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In 2015, the World Health Organization renamed mucinous bronchioloalveolar adenocarcinoma as pulmonary invasive mucinous adenocarcinoma (IMA). Due to its low incidence and unclear prognosis with surgical treatment, previous studies have presented opposing survival outcomes. We aimed to investigate the differences in surgical prognosis and prognosis-related risk factors by comparing IMA with non-mucinous invasive adenocarcinoma (NMA).
Primary adenocarcinoma of the bladder accounts for less than 2% of all bladder cancers. There is no report of such a case in a defunctionalized bladder. All reported cases of carcinoma in defunctionalized bladders were either squamous cell, signet ring cell, or transitional cell carcinoma, detected within an average of 5 years after urinary diversion, and all have been associated with chronic inflammation of the bladder. We report on 2 cases of adenocarcinoma that developed in defunctionalized bladders 30 and 8 years after ileal loop diversion for prune belly syndrome and neurogenic bladder, respectively.
Mucinous gastric carcinoma (MGC) is a rare histological subtype of gastric cancer. The clinicopathological characteristics and CT features of MGC remain controversial. This study aimed to determine the clinicopathological characteristics and CT features of MGC. We reviewed 62 patients with MGC and 104 patients with non-mucinous gastric carcinoma (NMGC), pathologically confirmed between 2003 and 2015. There are significant differences in some clinicopathological characteristics and CT features between MGC and NMGC. NMGC occurs preferentially in males and more frequently in the lower third of the stomach. Patients with MGC were characterized by larger tumor size, more advanced tumor stages (II and III) and fewer lymphatic invasions. Layered enhancement (83.3%) was the main pattern of MGC, while the most common pattern in NMGC was homogeneous enhancement (52.6%), followed by heterogonous enhancement (34.6%). The degree of enhancement of the inner layer in MGC was significantly higher than in NMGC (ΔCT of portal venous phase: 54.57 Hu vs. 47.19 Hu, P = 0.034), while the middle or outer layer in MGC was significantly less enhanced (ΔCT of portal venous phase: 19.07 Hu vs. 33.09 Hu, P <0.001). Calcifications were more common in MGC (P <0.001). ROC curves revealed that the most effective variables in distinguishing MGC and NMGC were ΔCT of the middle or outer layer in the arterial phase (AUC=0.774) and portal venous phase (AUC=0.774), followed by the attenuation value of the middle or outer layer in the unenhanced phase (AUC=0.763). Calcifications had a high specificity (98.7%) in the diagnosis of MGC. The accuracy (86.1%), sensitivity (83.3%) and specificity (87.2%) of layered enhancement in diagnosing MGC were all high. Therefore, MGC was more likely to have larger tumor size and more advanced tumor stage (II and III) than NMGC. The thicker gastric wall, layered enhancement pattern and calcification were highly suggestive CT features for differentiating MGC from NMGC.
There is a need to personalize the treatment for rectal cancer patients. The aim of this study was to analyze therapy response and prognosis after preoperative radiotherapy in rectal cancer patients with mucinous adenocarcinoma compared to those with non-mucinous adenocarcinoma. The study included retrospectively collected data from 433 patients, diagnosed with rectal cancer in the South East health care region in Sweden between 2004 and 2012. Patients with non-mucinous adenocarcinoma that received short-course radiotherapy before surgery had better overall survival, cancer specific survival, and disease-free survival, as well as distant- and local-recurrence-free survival (p = 0.003, p = 0.001, p = 0.002, p = 0.002, and p = 0.033, respectively) compared to the patients that received long-course radiotherapy with concomitant capecitabine. The results were still significant after adjusting for sex, age, stage, differentiation, and chemotherapy in the neoadjuvant and/or adjuvant setting, except for local-recurrence-free survival that was trending towards significance (p = 0.070). In patients with mucinous adenocarcinoma, no difference in survival was seen when comparing patients that had short-course radiotherapy and patients that had long-course radiotherapy. However, none of 18 patients with mucinous adenocarcinoma treated with long-course radiotherapy had local tumor progression, compared to 7% of 67 patients with non-mucinous adenocarcinoma. The results indicate that mucinous adenocarcinoma and non-mucinous adenocarcinoma may respond differently to radiotherapy.
