Comprehensive clinicopathologic features in autoimmune atrophic gastritis: Insights from a European cohort of 57 patients.

CONTEXT: Autoimmune atrophic gastritis (AAG) is a frequently underdiagnosed disease due to its broad-spectrum clinical presentation. The diagnosis is based on histological confirmation of corpus-restricted metaplastic chronic atrophic gastritis. OBJECTIVE: To thoroughly describe the histological features of a European cohort of AAG patients. DESIGN: Clinical and pathological data of 57 out of 676 patients diagnosed with AAG were reviewed. RESULTS: Thirty-nine patients were female and eighteen were male. The mean age was 62 years. Antibodies were identified in 32/42 patients (76 %). Vitamin B12 levels were low (< 200 pg/mL) in 37/54 patients (69 %). Serum gastrin levels was elevated (> 115 pg/mL) in all cases tested. Associated autoimmune/inflammatory conditions were identified in 20/57 patients (35 %). Histologically, deep chronic inflammation was present in 46/57 (81 %) patients. Complete destruction of oxyntic glands was observed in 45/57 (79 %) patients. Pyloric metaplasia was present in 54/57 (95 %) patients, intestinal metaplasia in 51/57 (89 %) patients, and pancreatic metaplasia in 20/57 (35 %) patients. Among ECL cell proliferation, linear hyperplasia was present in all 57/57 patients, micronodular hyperplasia in 55/57 patients, and adenomatoid hyperplasia in 10/57 patients. ECL cell dysplasia was identified in 5/57 patients, and neuroendocrine microtumor in 4/57 patients. CONCLUSIONS: The diagnosing of AAG remains challenging due to the greater variability in symptoms than previously recognized. It is important to consider chronic AAG, especially with other concurrent autoimmune conditions. The importance of accurate diagnosis and surveillance is based on the potential development of type 1 gastric neuroendocrine tumor and increased risk of gastric adenocarcinoma.

Nephrogenic Adenoma: A Pitfall on Frozen Section of Urethral Strictures.

Urethral strictures are a common cause of urinary obstruction which can be treated with surgical resection. Frozen sections are rare and pose a diagnostic challenge to pathologists due to the presence of benign lesions such as nephrogenic adenoma. We retrospectively examined all specimens of urethral stricture resections submitted to pathology at our institution from 2012 to 2022 (n = 258). Final pathology reports were searched to identify patients with dysplasia, carcinoma, or nephrogenic adenoma. When available, frozen section reports were also examined and compared to the final report, and additional clinical history and microscopic images were collected for patients with nephrogenic adenoma. Nephrogenic adenoma was identified in 3.8% (10/258) of urethral stricture resections. Dysplasia was identified in one patient who underwent two separate resections, and squamous cell carcinoma was found in one resection. Intraoperative frozen section was requested in 3.4% of resections (9/258). In two resections, an initial diagnosis of squamous cell carcinoma was initially favoured, however when reviewed with a genitourinary pathologist the diagnosis was changed to "reactive process" with a final diagnosis of nephrogenic adenoma. Nephrogenic adenoma can be challenging on frozen section due to variable architectural patterns, inflammation, and reactive changes. While urethral strictures are relatively common, their assessment by frozen section is rare and pathologists may lack familiarity with the variable morphology of benign entities that can be seen on frozen section resulting in their misinterpretation. We highlight this potential diagnostic pitfall and demonstrate the value of a second opinion prior to definitive frozen section diagnosis of malignancy.

TFE3-rearranged RCC with osseous metaplasia found on bone mass densitometry.

Introduction and importance: Renal cell carcinoma (RCC) is the most common primary renal malignancy in patients between the ages of 50 and 70. A rare described variant of RCC is transcription factor for immunoglobulin heavy-chain enhancer 3 (TFE3) rearranged RCC. Osseous metaplasia, which refers to the occurrence of normal bone tissue in soft tissue, has been observed in all subtypes of renal cell carcinoma (RCC); however, only three previous case reports have documented the occurrence of osseous metaplasia in TFE3-rearranged RCC. Case presentation: We present a case of a 65-year-old woman presenting with an incidentally discovered calcified Bi-lobed renal mass detected on bone densitometry composed of a calcified thick-walled cyst measuring 7×6.5×6.5 cm showing intraluminal densities and heterogeneous content, and a lobulated partially exophytic renal mass measuring 4.5×5.5×4.5 cm. The patient underwent robotic-assisted radical nephrectomy confirming the diagnosis of RCC with osseous metaplasia extending into the pelvic calyces and renal sinus fat implicating a pathological stage of T3a. Clinical discussion: TFE3-rearranged RCCs represent a rare sub-classification in adult RCCs. It may be associated with unfavorable prognosis and aggressive patterns of disease in the presence of osseous metaplasia. Conclusion: This is the first case in the literature of TFE3-rearranged RCC with osseous metaplasia on bone mass densitometry scan and the fourth case of TFE3-rearranged RCC with osseous metaplasia. The patient is to be treated as a high-risk patient and to be monitored closely for recurrence of malignancy, as indicated in the EAU guidelines.

