addition to basic immunohistochemical analyses in the diagnostics of non-small cell lung cancer

Micke

Botling

Mattsson

et al. 2019

Sci Rep

View full text Add to dashboard Cite

show abstract

“…The red arrow in the representative image indicates a typical goblet cell in an irregular gastric gland in the DCA group ( Figure 9a ). Second, since 65.2% of cases of IM columnar cells that secreted intestinal mucus showed AB-positive staining due to the presence of acidic mucin, 44 AB/PAS staining was further performed to identify the type of mucin. Consequently, mucosal columnar cells in the control mice were stained magenta with PAS, indicating the presence of neutral mucin, whereas columnar cells in the bottoms of glands and the fovea of gastric mucosa in all cases in the DCA group reacted with AB and were stained blue-violet ( Figure 9b ).…”

Section: Resultsmentioning

confidence: 99%

Deoxycholic acid induces gastric intestinal metaplasia by activating STAT3 signaling and disturbing gastric bile acids metabolism and microbiota

et al. 2022

View full text Add to dashboard Cite

Intestinal metaplasia (IM) is the inevitable precancerous stage to develop intestinal-type gastric cancer (GC). Deoxycholic acid (DCA) is the main bile acid (BA) component of duodenogastric reflux and has shown an increased concentration during the transition from chronic gastritis to IM associated with continued STAT3 activation. However, the mechanisms underlying how DCA facilitates IM in the gastric epithelium need exploration. We evaluated IM and bile reflux in corpus tissues from 161 subjects undergoing GC screening. Cell survival and proliferation, proinflammatory cytokine expression and TGR5/STAT3/KLF5 axis activity were measured in normal human gastric cells, cancer cells, and organoid lines derived from C57BL/6, FVB/N and insulin-gastrin (INS-GAS) mice treated with DCA. The effects of DCA on IM development were determined in INS-GAS mice with long-term DCA supplementation, after which the gastric bacterial and BA metabolic profiles were measured by 16S rRNA gene sequencing and LC-MS. We revealed a BA-triggered TGR5/STAT3/KLF5 pathway in human gastric IM tissues. In gastric epithelial cells, DCA promoted proliferation and apoptotic resistance, upregulated proinflammatory cytokines and IM markers, and facilitated STAT3 phosphorylation, nuclear accumulation and DNA binding to the KLF5 promoter. DCA triggered STAT3 signaling and the downstream IM marker KLF5 in mouse gastric organoids in vitro and in vivo . In INS-GAS mice, DCA promoted the accumulation of serum total BAs and accelerated the stepwise development of gastric IM and dysplasia. DCA induced gastric environmental alterations involving abnormal BA metabolism and microbial dysbiosis, in which the Gemmobacter and Lactobacillus genera were specifically enriched. Lactobacillus genus enrichment was positively correlated with increased levels of GCA, CA, T-α-MCA, TCA and β-MCA in DCA-administrated INS-GAS mice. DCA promotes nuclear STAT3 phosphorylation, which mediates KLF5 upregulation associated with gastric inflammation and IM development. DCA disturbs the gastric microbiome and BA metabolism homeostasis during IM induction.

show abstract

“…Moreover, the Alcian blue (pH 2.5) mucin stain specifically detects acidic mucin, presenting a positive result for intestinal-type G.C. [46]. Notably, the H+/K+ ATPase-Cre; LKB1 L/L ; PTEN L/L mice exhibited strong Alcian blue staining in the lower region and isthmus of the gland lesions, setting them apart from wild-type mice stomach (Figure 5).…”

Section: H+/k+ Atpase-cre Lkb1 L/l Pten L/l Mice Develop Intestinal-t...mentioning

confidence: 99%

Development of a Genetically Engineered Mouse Model Recapitulating LKB1 and PTEN Deficiency in Gastric Cancer Pathogenesis

Fang,

Hung,

Lau

et al. 2023

Cancers

View full text Add to dashboard Cite

The LKB1 and PTEN genes are critical in gastric cancer (G.C.) development. LKB1, a robust tumor suppressor gene, encodes a serine/threonine kinase that directly triggers the activation of AMPK—an integral cellular metabolic kinase. The role of the LKB1 pathway extends to maintaining the stability of epithelial junctions by regulating E-cadherin expression. Conversely, PTEN, a frequently mutated tumor suppressor gene in various human cancers, emerges as a pivotal negative regulator of the phosphoinositide 3-kinase (PI3K) signaling pathway. This study is set to leverage the H+/K+ ATPase Cre transgene strain to precisely target Cre recombinase expression at parietal cells within the stomach. This strategic maneuver seeks to selectively nullify the functions of both LKB1 and PTEN in a manner specific to the stomach, thereby instigating the development of G.C. in a fashion akin to human gastric adenocarcinoma. Moreover, this study endeavors to dissect the intricate ways in which these alterations contribute to the histopathologic advancement of gastric tumors, their potential for invasiveness and metastasis, their angiogenesis, and the evolving tumor stromal microenvironment. Our results show that conditional deletion of PTEN and LKB1 provides an ideal cancer microenvironment for G.C. tumorigenesis by promoting cancer cell proliferation, angiogenesis, and metastasis.

show abstract

Mucin histochemistry of stomach in metaplasia and adenocarcinoma: An observation

Cited by 8 publications

References 15 publications

Mucin staining is of limited value in addition to basic immunohistochemical analyses in the diagnostics of non-small cell lung cancer

Mucin staining is of limited value in addition to basic immunohistochemical analyses in the diagnostics of non-small cell lung cancer

Deoxycholic acid induces gastric intestinal metaplasia by activating STAT3 signaling and disturbing gastric bile acids metabolism and microbiota

Development of a Genetically Engineered Mouse Model Recapitulating LKB1 and PTEN Deficiency in Gastric Cancer Pathogenesis

Contact Info

Product

Resources

About