Colorectal cancer is a highly heterogeneous disease. Most colorectal cancers are classical adenocarcinoma, and mucinous adenocarcinoma is a unique histological subtype that is known to respond poorly to chemoradiotherapy. The difference in prognosis between mucinous adenocarcinoma and classical adenocarcinoma is controversial. Here, to gain insight into the differences between classical adenocarcinoma and mucinous adenocarcinoma, we analyse 7 surgical tumour samples from 4 classical adenocarcinoma and 3 mucinous adenocarcinoma patients by single-cell RNA sequencing. Our results indicate that mucinous adenocarcinoma cancer cells have goblet cell-like properties, and express high levels of goblet cell markers (REG4, SPINK4, FCGBP and MUC2) compared to classical adenocarcinoma cancer cells. TFF3 is essential for the transcriptional regulation of these molecules, and may cooperate with RPS4X to eventually lead to the mucinous adenocarcinoma mucus phenotype. The observed molecular characteristics may be critical in the specific biological behavior of mucinous adenocarcinoma.
Though invasive mucinous adenocarcinoma of the lung (IMA) is pathologically distinctive, the molecular mechanism driving IMA is not well understood, which hampers efforts to identify therapeutic targets. Here, by analyzing gene expression profiles of human and mouse IMA, we identified a Mucinous Lung Tumor Signature of 143 genes, which was unexpectedly enriched in mucin-producing gastrointestinal, pancreatic, and breast cancers. The signature genes included transcription factors FOXA3, SPDEF, HNF4A, mucins MUC5AC, MUC5B, MUC3, and an inhibitory immune checkpoint VTCN1/B7-H4 (but not PD-L1/B7-H1). Importantly, induction of FOXA3 or SPDEF along with mutant KRAS in lung epithelium was sufficient to develop benign or malignant mucinous lung tumors, respectively, in transgenic mice. FOXA3 and SPDEF induced MUC5AC and MUC5B, while HNF4A induced MUC3 in human mucinous lung cancer cells harboring a KRAS mutation. ChIP-seq combined with CRISPR/Cas9 determined that upstream enhancer regions of the mucin genes MUC5AC and MUC5B, which were bound by SPDEF, were required for the expression of the mucin genes. Here, we report the molecular signature and gene regulatory network driving mucinous lung tumors.
Increasing evidence links Notch-1 signaling with the maintenance of intestinal architecture and homeostasis. Dysfunction in the common Notch-1 pathway transcription factor recombinant binding protein suppressor of hairless (RBP-J) is associated with loss of epithelial barrier integrity and aberrant conversion of proliferative crypt cells into goblet cells. Furthermore, we have recently discovered that epithelial Notch-1 is indispensable in bridging innate and adaptive immunity in the gut and is required for supporting protective epithelial pro-inflammatory responses. Yet, the epithelial specific function of Notch-1 in intestinal tumorigenesis remains unknown. We generated Villin-Cre/Notch-1 fl/fl (VN -/- ) mice that are selectively deficient in Notch-1 in intestinal epithelial cells. Intestinal epithelial Notch-1 preserved barrier function and integrity, whereas lack of epithelial Notch-1 induced goblet cell hyperplasia, spontaneous serrated lesions, multifocal low- and high-grade dysplasia and colonic mucinous neoplasms in mice. Over time, VN -/- mice displayed high occurrence of colorectal mucinous adenocarcinomas, which correlated with increased levels of mitogenic, angiogenic and pro-tumorigenic gene expression. Finally, we found that the expression of Notch-1 is significantly reduced in human colorectal mucinous adenocarcinoma when compared to colorectal adenocarcinoma. Taken together, our findings reveal a novel and critical protective role for Notch-1 in controlling intestinal tumorigenesis.