Identification of Lipomatous Metaplasia in a Cortisol-secreting Adrenocortical Adenoma Treated With Mifepristone.

Adrenal adenomas are benign tumors of the adrenal cortex that may secrete excess hormones, such as cortisol. They are most commonly discovered during imaging studies for unrelated problems. Lipomatous metaplasia is a rare degenerative change in adrenal adenomas, characterized by the presence of adipose tissue and hematopoietic elements within the tumor. In this report, we present a case of an adrenal adenoma with lipomatous metaplasia in a patient with hypertension, hyperlipidemia, and type II diabetes mellitus. The discovery of this adrenal mass was prompted by an evaluation of the patient's progressive hirsutism. The tumor was found to be secreting cortisol, leading to Cushing syndrome. The patient subsequently underwent surgical resection of the mass after being treated with mifepristone. The histopathological examination confirmed it to be an adrenal cortical neoplasm with lipomatous metaplasia, characterized by uncertain malignant potential. The patient did well postoperatively. Three months after left adrenalectomy, the patient's hirsutism, A1c, and hypertension improved, allowing a reduction in antihypertensives. Her body mass index stabilized, her triglyceride decreased, and her dehydroepiandrosterone sulfate level normalized. She continued to do well at follow-up visits. Overall, this was a rare case of a functioning adrenal adenoma with lipomatous metaplasia, presenting both diagnostic and therapeutic challenges.

p53 mutation biases squamocolumnar junction progenitor cells towards dysplasia rather than metaplasia in Barrett's oesophagus.

BACKGROUND: While p53 mutations occur early in Barrett's oesophagus (BE) progression to oesophageal adenocarcinoma (EAC), their role in gastric cardia stem cells remains unclear. OBJECTIVE: This study investigates the impact of p53 mutation on the fate and function of cardia progenitor cells in BE to EAC progression, particularly under the duress of chronic injury. DESIGN: We used a BE mouse model (L2-IL1ß) harbouring a Trp53 mutation (R172H) to study the effects of p53 on Cck2r+ cardia progenitor cells. We employed lineage tracing, pathological analysis, organoid cultures, single-cell RNA sequencing (scRNA-seq) and computational analyses to investigate changes in progenitor cell behaviour, differentiation patterns and tumour progression. Additionally, we performed orthotopic transplantation of sorted metaplastic and mutant progenitor cells to assess their tumourigenic potential in vivo. RESULTS: The p53 mutation acts as a switch to expand progenitor cells and inhibit their differentiation towards metaplasia, but only amidst chronic injury. In L2-IL1ß mice, p53 mutation increased progenitors expansion and lineage-tracing with a shift from metaplasia to dysplasia. scRNA-seq revealed dysplastic cells arise directly from mutant progenitors rather than progressing through metaplasia. In vitro, p53 mutation enhanced BE progenitors' organoid-forming efficiency, growth, DNA damage resistance and progression to aneuploidy. Sorted metaplastic cells grew poorly with no progression to dysplasia, while mutant progenitors gave rise to dysplasia in orthotopic transplantation. Computational analyses indicated that p53 mutation inhibited stem cell differentiation through Notch activation. CONCLUSIONS: p53 mutation contributes to BE progression by increasing expansion and fitness of undifferentiated cardia progenitors and preventing their differentiation towards metaplasia.

Gastric Cancer and Intestinal Metaplasia: Differential Metabolic Landscapes and New Pathways to Diagnosis.

