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At least 19 recordsLinked to original sources
PubMed1976

Adenocarcinoma of the kidney. II. Enzyme histochemistry of renal adenocarcinomas induced in rats by N-(4'-fluoro-4-biphenylyl)acetamide.

Activities of a broad spectrum of enzymes were studied histochemically in renal adenocarcinomas induced in young male F344 rats by chronic dietary administration of the carcinogen N(4'-fluoro-4-biphenylyl)acetamide. Enzymes included were: dehydrogenases of glucose-6-phosphate, lactate, succinate, malate, and alpha-glycerophosphate; peroxidase (catalase); glucose-6-phosphatase; alkaline and acid phosphatase; Mg2+ ATPase; 5'-nucleotidase; and aminopeptidase. Levels of enzyme activity were estimated visually and scored from 0 (not detectable) to a maximum of 5 (intense). Comparison of estimated activity for each enzyme was made between small neoplastic nodules (stage III tumors) and large adenocarcinomas (stage IV tumors) and between tumors and portions of normal proximal tubules in parenchyma of kidneys from untreated control rats. The results, which revealed nearly identical levels of activity for most enzymes in both stages III and IV tumors, suggested similar metabolic and biologic behavior of these lesions. However, when data for tumors were compared with data for normal proximal tubules, striking differences were observed consistent with: 1) a marked shift of energy metabolism from oxidative to glycolytic production of ATP, with a corresponding reduction in mitochondrial respiration; and 2) simplification of plasma membrane specializations that were possibly associated with a reduction or loss of transport function. These findings were compared with other histochemical, biochemical, and ultrastructural studies of renal adenocarcinomas in rats and man.

Adenocarcinoma↗
PubMed1979

Paneth cell-rich papillary adenocarcinoma and a mucoid adenocarcinoma occurring synchronously in colon: a light and electron microscopic study.

A 71-year-old man who presented with iron deficiency anaemia and weight loss was found to have two colonic tumours: a mucoid adenocarcinoma at the splenic flexure and a papillary adenocarcinoma rich in Paneth cells in the ascending colon. The light and ultrastructural features of the neoplastic cells are described, and the significant of the presence of neoplastic Paneth cells is discussed.

Adenocarcinoma, Mucinous↗
PubMed2025

KLF5 facilitates lung adenocarcinoma metastasis by regulating the epithelial-mesenchymal transition pathway through RHPN2.

BACKGROUND: Distant metastasis is a primary factor contributing to the significantly shorter survival time of patients with advanced lung adenocarcinoma. The transcription factor Kruppel-like factor 5 (KLF5) facilitates the progression of lung adenocarcinoma. However, the specific mechanism by which KLF5 is involved in the tumor metastasis of lung adenocarcinoma metastasis remains largely unclear. METHODS: Using bioinformatic analysis, Rhophilin Rho GTPase Binding Protein 2 (RHPN2) was identified as a potential downstream target gene for KLF5; it plays a crucial role in the regulation of the epithelial-mesenchymal transformation pathway in lung adenocarcinoma. Western blotting and immunohistochemistry were performed to examine RHPN2 expression in lung adenocarcinoma. In vivo and in vitro experiments were conducted to explore the regulatory role of RHPN2 on the cell growth and metastasis of lung adenocarcinoma. Chromatin immunoprecipitation sequencing was used to analyze the direct binding activity between KLF5 and RHPN2 promoter regions. Luciferase activity assay was performed to verify the transcriptional activation effect of KLF5 on RHPH2. RESULTS: RHPN2 was highly expressed in lung adenocarcinoma; patients with lung adenocarcinoma who showed high RHPN2 expression had a poor prognosis. In vivo and in vitro experiments showed that RHPN2 promoted cell growth and metastasis and activated the epithelial-mesenchymal transformation pathway in lung adenocarcinoma. KLF5 directly bound to the promoter region of RHPN2 and upregulated its expression in lung adenocarcinoma through transcriptional activation. In addition, rescue experiments confirmed that KLF5 facilitated the progression of lung adenocarcinoma in an RHPN2-dependent manner. CONCLUSION: Our study offers insights into the potential mechanisms of metastasis in lung adenocarcinoma and highlights RHPN2 as a potential therapeutic target.