Colorectal mucinous adenocarcinoma (MAC) and serrated adenocarcinoma (SAC) share many characteristics, including right-side colon location, frequent mucin production, and various molecular features. This study examined the frequency of SAC morphology in MACs. We assessed the correlation of SAC morphology with clinicopathological parameters, molecular characteristics, and patient prognosis. Eighty-eight colorectal MACs were collected and reviewed for SAC morphology according to Makinen's criteria. We sequenced KRAS and BRAF, assessed CpG island methylator phenotype (CIMP) frequency, and analyzed DNA mismatch repair enzyme levels using immunohistochemistry in tumor samples. SAC morphology was observed in 38% of MACs, and was associated with proximal location (P=0.001), BRAF mutation (P=0.042), CIMP-positive status (P=0.023), and contiguous traditional serrated adenoma (P=0.019). Multivariate analysis revealed that MACs without both SAC morphology and CIMP-positive status exhibited 3.955 times greater risk of cancer relapse than MACs having both characteristics or either one (P=0.035). Our results show that two MAC groups with distinct features can be identified using Makinen's criteria, and suggest a favorable prognostic role for the serrated neoplastic pathway in colorectal MAC.
Mucinous adenocarcinoma of the rectum is an infrequently encountered histological subtype that is associated with an impaired response to chemoradiotherapy and a worse overall prognosis. A genomic profile analysis of mucinous rectal tumors has not yet been performed. The aim of this study was to comprehensively describe the burden of somatic mutations and copy number variation as well as perform mutational signature and microbial analysis of an in-house collected cohort of mucinous adenocarcinoma of the rectum.
The value of adjuvant chemotherapy for rectal cancer patients is debated and varies in different subgroups. One such subgroup is mucinous adenocarcinoma (MAC), which is more treatment resistant compared to non-mucinous adenocarcinoma (NMAC). To date, mucinous histology is not taken into account when deciding on adjuvant treatment strategy. This is the first study to exclusively include patients with rectal cancer, then separate MAC and NMAC and compare the survival in patients that had or did not have adjuvant chemotherapy.
Mucinous adenocarcinoma (MA) is a subtype of colorectal cancer (CRC) associated with a higher incidence of local extension and worse survival compared to non-mucinous adenocarcinoma, but few studies have investigated surgery-related predictors for recurrence of MA. Therefore, we aimed to elucidate the predictors for local recurrence and remote metastasis of MA after surgery.
Mucinous adenocarcinoma of the salivary gland (MAC) is a lethal cancer with unknown molecular etiology and a high propensity to lymph node metastasis. Mostly due to its orphan status, MAC remains one of the least explored cancers that lacks cell lines and mouse models that could help translational and pre-clinical studies. Surgery with or without radiation remains the only treatment modality but poor overall survival (10-year, 44%) underscores the urgent need for mechanism-based therapies.
According to the latest the World Health Organization (WHO) classification in 2015, invasive mucinous adenocarcinoma (IMA) is defined as a new pathological subtype of lung adenocarcinoma (LUAD). However, whether this rare subtype of lung pathology has any difference in prognosis than conventional LUAD is debatable. Our study attempted to compare clinical characteristics and prognosis of IMA vs. noninvasive mucinous adenocarcinomas (NMA).