Gastric cancer (GC) is the fifth most common cause of cancer-related death worldwide. Early detection is crucial for improving survival rates and treatment outcomes. However, accurate GC-specific biomarkers remain unknown. This study aimed to identify the metabolic differences between intestinal metaplasia (IM) and GC to determine the pathways involved in GC. A metabolic analysis of IM and tissue samples from 37 patients with GC was conducted using ultra-performance liquid chromatography with tandem mass spectrometry. Overall, 665 and 278 significant features were identified in the aqueous and 278 organic phases, respectively, using false discovery rate analysis, which controls the expected proportion of false positives among the significant results. sPLS-DA revealed a clear separation between IM and GC samples. Steroid hormone biosynthesis, tryptophan metabolism, purine metabolism, and arginine and proline metabolism were the most significantly altered pathways. The intensity of 11 metabolites, including N1, N2-diacetylspermine, creatine riboside, and N-formylkynurenine, showed significant elevation in more advanced GC. Based on pathway enrichment analysis and cancer stage-specific alterations, we identified six potential candidates as diagnostic biomarkers: aldosterone, N-formylkynurenine, guanosine triphosphate, arginine, S-adenosylmethioninamine, and creatine riboside. These metabolic differences between IM and GC provide valuable insights into gastric carcinogenesis. Further validation is needed to develop noninvasive diagnostic tools and targeted therapies to improve the outcomes of patients with GC.

Protein Biomarkers of Gastric Preneoplasia and Cancer Lesions in Blood: A Comprehensive Review.

Gastric cancer (GC) is a major cause of cancer-related mortality worldwide. It is often associated with a bad prognosis because of its asymptomatic phenotype until advanced stages, highlighting the need for its prevention and early detection. GC development is preceded by the emergence of gastric preneoplasia lesions (GPNLs), namely atrophic gastritis (AG), intestinal metaplasia (IM), and dysplasia (DYS). GC is currently diagnosed by endoscopy, which is invasive and costly and has limited effectiveness for the detection of GPNLs. Therefore, the discovery of non-invasive biomarkers in liquid biopsies, such as blood samples, in order to identify the presence of gastric preneoplasia and/or cancer lesions at asymptomatic stages is of paramount interest. This comprehensive review provides an overview of recently identified plasma/serum proteins and their diagnostic performance for the prediction of GPNLs and early cancer lesions. Autoantibodies appear to be promising biomarkers for AG, IM and early gastric cancer detection, along with inflammation and immunity-related proteins and antibodies against H. pylori virulence factors. There is a lack of specific protein biomarkers with which to detect DYS. Despite the need for further investigation and validation, some emerging candidates could pave the way for the development of reliable, non-invasive diagnostic tests for the detection and prevention of GC.

Autoimmune gastritis studies and gastric cancer: True renaissance or bibliometric illusion.

A bibliometric analysis of studies dedicated to autoimmune gastritis (AIG) recently published demonstrated a noteworthy surge in publications over the last three years. This can be explained by numerous publications from different regions of the world reporting the results of several studies that stimulated reassessment of our view of AIG as a precancerous condition. Follow-up studies and retrospective analyses showed that the risk of gastric cancer (GC) in AIG patients is much lower than expected if the patients ever being infected with Helicobacter pylori (H. pylori) were excluded. The low prevalence of precancerous lesions, such as the incomplete type of intestinal metaplasia, may explain the low risk of GC in AIG patients because the spasmolytic polypeptide-expressing metaplasia commonly observed in AIG does not involve clonal reprogramming of the gastric gland and can be considered as an adaptive change rather than a true precancerous lesion. However, changes in gastric secretion due to the progression of gastric atrophy during the course of AIG cause changes in the gastric mic-robiome, stimulating the growth of bacterial species such as streptococci, which may promote the development of precancerous lesions and GC. Thus, Streptococcus anginosus exhibited a robust proinflammatory response and induced the gastritis-atrophy-metaplasia-dysplasia sequence in mice, reproducing the well-established process for carcinogenesis associated with H. pylori. Prospective studies in H. pylori-naïve patients evaluating gastric microbiome changes during the long-term course of AIG might provide an explanation for the enigmatic increase in GC incidence in the last decades in younger cohorts, which has been reported in economically developed countries.

Confocal laser endomicroscopy as a new diagnostic tool for poorly differentiated gastric adenocarcinoma.