Humans↗
PubMed2026

Comprehensive Profiling of Claudin 18.2 Immunohistochemical Expression in 564 Surgically Resected Gastric and Gastroesophageal Junction Adenocarcinomas.

Claudin 18 isoform 2 (CLDN18.2) is a novel therapeutic target for advanced, HER2-negative gastric/gastroesophageal junction (GEJ) adenocarcinoma positive for CLDN18.2 immunohistochemical (IHC) expression, defined as &#x2265;75% tumor cells with moderate-to-strong membranous staining. Clinical studies for emerging CLDN18.2-targeted therapeutics have used less stringent enrollment criteria to test the efficacy of such therapies in patients with moderate-to-low CLDN18.2 IHC expression. Anticipating the advent of such treatments, this study aimed to provide a comprehensive survey of CLDN18.2 expression using a clinical trial-validated CLDN18.2 monoclonal antibody in surgically resected gastric/GEJ adenocarcinomas and characterize CLDN18.2-positive carcinomas using both high- and low-expression thresholds. Crisp membranous CLDN18.2 staining was detected in 59% (335/564) carcinomas, including 57% (164/286) of gastric and 62% (171/278) of GEJ adenocarcinomas. Most gastric (147/164, 90%) and GEJ (166/171, 97%) adenocarcinomas with staining demonstrated moderate or strong staining intensity. Using the high-expression threshold (&#x2265;75% tumor cells with moderate-to-strong staining), positive CLDN18.2 expression was observed in 20% (57/286) of gastric and 27% (75/278) of GEJ adenocarcinomas and was associated with Epstein-Barr virus status (P < .001) and stage I gastric adenocarcinomas (P = .02) but stage IV GEJ adenocarcinomas (P = .03). Using a low-expression threshold (&#x2265;10% tumor cells with membranous staining), positive CLDN18.2 remained significantly associated with stage I (P = .004) and showed an unadjusted association with improved disease-specific survival in gastric adenocarcinomas (P = .045), which was not retained in multivariable analysis. Whole transcriptomic analysis showed concordance between IHC and CLDN18 messenger RNA expression. Transcriptomic alterations in CLDN18.2 IHC-positive gastric adenocarcinomas included pathways in drug resistance and tumor invasion. In summary, our study presents a detailed characterization of the prevalence and distribution of CLDN18.2 IHC expression patterns. Our results showed that 59% surgically resected gastric/GEJ adenocarcinomas exhibited CLDN18.2 staining. CLDN18.2 IHC positivity defined by both high- and low-expression thresholds may be associated with early-stage gastric adenocarcinoma. These findings expand our recognition of patients who may benefit from CLDN18.2-targeted therapy.

CLDN18.2↗
PubMed2025

Suppression of LKB1-mutant lung adenocarcinoma by natural killer cells from females.

BACKGROUND: This study addressed the enigma of sex differences in smoking-related lung cancer, particularly focusing on the low LKB1 mutation frequency in female patients with lung adenocarcinoma. METHODS: Sex bias was studied with a genetically engineered mouse model and various tail-vein injection models. Immune cells were analyzed by antibody-depletion study, flow cytometry, and immunofluorescence. The relevance of our findings to human disease was validated by evaluating various lung adenocarcinoma datasets. All statistical tests are 2-sided. RESULTS: A statistically significant percentage of females are resistant to LKB1-mutant tumor formation in our models, reflecting this sex difference in humans. Natural killer (NK) cells were identified as a critical factor in this sex-biased response. This sex difference was observed primarily in LKB1-mutant lung adenocarcinoma, probably due to their low major histocompatibility complex class I level, making them the ideal target for NK cells through the missing-self recognition. Although females resistant to LKB1-mutant lung adenocarcinoma formation did not have enhancement of any specific NK subpopulation, our immunofluorescence analysis revealed high numbers of NKs in female lungs even with the presence of LKB1-mutant lung adenocarcinoma. Our gene set enrichment analysis of The Cancer Genome Atlas-lung adenocarcinoma dataset also showed that female LKB1-mutant lung adenocarcinoma patients have a stronger NK-mediated response after adjusting for other male-female differences using the LKB1 wild-type lung adenocarcinoma dataset. CONCLUSION: Females have a stronger NK-mediated response against LKB1-mutant lung adenocarcinoma, which was present in our mouse model and the human lung adenocarcinoma dataset. This study revealed a novel role of NK cells in suppressing LKB1-mutant lung adenocarcinoma in females, which should be assessed in the clinical setting in the future.

