No abstract available.
Central Nervous System* ; Solitary Fibrous Tumors*

This review explores spatial mapping technologies in cancer research, highlighting their crucial role in understanding the complexities of the tumor microenvironment (TME). The TME, which is an intricate ecosystem of diverse cell types, has a significant impact on tumor dynamics and treatment outcomes. This review closely examines cutting-edge spatial mapping technologies, categorizing them into capture-, imaging-, and antibody-based approaches. Each technology was scrutinized for its advantages and disadvantages, factoring in aspects such as spatial profiling area, multiplexing capabilities, and resolution. Additionally, we draw attention to the nuanced choices researchers face, with capture-based methods lending themselves to hypothesis generation, and imaging/antibody-based methods that fit neatly into hypothesis testing. Looking ahead, we anticipate a scenario in which multi-omics data are seamlessly integrated, artificial intelligence enhances data analysis, and spatiotemporal profiling opens up new dimensions.

Myxoid liposarcoma is a subtype of liposarcoma. This specific subtype can be identified based on its characteristic histological and cytogenetical features. The tumor has a fusion transcript of the CHOP and TLS genes, which is caused by t(12;16)(q13;p11). Most of the fusion transcripts that have been identified fall into three categories, specifically type I (exons 7-2), type II (exons 5-2), and type III (exons 8-2). A total of seven myxoid liposarcomas associated with the rare phenomenon of cartilaginous differentiation have been documented in the literature. Currently, only one of these cases has been cytogenetically analyzed, and the analysis indicated that it was a type II TLS-CHOP fusion transcript in both the typical myxoid liposarcoma and cartilaginous areas. This study presents a second report of myxoid liposarcoma with cartilaginous differentiation, and includes a cytogenetical analysis of both the myxoid and cartilaginous areas.
Cartilage ; Liposarcoma ; Liposarcoma, Myxoid

BACKGROUND: Naked cuticle Drosophila 1 (NKD1) has been related to non-small cell lung cancer in that decreased NKD1 levels have been associated with both poor prognosis and increased invasive quality. METHODS: Forty cases of lung adenocarcinoma staged as Tis or T1a were selected. Cases were subclassified into adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA), and small adenocarcinoma (SAD). Immunohistochemical studies for NKD1 were performed. RESULTS: Forty samples comprised five cases of AIS (12.5%), eight of MIA (20.0%), and 27 of SAD (67.5%). AIS and MIA showed no lymph node metastasis and 100% disease-free survival, whereas among 27 patients with SAD, 2 (7.4%) had lymph node metastasis, and 3 (11.1%) died from the disease. Among the 40 cases, NKD1-reduced expression was detected in 8 (20%) samples, whereas normal expression was found in 15 (37.5%) and overexpression in 17 (42.5%). Loss of NKD1 expression was significantly associated with lymph node metastasis (p=0.001). All cases with predominant papillary pattern showed overexpression of NKD1 (p=0.026). CONCLUSIONS: Among MIA and SAD, MIA had better outcomes than SAD. Down-regulated NKD1 expression was closely associated with nodal metastasis, and overexpression was associated with papillary predominant adenocarcinoma.
Adenocarcinoma ; Carcinoma, Non-Small-Cell Lung ; Disease-Free Survival ; Drosophila ; Humans ; Immunohistochemistry ; Lung ; Lung Neoplasms ; Lymph Nodes ; Neoplasm Metastasis ; Prognosis

No abstract available.
Adenocarcinoma* ; Carcinoma, Papillary* ; Neoplasm Metastasis* ; Thyroid Gland*

BACKGROUND: The epidermal growth factor receptor (EGFR) is a surrogate marker for basal-like breast cancer. A recent study suggested that EGFR may be used as a target for breast cancer treatment. METHODS: A total of 706 invasive ductal carcinomas (IDC) of the breast were immunophenotyped, and 82 cases with EGFR protein expression were studied for EGFR gene amplification. RESULTS: EGFR protein was expressed in 121 of 706 IDCs (17.1%); 5.9% were of luminal type, 25.3% of epidermal growth factor receptor 2 (HER-2) type, and 79.3% of basal-like tumors. EGFR gene amplification and high polysomy (fluorescent in situ hybridization [FISH]-positive) were found in 18 of 82 cases (22.0%); 41.2% of the HER-2+, EGFR+, cytokeratin 5/6- (CK5/6-) group, 11.2% of the HER-2-, EGFR+, CK5/6- group, and 19.1% of the HER-2-, EGFR+, CK5/6+ group. FISH-positive cases were detected in 8.3% of the EGFR protein 1+ expression cases, 15.9% of 2+ expression cases, and 38.5% of 3+ expression cases. In group 2, the tumors had a high Ki-67 labeling (>60%), but the patients showed better disease-free survival than those with tumors that co-expressed HER-2 or CK5/6. CONCLUSIONS: EGFR-directed therapy can be considered in breast cancer patients with EGFR protein overexpression and gene amplification, and its therapeutic implication should be determined in HER-2 type breast cancer patients.
Biomarkers ; Breast ; Breast Neoplasms ; Carcinoma, Ductal ; Disease-Free Survival ; Gene Amplification ; Genes, erbB-1 ; Humans ; In Situ Hybridization ; Keratins ; Phenobarbital ; Receptor, Epidermal Growth Factor