Gastric cancer (GC) is a multifactorial disease, where both environmental and genetic features can have an impact on its occurrence and development. GC represents one of the leading causes of cancer-related deaths worldwide. GC is most frequent in males and is believed to arise from a series of premalignant lesions. The detection of GC at an early stage is crucial because early GC, which is an invasive stomach cancer confined to the mucosal or submucosal lining, may be curable with a reported 5-year survival rate of more than 90%. Advanced GC usually has a poor prognosis despite current treatment standards. The diagnostic efficacy of conventional endoscopy (with light endoscopy) is currently limited. Confocal laser endomicroscopy is a novel imaging technique that allows real-time in vivo histological examination of mucosal surfaces during endoscopy. Confocal laser endomicroscopy may be of great importance in the surveillance of precancerous gastric lesions and in the diagnosis of GC. In this editorial we commented on the article about this topic published by Lou et al in the recent issue of the World Journal of Clinical Cases.

Unveiling Cancer-Related Metaplastic Cells in Both Helicobacter pylori Infection and Autoimmune Gastritis.

BACKGROUND & AIMS: Gastric metaplasia may arise as a consequence of chronic inflammation and is associated with an increased risk of gastric cancer development. Although Helicobacter pylori (Hp) infection and autoimmune gastritis (AIG) both induce gastric metaplasia, possible distinctions in resulting metaplastic cells and their respective cancer risks requires further investigation. METHODS: Using both mouse models and human participants, we scrutinized the metaplasia originating from Hp infection and AIG. Gastric pathology and metaplasia were examined through histopathologic assessment. Molecular features of metaplastic cells were defined using single-cell transcriptomics in murine models of Hp infection and AIG, as well as in human biopsy specimens from patients with Hp infection and AIG. Expression of a newly defined cancer-related metaplastic biomarker was confirmed through immunofluorescence. RESULTS: Metaplasia in Hp infection and AIG displayed comparable histopathologic and transcriptional features. Diverse metaplastic subtypes were identified across both disease settings, with subtle differences in the prevalence of certain subtypes between inflammatory contexts. Notably, Hp infection did not drive a unique metaplastic cell phenotype. One metaplastic subtype, which resembled incomplete intestinal metaplasia and shared transcriptional features with gastric cancer, was identified in both diseases. This cancer-like metaplastic subtype was characterized by expression of the cancer-associated biomarker alanyl aminopeptidase N/CD13. CONCLUSION: Both Hp infection and AIG trigger a diverse array of metaplastic cell types. Identification of a cancer-related metaplastic cell uniquely expressing alanyl aminopeptidase N/CD13, present in both Hp- and AIG-induced gastritis, indicates the carcinogenic capacity of both diseases. This discovery can guide early detection and risk stratification for patients with chronic gastritis.

Predicting Regression of Barrett's Esophagus-Can All the King's Men Put It Together Again?

The primary pre-neoplastic lesion of the lower esophagus in the vicinity of the gastroesophageal junction (GEJ) is any Barrett's esophageal lesions (BE), and esophageal neoplasia has increased in the US population with predispositions (Caucasian males, truncal obesity, age, and GERD). The responses to BE are endoscopic and screening cytologic programs with endoscopic ablation of various forms. The former have not been proven to be cost-effective and there are mixed results for eradication. A fresh approach is sorely needed. We prospectively followed 2229 mostly male veterans at high risk for colorectal cancer in a 27-year longitudinal long-term study, collecting data on colorectal neoplasia development and other preneoplastic lesions, including BE and spontaneous regression (SR). Another cross-sectional BE study at a similar time period investigated antigenic changes at the GEJ in both BE glandular and squamous mucosa immunohistochemistry and the role of inflammation. Ten of the prospective cohort (21.7%) experienced SR out of a total of forty-six BE patients. Significant differences between SR and stable BE were younger age (p < 0.007); lower platelet levels (p < 0.02); rectal p87 elevation in SR (p < 0.049); a reduced innate immune system (InImS) FEREFF ratio (ferritin: p87 colonic washings) (p < 0.04). Ancillary testing showed a broad range of neoplasia biomarkers. InImS markers may be susceptible to intervention using commonplace and safe medical interventions and encourage SR.

Transdifferentiation occurs without resetting development-specific DNA methylation, a key determinant of full-function cell identity.