Killer Cells, Natural↗
PubMed1979

Distinction between endocervical and endometrial adenocarcinoma with immunoperoxidase staining of carcinoembryonic antigen in routine histological tissue specimens.

The differential diagnosis of endocervical and endometrial adenocarcinomas can be improved by the demonstration of carcinoembryonic antigen (CEA) in tissue by means of immunoperoxidase staining. Tissue from 131 (80%) of 163 patients with endocervical adenocarcinoma but only 11 (8%) of 137 patients with endometrial adenocarcinoma was CEA-positive. The commonest exceptions were endocervical mesonephroid adenocarcinomas (which were CEA-negative) and endometrial adenosquamous carcinomas (which were CEA-positive). After exclusion of these on simple morphological criteria, 86 of 107 endocervical adenocarcinomas (80%) were CEA-positive, and all 122 endometrial adenocarcinomas were CEA-negative. The remarkable difference in the expression of CEA between endocervical and endometrial adenocarcinomas suggests a novel application of immunohistochemistry in routine clinical practice.

Adenocarcinoma↗
PubMed2026

TMEM33 regulates the proliferation and migration of lung adenocarcinoma by promoting the PI3K/AKT/mTOR signaling pathway.

Lung adenocarcinoma is a common type of lung cancer with high incidence and mortality rates. TMEM33, a tumor-associated protein, has not been fully elucidated in lung adenocarcinoma. To explore the expression of TMEM33 in lung adenocarcinoma, its impact on tumor progression, and its role in the PI3K/AKT/mTOR signaling pathway. Key genes associated with lung adenocarcinoma were screened using the Gene Expression Omnibus (GEO) dataset GSE140797 in combination with a weighted correlation network analysis (WGCNA). Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed on these key genes. TMEM33 expression in Lung adenocarcinoma patients was validated using data from the TCGA database. The directly interactive molecules were screened through a bioinformatics method. Cellular assays (Western Blot, CCK8, colony formation, scratch assay, Trans well assay) and a nude mouse model were used to investigate the effects of TMEM33 on cell proliferation, migration, and tumor growth. TMEM33 is highly expressed in lung adenocarcinoma tissues (P&#x2009;<&#x2009;0.05) and associated with poor prognosis. Overexpression of TMEM33 promotes cell proliferation and migration, and activates the PI3K/AKT/mTOR signaling pathway (P&#x2009;<&#x2009;0.01). In the nude mouse model, TMEM33 overexpression increases tumor volume (P&#x2009;<&#x2009;0.001), and PI3K/AKT pathway inhibition suppresses these effects (P&#x2009;<&#x2009;0.05, P&#x2009;<&#x2009;0.01). TMEM33 acts as an oncogene in lung adenocarcinoma by activating the PI3K/AKT/mTOR pathway, providing new therapeutic targets.

Cell migration↗
PubMed2026

STK11 Mutations and Deletions Define an Aggressive Molecular Subgroup of Cervical Adenocarcinoma.

Cervical adenocarcinoma accounts for 15%-20% of cervical cancers and is associated with poorer survival and reduced response to screening and immunotherapy compared with squamous cell carcinoma (SCC). The genomic drivers underlying this molecular subgroup remain incompletely characterized. Whole-exome sequencing was performed on 302 invasive cervical cancers from Guatemala and Venezuela. Structural variation analysis was conducted using SNP-array and whole-genome sequencing data. Findings were replicated in more than 4600 additional cervical cancer samples from TCGA, AACR Project GENIE, MSKCC, and Caris datasets. TP53 mutations were more frequent in adenocarcinoma than SCC, particularly in HPV-negative tumors. STK11 alterations, including mutations and focal deletions, were significantly enriched in HPV-positive adenocarcinomas compared with SCC and affected 23% of adenocarcinomas overall. Whole-genome analyses identified recurrent focal deletions, inversions, chromosomal rearrangements, and breakage-fusion-bridge events involving chromosome 19p and STK11 that were not detected by exome sequencing alone. STK11 alterations were associated with younger age at diagnosis, poorer overall survival, and inferior outcomes following immune checkpoint inhibitor (ICI) therapy. STK11 alterations significantly co-occurred with YAP1 amplification but were largely mutually exclusive with PIK3CA mutation. Cervical adenocarcinomas also demonstrated significantly lower CD274 (PD-L1) expression than SCC. STK11 alterations define a distinct molecular subgroup of cervical adenocarcinoma characterized by structural disruption of chromosome 19p, younger age at onset, and poorer clinical outcomes. These findings have implications for molecular classification and future targeted therapeutic approaches in cervical cancer.