Whether invasive mucinous adenocarcinoma (IMA) and colloid adenocarcinoma (ICA) of the lung represent separate tumour entities, or simply lie within a spectrum of phenotypic variability, is worth investigating. Fifteen ICA, 12 IMA, 9 ALK-rearranged adenocarcinomas (ALKA), 8 non-mucinous KRAS-mutated adenocarcinomas (KRASA) and 9 mucinous breast adenocarcinomas (MBA) were assessed by immunohistochemistry for alveolar (TTF1, cytoplasmic MUC1), intestinal (CDX-2, MUC2), gastric (membrane MUC1, MUC6), bronchial (MUC5AC), mesenchymal (vimentin), neuroendocrine (chromogranin A, synaptophysin), sex steroid hormone-related (oestrogen and progesterone receptors), pan-mucinous (HNF4A) and pan-epithelial (keratin 7) lineage biomarkers and by targeted next generation sequencing (TNGS) for 50 recurrently altered cancer genes. Unsupervised clustering analysis using molecular features identified cluster 1 (IMA and ICA), cluster 2 (ALKA and KRASA) and cluster 3 (MBA) (p < 0.0001). Cluster 1 showed four histology-independent sub-clusters (S1 to S4) pooled by HFN4A and MUC5AC but diversely reacting for TTF1, MUC1, MUC2, MUC6 and CDX2. Sub-cluster S1 predominantly featured intestinal-alveolar, S2 gastrointestinal, S3 gastric and S4 alveolar differentiation. In turn, KRASA and ALKA shared alveolar lineage alongside residual MUC5AC expression, with additional focal CDX2 and diffuse vimentin, respectively. A proximal-to-distal scheme extending from terminal (TB) and respiratory (RB) bronchioles to alveolar cells was devised, where S3 originated from distal TB (cellular mucinous adenocarcinoma), S2 from proximal RB (secreting mucinous adenocarcinoma), S1 from intermediate RB (mucin lake-forming colloid adenocarcinoma), S4 from distal RB (colloid alveolar adenocarcinoma), KRASA from juxta-alveolar RB (KRAS-mutated non-mucinous adenocarcinoma) and ALKA from juxta-bronchial alveolar cells (ALK-translocated adenocarcinoma). TNGS analysis showed KRAS, LKB1, TP53, APC and CDKN2A mutation predominance. In conclusion, IMA and ICA are basket categories, which likely originate from distinct domains of stem/progenitor cells spatially distributed along bronchioles upon common molecular features and genetic alterations.
The epidemiology and clinical outcome of gastrointestinal mucinous adenocarcinoma (MA) are not well illustrated. The present study aimed to explore the evolving epidemiology and prognostic factors that affect the survival of patients with MA in the gastrointestinal tract. A retrospective and population-based study was conducted to determine the annual age-adjusted incidence, overall survival (OS) and survival trend of gastrointestinal mucinous MA using nationally representative data from the Surveillance, Epidemiology, and End Results (SEER) program between 2000 and 2014. A Kaplan-Meier curve and a Cox proportional regression model were used to evaluate prognostic factors for this disease. Of the 51632 cases, females accounted for 50.5% (26058). The annual incidence of MA steadily decreased from 2000 to 2014. This trend occurred across all stages, grades and sites, apart from the appendix. In the SEER 18 registry grouping (2000-2014), the highest incidence was 3.333 per 100,000 persons for the colon. The median OS varied significantly between different primary sites, stages, grades, and age of clinical diagnosis, and the time period of diagnosis, according to a multivariable analysis. The five-year OS of gastrointestinal MA improved gradually between 2000 and 2014. The improvement in survival over the same interval was more pronounced in the subgroup of distant gastrointestinal MA. All sites along the alimentary tract, with the exception of the appendix, showed a decrease in the incidence of MA. Improved survival rates were observed for most of the gastrointestinal tract, especially for patients with advanced stage disease. MA in the upper gastrointestinal tract was less frequent but had poorer survival than colorectal MA. Clinicians should consider the primary tumour site when making therapeutic guidelines and treatment decisions for gastrointestinal MA.
Objective: This study aimed to develop and validate predictive models using clinical parameters, radiomic features, and a combination of both for invasive mucinous adenocarcinoma (IMA) of the lung in patients with lung adenocarcinoma. Method: A total of 173 and 391 patients with IMA and non-IMA, respectively, were retrospectively analyzed from January 2017 to September 2022 in our hospital. Propensity Score Matching was used to match the 2 groups of patients. A total of 1037 radiomic features were extracted from contrast-enhanced computed tomography (CT). The patients were randomly divided into training and test groups at a ratio of 7:3. The least absolute shrinkage and selection operator algorithm was used for radiomic feature selection. Three radiomics prediction models were applied: logistic regression (logistic), support vector machine (SVM), and decision tree. The best-performing model was adopted, and the radiomics score (Radscore) was then computed. A clinical model was developed using logistic regression. Finally, a combined model was established based on a clinical model and a radiomics model. The area under the receiver operating characteristic (ROC) curve (AUC) and decision curve analysis were used to evaluate the predictive value of the developed models. Results: Both clinical and radiomics models established using the logistic method showed the best performance. The Delong test revealed that the combined model was superior to the clinical and radiomics models (P = .018 and .020, respectively). The ROC-AUC (also decision curve analysis) of the combined model was 0.840 and 0.850 in the training and testing groups, respectively, which showed good predictive performance for IMA. The Brier scores for the combined model were 0.161 and 0.154 in the training and testing groups, respectively. Conclusion: The combined model incorporating radiomic CT features and clinical predictors may have the potential to predict IMA in patients with lung cancer.
