Histopathological examination from the excisional specimen revealed a well-circumscribed dermal to subcutaneous tumor with ample sclerotic collagen bundles, an increased number of CD34 positive spindled cells, and prominent S-100 positive mature adipocytes comprising greater than 50% of the tumor.
The tumor in all the 21 cases recruited for the study showed immunohistochemical positivity for SAT6, while CD34 was positive in all the 18 tumor in which it was performed.
EMA, PR, S100, p53, and CD34 were expressed in 94%, 73%, 49%, 26%, and 23% of the tumors, respectively. p53 expression correlated positively with Ki-67 and World Health Organization (WHO) grade (r<sub>τ</sub> = 0.31 and r<sub>τ</sub> = 0.4, respectively).
Immunohistochemical expression of anti-angiogenic isoform of VEGF<sub>165</sub>b subunit, VEGFR1, VEGFR2, and microvessel density (CD34) were assessed in the tumour tissue and in the non-tumorous surrounding margins.
By immunohistochemistry, the tumor cells showed patchy positivity for CD34 and diffuse intranuclear positivity for STAT6, along with cytoplasmic positivity for MIC2 and BCL2.
Four serial sections were cut and stained in order to assess the following parameters: tumor grading with Hematoxylin-Eosin (H-E), tumor cells architecture (GÖ) with Gömöri technique, tumor stroma architecture (TC) with Goldner's trichrome, and vascular network (VN) architecture with cluster of differentiation 34 (CD34) immunomarker.
Our findings suggest that (hCB)-CD34+ NSG mice are transient and/or incomplete carriers of the human immune system and, therefore, represent a suboptimal tool to study the interaction between tumor and immune cells.
Statistical analysis of epithelial cytoplasmic expression revealed association of MFAP5 expression with tumor size (P=0.046), high histologic grade (P=0.007), presence of lymph node metastasis (P=0.014), poor Nottingham Prognostic Index (NPI) (P=0.001), late stage (P=0.008), immunohistochemical subtypes of BC (P=0.018), and increased microvessel density using CD34 immunostianing (P=0.04).
Also, in a Lewis lung carcinoma cell allograft model, the tumor size in Rx3+/‑ mice was significantly larger than that in WT mice, and the EPC cell population (CD34+/VEGFR2+ cells) recruited to the tumor was greater in the Rx3+/‑ mice compared with the WT mice.
All tested cases displayed concomitant loss of SMARCA4 and SMARCA2 and most tumors expressed epithelial markers (Pan-keratin or EMA) (n=29/30), SOX2 (n=26/27), and CD34 (n=17/27).
Thick-walled vessels in HLM were composed of mostly HMGA2-positive tumor cells, and HLM with HMGA2 overexpression also showed CD34-positive tumor vessel-supporting pericytes.
Superficial CD34 positive fibroblastic tumor (SCPFT) is a recently recognized, unique neoplasm with distinctive histomorphological features such as high pleomorphism, low mitotic rate, and diffuse CD34 reactivity.
Immunohistochemistry on human clinical specimens revealed that CXCR4 and a tumor vasculature marker CD34 were co-distributed in tumor vessels in human OSCC specimens.
By immunoperoxidase stains, the tumor cells are positive with the vascular markers CD31 and CD34 but negative with the epithelial marker cytokeratin AE1/AE3.
These effects were observed both at the bulk tumor level and in the most immature CD34⁺38<sup>-</sup> cell compartments containing the leukemic stem cells.