Humans↗
PubMed1977

The histomorphologic spectrum of endocervical (Müllerian) adenocarcinoma--a potential prognostic indicator.

A review of all patients with endocervical adenocarcinoma seen at the Universtiy of Kentucky Medical Center from 1962 through 1972 yielded 15 patients with tissue-verifiable primary endocervical adenocarcinoma that had no associated sarcomatous or squamoid features. These patients varied from 17 to 73 years old with a mean age of 47 years. A malignant clear cell pattern was present in 8 patients and in 3 of these individuals that prominent morphologic feature was associated with hobnail cells. Five patients with clear cell carcinomatous changes in the endocervix were born prior to the use of diethylstilbestrol (DES) and 2 of the remaining 3 patients were exposed to DES during the first trimester of pregnancy. Other morphologic types of endocervical adenocarcinoma included mucinous adenocarcinoma in 9 patients (60%) and basaloid adenocarcinoma in one patient (7%). Cellular atypia of endocervical glands, which in some areas was consistent with adenocarcinoma in situ was found in 9 of the 15 patients with invasive endocervical cancers. Both vessel invasion by tumor cells and tumor necrosis were associated with a poor prognosis.

Adenocarcinoma↗
PubMed1978

Potentialities of the cytological method in diagnosing adenocarcinoma of the lung.

Parallel cytological and histological studies were performed for 87 patients with pulmonary adenocarcinoma. Sputum, impression smears of the bronchial mucosa, aspirates from the bronchi, punctates of the tumor obtained transbronchially, pieces of tumor obtained at bronchoscopy, and operation material were examined. Considerable difficulties wre found in cytological diagnosis of adenocarcinomas due to degenerative changes in tumor cells, the presence of cells of the metaplastic columnar epithelium and marked anaplasia of tumor cells in adenocarcinoma with low differentiation. The frequency of diagnostic errors was 20.0--50.6% depending on the histological form of adenocarcinoma and the accompanying processes in bronchi. The cytological criteria improving the differential diagnosis of adenocarcinoma are presented. The validity of cytological diagnosis of adenocarcinoma does not depend on the nature of the material examined.

Adenocarcinoma↗
PubMed1978

Production of adenocarcinomas of the small intestines of Wistar rats fed panfuran-S containing 3-di(hydroxymethyl)amino-6-(5-nitro-2-furylethenyl)-1,2,4-triazine.

Panfuran-S in the diet produced a high incidence of invasive and metastatic adenocarcinomas of the duodenum and the jejunum in outbred Wistar rats. Depressed growth and incidence of cancer production were dose-dependent. Adenocarcinomas of the duodenum were present in 2 of 18 (11%) rats that received 1,750 ppm 3-di(hydroxymethyl)amino-6-(5-nitro-2-furylethenyl)-1,2,4-triazine (DHNT) in the diet and in 11 of 19 (58%) rats that received 3,500 ppm DHNT. Adenocarcinomas of the jejunum were present in 10 of 18 (56%) and 16 of 19 (84%) rats that received 1,750 and 3,500 ppm DHNT, respectively, for 35-37 weeks. The only other tumors observed were squamous cell papillomas of the forestomach. Histologically, most of the adenocarcinomas appeared tubular or papillary and were similar to adenocarcinomas in the small intestine of man and also to human intestinal-type adenocarcinoma of the stomach. This system provided a useful experimental model for the study of the pathogenesis of carcinoma of the small intestine.

Adenocarcinoma↗
PubMed1979

Adenocarcinoma of the lung: recent results from the Veterans Administration Lung Group.