Invasive mucinous lung adenocarcinoma (IMA) is a rare subtype of lung adenocarcinoma with no effective treatment option in advanced disease. KRAS mutations occur in 28-87% of the cases. NRG1 fusions were recently discovered in KRAS-negative IMA cases and otherwise negative for known driver oncogenes and could represent an attractive therapeutic target. Published data suggest that NRG1 fusions occur essentially in nonsmoking Asian women. From an IMA cohort of 25 French patients of known ethnicity, driver oncogenes EGFR, KRAS, BRAF, ERBB2 mutations, and ALK and ROS1 rearrangements presence were analyzed. In the IMA samples remaining negative for these driver oncogenes, an NRG1 rearrangement detection was performed by FISH. A driver oncogene was identified in 14/25 IMA, namely 12 KRAS mutations (48%), one ROS1 rearrangement (4%), and one ALK rearrangement (4%). The detection of NRG1 rearrangement by FISH was conducted in the 11 pan-negative IMA. One sample was NRG1FISH-positive and 100% of the tumor nuclei analyzed were positive. This NRG1-positive patient was a 61-year-old nonsmoking woman of Vietnamese ethnicity and was the sole patient of Asian ethnicity of the cohort. She died 6 months after the diagnosis with a pulmonary multifocal disease. NRG1FISH detection should be considered in patients with IMA pan-negative for known driver oncogenes. These results might suggest that NRG1 fusion is more frequent in IMA from Asian patient. Larger studies are needed.
The extent of bowel resection is widely debated in colon cancer surgery. Right hemicolectomy (RHC) and partial colectomy (PC) are the most common operation options for right-sided colon cancer (RCC). However, there are still no treatment guidelines or published studies to guide surgical options for mucinous adenocarcinoma (MAC) of RCC.
Invasive mucinous adenocarcinoma (IMA) is a mucinous variant of lepidic predominant lung adenocarcinoma (LPA) and associated with a worse prognosis. We postulated that cytokine expression would enable us to differentiate IMA from LPA in terms of prognosis and acquisition of pro-tumoural capacities. A 30-cytokine panel was assessed in bronchoalveolar lavage fluids (BALF) from IMA (n=38), LPA (n=25) and control samples (n=7). We investigated the expression of differentially expressed cytokines and splice variants of their receptors in surgical samples. The presence of EGFR and KRAS mutations were determined. We also examined the expression of cytokines and splice variants of their receptors in different cell lines, exploring their functional impact on signalling pathways, proliferation and migration. Only C-X-C motif chemokine 10 (CXCL10) was differentially expressed, namely overexpressed in IMA BALF compared with LPA. CXCL10 overexpression in BALF was linked to a worse prognosis. In surgical samples, CXCL10 and its receptor C-X-C motif chemokine receptor 3 (CXCR3) were overexpressed in IMA compared to LPA. A pro-tumoural CXCR3-A splice variant was overexpressed in IMA, suggesting a CXCL10/CXCR3-A autocrine loop in IMA. CXCL10 and CXCR3 expression were not correlated with EGFR or KRAS status. CXCL10 up-regulated CXCR3-A expression, Erk1/2 phosphorylation and enhanced migration in the mucinous H2228 cell line. CXCL10/CXCR3-A may play a pro-tumoural role in IMA via an autocrine mechanism.
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