A number of studies have demonstrated that it is possible to directly convert one cell type to another by factor-mediated transdifferentiation, but in the vast majority of cases, the resulting reprogrammed cells are unable to maintain their new cell identity for prolonged culture times and have a phenotype only partially similar to their endogenous counterparts. To better understand this phenomenon, we developed an analytical approach for better characterizing trans-differentiation-associated changes in DNA methylation, a major determinant of long-term cell identity. By examining various models of transdifferentiation both in vitro and in vivo, our studies indicate that despite convincing expression changes, transdifferentiated cells seem unable to alter their original developmentally mandated methylation patterns. We propose that this blockage is due to basic developmental limitations built into the regulatory sequences that govern epigenetic programming of cell identity. These results shed light on the molecular rules necessary to achieve complete somatic cell reprogramming.

Predictive Neuromarker Patterns for Calcification Metaplasia in Early Tendon Healing.

Unsuccessful tendon healing leads to fibrosis and occasionally calcification. In these metaplastic drifts, the mouse AT preclinical injury model represents a robust experimental setting for studying tendon calcifications. Previously, calcium deposits were found in about 30% of tendons after 28 days post-injury. Although a neuromediated healing process has previously been documented, the expression patterns of NF200, NGF, NPY, GAL, and CGRP in mouse AT and their roles in metaplastic calcific repair remain to be explored. This study included a spatiotemporal analysis of these neuromarkers during the inflammatory phase (7 days p.i.) and the proliferative/early-remodelling phase (28 days p.i.). While the inflammatory phase is characterised by NF200 and CGRP upregulation, in the 28 days p.i., the non-calcified tendons (n = 16/24) showed overall NGF, NPY, GAL, and CGRP upregulation (compared to 7 days post-injury) and a return of NF200 expression to values similar to pre-injury. Presenting a different picture, in calcified tendons (n = 8), NF200 persisted at high levels, while NGF and NPY significantly increased, resulting in a higher NPY/CGRP ratio. Therefore, high levels of NF200 and imbalance between vasoconstrictive (NPY) and vasodilatory (CGRP) neuromarkers may be indicative of calcification. Tendon cells contributed to the synthesis of neuromarkers, suggesting that their neuro-autocrine/paracrine role is exerted by coordinating growth factors, cytokines, and neuropeptides. These findings offer insights into the neurobiological mechanisms of early tendon healing and identify new neuromarker profiles predictive of tendon healing outcomes.

Characterization of Metronidazole, Clarithromycin and Amoxicillin Resistance Genes in Helicobacter pylori Isolated from Gastroenteritis Patients.

BACKGROUND: Helicobacter pylori (H. pylori)is a Gram-negative, microaerophilic, and spiral shape bacterium that resides inside the human stomach. The human stomach serves as its primary reservoir. Complaints about stomach complication due to H. pylori infections are reported in the majority of populations around the globe. Chronic gastritis and intestinal metaplasia of the gastric mucosa are major complications of a long-term H. pylori infections that can lead to gastric cancer in severe cases. This study aims to characterize H. pylori isolates from gastroenteritis patients and to determine the resistance of H. pylori to various antibiotics. METHODS: In the current study, a total of (n = 80) gastric biopsy samples were randomly collected from gastroenteritis patients in brain-heart infusion broth. These were inoculated on Columbia blood agar supplemented with Helicobacter pylori selective supplement (DENT). After culturing, Microscopy and biochemical tests were performed. The susceptibility profile of H. pylori isolates was evaluated using the Kirby Bauer disk diffusion method. On the basis of the drug resistance profile, a total of (n = 20) isolates including (n = 10) from females and (n = 10) from males were selected for the detection and characterization of resistant genes. After confirmation of H. pylori using 16s rRNA, polymerase chain reaction (PCR) was done for the detection of resistance genes including Metronidazole resistance (rdxA gene), Clarithromycin resistance (23s rRNA gene) and Amoxicillin resistance (Penicillin-binding protein A1 (pbpA1) gene). RESULTS: In a total of (n = 80) samples, H. pylori was isolated from 72.5% (n = 58) samples. Among the positive patients, there were 62% (n = 36) of female positive patients while in males, its ratio was 38% (n = 22). It was more common in the age between 30-50 years 55.17% (n = 32). It has shown the highest resistance towards Metronidazole 90% (n = 52), and the lowest toward Levofloxacin 65% (n = 38). Metronidazole resistance gene (rdxA gene) was detected in (n = 13) isolates including (n = 9) isolates from females and (n = 4) from males. In the case of, the Clarithromycin resistance gene (23s rRNA) (n = 10) was positive for H. pylori including (n = 6) isolates from females and (n = 7) were positive for Amoxicillin (pbpA1 gene) including (n = 2) in female and (n = 5) from male patients. CONCLUSION: This study highlights the increasing incidence of H. pylori infections in both male and female patients. It also revealed the current status of antibiotic resistance and its resistance genes in patients facing gastrointestinal issues. Continuous surveillance of resistant clones will help in formulating strategies that can help in combating of resistant clone. It will also help clinician in proper prescription and management of H. pylori infections.