Adenocarcinoma has become the most common type of cancer of the lung. Its distinct natural history necessitates separation from the other cell types. Results from recent Veterans Administration Lung Group studies show that local-regional failure occurred in 59% of patients after irradiation for adenocarcinoma limited to the thorax. Data from 300 consecutive autopsies reveal that death was caused by intrathoracic complications of the tumor in 38%, and by metastases in 57% of patients. Adenocarcinoma has an intermediate risk of local and distant failure when compared to squamous and small-cell carcinoma. However, brain metastases are most frequent with adenocarcinoma. Preliminary results suggest that prophylactic brain irradiation decreases the frequency of brain metastases. Patients with adenocarcinoma are more likely than those with other cell types to have metastases only in the brain. Prophylactic brain irradiation may make the greatest contribution to improved survival in pateints with adenocarcinoma of the lung.

Adenocarcinoma↗
PubMed2025

Impaired natural killer cell maturation in lung adenocarcinoma driven by FABP4 and SPON2 downregulation through disrupted lipid metabolism.

BACKGROUND: Although natural killer (NK) cells play a crucial role in antitumor immunity, the metabolic changes driving their dysfunction in lung adenocarcinoma remain poorly understood. This study investigates how these metabolic modifications impact NK cell function within the lung adenocarcinoma microenvironment. METHODS: A total of 13 pairs of lung adenocarcinoma samples were obtained from The Cancer Genome Atlas. Differential gene expression, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and single-cell metabolic quantification analyses were used to characterize the transcriptomic, pathway, and metabolic signatures of NK cells. The developmental trajectory was reconstructed via pseudotime analysis. The fatty acid-binding protein 4 (FABP4) and spondin2 (SPON2) expression was examined using immunofluorescence (IF) and immunohistochemistry (IHC) in patients with lung adenocarcinoma. In NK cells with FABP4 downregulation, FABP4 function was analyzed using antibody-independent cell-mediated cytotoxicity assays, flow cytometry (FCM), and liquid chromatography-mass spectrometry. RESULTS: The number of NK cells was significantly decreased in the lung adenocarcinoma microenvironment. FABP4 and SPON2 expression was significantly lower in NK cells within tumor tissues than in the adjacent tissues. FABP4 expression was significantly lower in tumor tissues than in the adjacent tissues, whereas no significant difference in SPON2 expression was observed. The cytotoxic function of NK cells with decreased FABP4 levels was impaired. Non-targeted lipid metabolism analysis indicated that differentially expressed lipids in NK cells with low FABP4 levels were functionally enriched in the glycerophospholipid metabolism pathway compared to those in normal NK cells. CONCLUSIONS: The study findings present new evidence showing that low FABP4 and SPON2 gene expression may impair NK cell maturity by affecting lipid metabolism in lung adenocarcinoma. These results provide a new perspective on restoring immune function in patients with lung cancer.

FABP4↗
PubMed1976

Feline intestinal adenocarcinoma. A clinicopathologic study of 22 cases.

Twenty-two cases of intestinal adenocarcinoma were diagnosed in an 11-year survey of 3145 feline necropsies. Histologically, tumors were grouped into four classes: (1) carcinoma with solid groups of cells, (2) adenocarcinoma with solid and acinar cells, (3) papillary adenocarcinoma, and (4) mucinous adenocarcinoma. Tumors were commonest in the ileum. Connective tissue, as well as epithelial metaplasia, were associated more often in this group of intestinal adenocarcinomas nomas than seen before. Hypertrophy and hyperplasia of muscular layers of the unaffected sections of intestines were seen in most of the small bowel and in half of the large bowel carcinomas in this series.

Adenocarcinoma↗
PubMed1978

Steroid hormone receptor characterization of several histologic variants of a rat prostatic adenocarcinoma.