Gastrointestinal stromal tumors (GISTs) are rare digestive system malignancies with extragastrointestinal stromal tumors (EGISTs) being even less. Diagnosing GISTs usually requires the identification of c-kit (CD117) expression by immunohistochemical staining. A 53-year-old woman complaining of dyspepsia was referred for the evaluation of a 1.5-cm extrinsic compression at the greater curvature of the proximal antrum. EUS revealed a multiseptated mass with positive Doppler findings. Abdominal CT showed that she harbored a large, 20-cm mass in her abdominal cavity, most likely arising from the right ovary. Surgery revealed a hypervascular tumor arising from the mesentery and attached to the gastric lesser curvature. Pathological examination revealed negativity for c-kit, but positivity for the protein “Discovered on GIST-1” (DOG1), confirming the EGIST diagnosis. Herein, we report this rare case of a c-kit-negative EGIST originating in the mesentery, which was diagnosed based on staining for DOG1.

Gastrointestinal stromal tumors (GISTs) are rare digestive system malignancies with extragastrointestinal stromal tumors (EGISTs) being even less. Diagnosing GISTs usually requires the identification of c-kit (CD117) expression by immunohistochemical staining. A 53-year-old woman complaining of dyspepsia was referred for the evaluation of a 1.5-cm extrinsic compression at the greater curvature of the proximal antrum. EUS revealed a multiseptated mass with positive Doppler findings. Abdominal CT showed that she harbored a large, 20-cm mass in her abdominal cavity, most likely arising from the right ovary. Surgery revealed a hypervascular tumor arising from the mesentery and attached to the gastric lesser curvature. Pathological examination revealed negativity for c-kit, but positivity for the protein “Discovered on GIST-1” (DOG1), confirming the EGIST diagnosis. Herein, we report this rare case of a c-kit-negative EGIST originating in the mesentery, which was diagnosed based on staining for DOG1.

Purpose: The most recent 2017 World Health Organization (WHO) classification of pancreatic neuroendocrine neoplasms (PanNENs) has refined the three-tiered 2010 scheme by separating grade 3 pancreatic neuroendocrine tumors (G3 PanNETs) from poorly differentiated pancreatic neuroendocrine carcinomas (PanNECs). However, differentiating between G3 Pan- NETs and PanNECs is difficult in clinical practice. Materials and Methods: Eighty-two surgically resected PanNENs were collected from 16 institutions and reclassified according to the 2017 WHO classification based on the histological features and proliferation index (mitosis and Ki-67). Immunohistochemical stains for ATRX, DAXX, retinoblastoma, p53, Smad4, p16, and MUC1 were performed for 15 high-grade PanNENs. Results: Re-classification resulted in 20 G1 PanNETs (24%), 47 G2 PanNETs (57%), eight G3 well-differentiated PanNETs (10%), and seven poorly differentiated PanNECs (9%). PanNECs showed more frequent diffuse nuclear atypia, solid growth patterns and apoptosis, less frequent organoid growth and regular vascular patterns, and absence of low-grade PanNET components than PanNETs. The Ki-67 index was significantly higher in PanNEC (58.2%± 15.1%) compared to G3 PanNET (22.6%±6.1%, p < 0.001). Abnormal expression of any two of p53, p16, MUC1, and Smad4 could discriminate PanNECs from G3 PanNETs with 100% specificity and 87.5% sensitivity. Conclusion Histological features supporting the diagnosis of PanNECs over G3 PanNETs were the absence of a low-grade PanNET component in the tumor, the presence of diffuse marked nuclear atypia, solid growth pattern, frequent apoptosis and markedly increased proliferative activity with homogeneous Ki-67 labeling. Immunohistochemical stains for p53, p16, MUC1, and Smad4 may be helpful in distinguishing PanNECs from G3 PanNETs in histologically ambiguous cases, especially in diagnostic practice when only small biopsied tissues are available.