Global prevalence of gastric intestinal metaplasia: a systematic review and meta-analysis.

BACKGROUND: Gastric intestinal metaplasia (GIM) is a precancerous lesion that increases the risk of gastric cancer. Several preliminary studies have examined the prevalence of GIM. The present systematic review and meta-analysis were conducted aimed estimating the global prevalence of GIM. METHODS: The present systematic review and meta-analysis was conducted based on the PRISMA reporting guidelines in the range of 1988-2022. Articles related to the purpose of the study were obtained from Embase, PubMed, Scopus, Web of Science (WOS), MagIran, SID databases, and Google Scholar search engine using relevant and validated keywords in MeSH/Emtree. Inclusion criteria were observational articles, access to the full text of the article, and articles that reported prevalence. Heterogeneity among studies was examined using the I2 index. The random effects model was used in this review due to the high heterogeneity between the results of the studies. Data were statistically analyzed using the Comprehensive Meta-Analysis (CMA) software. RESULTS: In the initial search, 4946 studies were found, of which 20 articles with a sample size of 57,263 met all the criteria for inclusion in the study. The global prevalence of GIM was 17.5% (95% confidence interval: 14.6-20.8%). The highest percentage of prevalence of GIM belonged to American continent with 18.6% (95% confidence interval: 13.8-24.6%) and patients with gastroesophageal reflux with 22.9% (95% confidence interval: 9.9-44.6%). CONCLUSION: The results of this study showed that the prevalence of GIM in the world is high and needs further investigation. Therefore, it is recommended to be given more attention by experts, officials, and health policymakers.

Pseudoinvasion and squamous metaplasia/morules in colorectal adenomatous polyp: a case report and literature review.

BACKGROUND: Submucosal pseudoinvasion and squamous metaplasia (SM) are incidental and special morphological findings in colorectal adenomas, and both can mimic invasive carcinoma. The coexistence of these two findings further increases the risk of misdiagnosis, posing a great diagnostic challenge to pathologists. From 1979 to 2022, only 8 cases have been reported, which was extremely rare. In this report, we presented a case of sigmoid colon adenoma accompanied by pseudoinvasion and SM. Additionally, relevant literature was analyzed to summarize the clinical and pathological characteristics. CASE PRESENTATION: A 51-year-old Chinese male patient presented with fresh blood after defecation. Electronic colonoscopy revealed multiple polyps, which were removed using a snare and subjected to high-frequency electrocoagulation resection. The largest polyp, located in the sigmoid colon, was a thick pedunculated and lobulated polyp with a maximum diameter of 2.8 cm. The surface of the polyp showed slight ruggedness and redness, and it was sent for pathological examination. Grossly, the polyp had a lobulated and slightly rough surface. Microscopically, it showed a tubulovillous adenoma with focal high-grade dysplasia and mucosal muscle hyperplasia. Glandular elements were observed in the submucosal layer, forming a well-defined lobular structure. Some of the glands displayed cystic change, and focal SM could be seen within the adenoma. SM could manifest as discrete solid cell nests of varying sizes or cribriform-morular-like structures. Immunohistochemical staining showed that SM cells were diffusely positive for cytokeratin 5/6 (CK5/6); p40, p63, and cytokeratin 20 (CK20) were negative; while caudal type homeobox 2 (CDX2) was weakly positive. ß-catenin showed abnormal nuclear expression, and an extremely low Ki67 proliferation index was observed. CONCLUSIONS: Coexistence of SM and pseudoinvasion in colorectal adenomas is highly rare. It is more commonly observed in males and tends to occur in the sigmoid colon. It primarily manifests in tubulovillous adenoma and tubular adenoma, with a majority of cases exhibiting a pedicle. Histologically, it is similar to invasive lesions. The cystic dilation of the submucosal glands, hemosiderin deposition, and the presence of a lamina propria around the submucosal glands without adjacent desmoplastic reaction, suggest pseudoinvasion rather than cancer. The bland cytological morphology and Immunohistochemical markers play a crucial role in distinguishing SM from true invasive lesions.