Several histologic variants of the transplantable R-3327 prostatic adenocarcinoma carried in male Copenhagen rats have been characterized and the histologic types have been correlated with steroid hormone receptor content. One type is clearly an adenocarcinoma; this tumor is hormonally responsive and contains substantial amounts of both androgen and estrogen receptors. In contrast, another histologic type, a fibrosarcoma, is hormonally nonresponsive and does not contain either receptor. A third histologic variant is classified as a carcinosarcoma and contains histological elements of both adenocarcinoma and fibrosarcoma and is also hormonally responsive. This tumor contains lower receptor levels than the adenocarcinomas but more than the fibrosarcomas. The androgen receptor appears to be identical in the different histologic forms of the tumor: the sedimentation coefficient is 7.8S and the dissociatiln constant for methyltrienolone is 4 x 10(-9) M. Similarly, the estrogen receptor from the different histologic forms of the tumor has a sedimentation coefficient of 8.3S and the dissociation constant for estradiol is 7 x 10(-10) M. These findings clearly distinguish the cytosol binding macromolecules from plasma binding proteins, and classify them as steroid hormone receptors. Further, rat serum was devoid of androgen and estrogen binding in the 8S region. Normal prostate tissue from Copenhagen rats contained low levels of an androgen receptor, but no estrogen receptor. It is possible that during growth and/or passage of the R-3327 tumor, the hormonally responsive adenocarcinoma cells do not survive and there is a gradual emergence of the nonresponsive fibrosarcoma. If, as we suspect, the receptors are found in the epithelial cells and not the stromal cells, there clearly should be considerable variation of receptor content in the different intermediary histologic forms of the tumor.

Adenocarcinoma↗
PubMed2026

Co-occurrence of bronchiolar adenoma and lung adenocarcinoma: a study of nine cases revealing distinct clonal origins via integrated histologic, immunophenotypic and molecular analysis.

PURPOSE: This study sought to elucidate the possible biological association between BA and lung adenocarcinoma through an analysis of cases in which both lesions coexist within the same specimen. METHODS: In our cohort, the BA and lung cancer components of nine concurrent-type BAs were microdissected using the Millisect system and subjected to whole-exome sequencing (WES). Their histopathological, immunohistochemical, and genomic profiles were comparatively evaluated. RESULTS: Histopathologically, the BA regions of concurrent-type BAs exhibited a classic bilayered architecture, composed of continuous luminal and basal cell layers. The adjacent monolayered concurrent components were diagnosed as adenocarcinoma in situ (AIS, N&#x202f;=&#x202f;4), minimally invasive adenocarcinoma (MIA, N&#x202f;=&#x202f;2), and invasive adenocarcinoma (ADC, N&#x202f;=&#x202f;3). Immunohistochemically, both luminal and basal cells in BA regions expressed thyroid transcription factor 1 (TTF1), albeit with more heterogeneous staining intensity compared to that observed in tumor components. Molecularly, EGFR mutations were the most frequently identified in either BA or tumor components, or in both (Case 9). In BA components, mutations included exon 19 p.S752F, exon 19 deletions (p.L747_T751delinsP and p.E746_T751delinsVP), and compound G719C/S768I mutations. Tumor components harbored exon 28 S1130C, exon 19 indel (p.E746_S752delins), and exon 18 p.G719C mutations. Notably, only three cases demonstrated limited overlap of mutations and copy number variations (CNVs) between the two components. Phylogenetic analysis revealed that six cases shared truncal alterations in genes including KMT2A, PIK3CA, SETD2, MITF, PBRM1, and SRSF3, one case harbored a shared canonical EGFR mutation (p.G719C), with an additional p.S768I alteration uniquely detected in the BA component. CONCLUSION: There is insufficient evidence to support BA as a premalignant lesion for lung adenocarcinoma base on morphological and molecular variables, and they may represent distinct pathological entities.

Concurrent-type bronchiolar adenoma↗
PubMed1978

Adenocarcinoma of the bladder as seen at Ochsner Medical Institutions.

Adenocarcinoma of the bladder is an uncommon malignancy comprising less than 2% of all bladder tumors. Eleven cases of adenocarcinoma of the bladder were seen from 1947 to 1977 at the Ochsner Medical Institutions. Six of the tumors were urachal in origin, and five involved the base and lateral walls of the bladder. Six patients were treated with total cystectomy, four with segmental cystectomy, and one with radiation therapy only. The average survival time for the patients with urachal adenocarcinoma was 2.8 years and for those with vesical adenocarcinoma, 2.4 years. Although segmental cystectomy is recommended by some, the authors recommend radical cystectomy for all patients with adenocarcinoma of the bladder.

Adenocarcinoma↗