A Rare Case of Synovial Chondromatosis in the Proximal Interphalangeal Joint of the Right Index Finger.

Synovial chondromatosis is a rare condition that is also known as Reichel syndrome. It is a disorder that affects the monoarticular joints. The proliferation and metaplasia of the synovial cartilage are its defining characteristics. Many tiny, intra-articular osseocartilaginous loose bodies are formed as a result of this proliferation. They are fed by the synovial fluid once they break off from the synovial surface and enter the joint cavity, where they develop into calcification and ossification. If left untreated, it usually causes the afflicted joint to malfunction severely. Large joints such as the knee, hip, elbow, and shoulder joints are frequently the sites of nodular proliferation. Smaller joints such as the hand's interphalangeal and metacarpal joints and thumb are among the more unusual locations. Although the disease usually resolves on its own, conservative management options include painkillers, activity modification, and cryotherapy. Surgical options include synovectomy, which is the gold standard procedure and involves removing the loose bodies. The following case study presents a 60-year-old female patient with a rare instance of synovial chondromatosis. She presented to the outpatient department (OPD) due to escalating pain and swelling in the proximal interphalangeal (PIP) joint of her right index finger, which significantly restricted her range of motion. On the hand X-ray, several small, uniformly sized calcified bodies were visible within the synovium. After negative results from autoimmune disease tests, the patient was recommended for surgical exploration as the patient reported a six-month increase in pain and difficulty flexing his index finger. Surgical exploration of the PIP joint and adjacent proximal and middle phalanx revealed several small, evenly sized, firm, smooth, creamy-white nodules. Post-op, the patient was given a splint cast for a span of seven days, followed by physical therapy, and the range of motion was achieved by the end of six months.

Molecular evolution of intestinal-type early gastric cancer according to Correa cascade.

Early screening is crucial for the prevention of intestinal-type gastric cancer. The objective of the current study was to ascertain molecular evolution of intestinal-type gastric cancer according to the Correa cascade for the precise gastric cancer screening. We collected sequential lesions of the Correa cascade in the formalin-fixed and paraffin-embedded endoscopic submucosal dissection-resected specimens from 14 Chinese patients by microdissection, and subsequently determined the profiles of somatic aberrations during gastric carcinogenesis using the whole exome sequencing, identifying multiple variants at different Correa stages. The results showed that TP53, PCLO, and PRKDC were the most frequently mutated genes in the early gastric cancer (EGC). A high frequency of TP53 alterations was found in low-grade intraepithelial neoplasia (LGIN), which further increased in high-grade intraepithelial neoplasia (HGIN) and EGC. Intestinal metaplasia (IM) had no significant correlation with EGC in terms of mutational spectra, whereas both LGIN and HGIN showed higher genomic similarities to EGC, compared with IM. Based on Jaccard similarity coefficients, three evolutionary models were further constructed, and most patients showed linear progression from LGIN to HGIN, ultimately resulting in EGC. The ECM-receptor interaction pathway was revealed to be involved in the linear evolution. Additionally, the retrospective validation study of 39 patients diagnosed with LGIN indicated that PRKDC mutations, in addition to TP53 mutations, may drive LGIN progression to HGIN or EGC. In conclusion, the current study unveils the genomic evolution across the Correa cascade of intestinal-type gastric cancer, elucidates the underlying molecular mechanisms of gastric carcinogenesis, and provides some evidence for potential personalized gastric cancer surveillance.

Development of Esophageal Epidermoid Metaplasia in a Pediatric Patient After Stevens-Johnson Syndrome.

Esophageal epidermoid metaplasia (EEM) is a rare condition that has not been described in Stevens-Johnson syndrome (SJS) and has only been described once in pediatrics. Neither the relationship, treatment, nor surveillance between SJS, esophageal strictures, and EEM has been established. We report the first case of EEM in an 8-year-old girl with esophageal stricture after SJS. Pediatric patients presenting with dysphagia after SJS should be evaluated for esophageal stricture and subsequent EEM development. Owing to EEM's, association with esophageal squamous cell cancer, close follow-up, biopsy surveillance for dysplasia, endoscopic treatment, and TP53 genetic sequencing should be considered.