Immunohistochemistry is an integral technique for tissue-based diagnostics and biomarker detection with broad worldwide adoption. Advances in core chemistries, antibody design, and automation have ushered unprecedented sensitivity, specificity, and reproducibility in immunohistochemistry assays.
As a result, clinical immunohistochemistry assays that utilize dual-color approaches and mutation-specific antibodies provide novel tools in clinical diagnostics that until recently were in the realm of investigational research. This review provides an overview of innovations in clinical immunohistochemistry assays with emphasis on those used for patients with hematopoietic neoplasms.
Advances in clinical-grade immunohistochemistry techniques have allowed labs to develop and validate multiplex assays that improve diagnostic utility-such as CD5/PAX5 and TCF4/CD123 dual-color stains-and have the potential to enhance the specificity of biomarker detection. In addition, the increased availability of immunohistochemistry assays that detect mutant proteins (e.g., BRAF V600E and IDH1 R132H) provides a helpful replacement and/or adjunct for molecular testing.
These techniques are highly reproducible, entail reasonable technical and interpretation complexity, and are relatively cost-effective, making them valuable novel tools in modern cancer care. Multiplex and mutation-specific immunohistochemistry assays represent important innovations that provide improved utility in the context of personalized medicine and targeted therapy.

Anti-TSNARE1 IgG plasma levels differ by sex in patients with schizophrenia in a Chinese population.

It was recently reported that levels of plasma IgG antibodies against peptide antigens derived from proteins encoded by schizophrenia-associated genes are altered in individuals with schizophrenia treated with antipsychotics. This study aimed to replicate the initial finding in antipsychotic-naïve patients with first-episode schizophrenia and to explore the possible mechanism by which immune tolerance of B cells may be altered in this disease.
A total of 408 case-control plasma samples were collected for analysis of circulating IgG antibodies against fragments derived from TCF4, TSNARE1, ZNF804A, TRANK1, ERCC4, DPYD and CD25 using an in-house ELISA. The Mann-Whitney U-test revealed that patients with schizophrenia had a significant change in plasma anti-TSNARE1 and anti-CD25 IgG levels; male patients mainly contributed to the increased levels of anti-TSNARE1 IgG and anti-CD25 IgG.
Receiver operating characteristic (ROC) curve analysis revealed that the anti-TSNARE1 IgG assay had an area under the ROC curve of 0.625 with a sensitivity of 15.7% and a specificity of 95.2%. Work on a B-cell model revealed that TRANK1-derived antigen treatments could enhance the proportions of CD83+ cells and apoptotic B cells when compared with TSNARE1-derived antigen and vehicle treatment.
We conclude that there is a gender difference in autoimmune responses in schizophrenia and suggest that anti-TSNARE1 IgG may be indicative of schizophrenia in a subgroup of male patients.

Blastic Plasmacytoid Dendritic Cell Neoplasm: State of the Art and Prospects.

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an extremely rare tumour, which usually affects elderly males and presents in the skin with frequent involvement of the bone-marrow, peripheral blood and lymph nodes. It has a dismal prognosis, with most patients dying within one year when treated by conventional chemotherapies.
The diagnosis is challenging, since neoplastic cells can resemble lymphoblasts or small immunoblasts, and require the use of a large panel of antibodies, including those against CD4, CD56, CD123, CD303, TCL1, and TCF4. The morphologic and in part phenotypic ambiguity explains the uncertainties as to the histogenesis of the neoplasm that led to the use of various denominations.
Recently, a series of molecular studies based on karyotyping, gene expression profiling, and next generation sequencing, have largely unveiled the pathobiology of the tumour and proposed the potentially beneficial use of new drugs. The latter include SL-401, anti-CD123 immunotherapies, venetoclax, BET-inhibitors, and demethylating agents. The epidemiologic, clinical, diagnostic, molecular, and therapeutic features of BPDCN are thoroughly revised in order to contribute to an up-to-date approach to this tumour that has remained an orphan disease for too long.
 Immunohistochemistry Innovations for Diagnosis and Tissue-Based Biomarker Detection.

Expression and clinical significance of transcription factor 4 (TCF4) in epithelial ovarian cancer.

To investigate TCF4 expression in epithelial ovarian cancer, and to explore its correlation with clinicopathological parameters and clinical prognosis of epithelial ovarian cancer.From 2009 to 2017, 188 cases of paraffin-embedded epithelial ovarian cancer tissues and 41 paratumor ovarian tissues which had been confirmed at the memorial hospital of Sun Yat-sen University were collected in this study, and the expression of TCF4 was performed by immunohistochemistry using a polyclonal antibody specific for TCF4.
The expression of TCF4 protein was associated with disease progression free survival and overall survival in epithelial ovarian cancer patients; and TCF4 overexpression was associated with age, FIGO stage, lymph node metastasis, intraperitoneal metastasis, intestinal metastasis, vital status, intraperitoneal recurrence, and serum CA153.
Moreover, in a multivariate Cox regression analysis TCF4 overexpression was an indeed independent prognostic factor in epithelial ovarian cancer.TCF4 may play an oncogenic role in epithelial ovarian cancer, and TCF4 is a useful independent prognostic biomarker of epithelial ovarian cancer, and it may provide a candidate target therapy treatment in future.

Osteopontin production by TM4SF4 signaling drives a positive feedback autocrine loop with the STAT3 pathway to maintain cancer stem cell-like properties in lung cancer cells.

Transmembrane 4 L6 family proteins have been known to promote cancer. In this study, we demonstrated that transmembrane 4 L6 family member 4 (TM4SF4), which is induced by γ-radiation in non-small cell lung cancer (NSCLC) cells, is involved in epithelial-to-mesenchymal transition (EMT) and cancer stem cell (CSC) properties of NSCLC through the regulation of osteopontin (OPN).
Forced TM4SF4 overexpression in A549 cells increased the secretion of OPN, which activates CD44 or integrin signaling and thus maintains EMT-associated CSC-like properties. OPN, known as a downstream target of β-catenin/T-cell factor 4 (TCF-4), was induced by up-regulated β-catenin via TM4SF4-driven phosphorylation of glycogen synthase kinase 3b (GSK3β).
TCF4 complexed to promoter regions of OPN in TM4SF4-overexpressing A549 cells was also confirmed by chromatin immunoprecipitation. Knockout of either β-catenin or TCF4-suppressed OPN expression, demonstrating that both factors are essential for OPN expression in NSCLC cells.
OPN secreted by TM4SF4/GSK3β/β-catenin signaling activated the JAK2/STAT3 or FAK/STAT3 pathway, which also up-regulates OPN expression in an autocrine manner and consequently maintains the self-renewal and metastatic capacity of cancer cells.

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Neutralizing antibody to OPN blocked the autocrine activation of OPN expression, consequently weakened the metastatic and self-renewal capacity of cancer cells. Collectively, our findings indicate that TM4SF4-triggered OPN expression is involved in the persistent reinforcement of EMT or cancer stemness by creating a positive feedback autocrine loop with JAK2/STAT3 or FAK/STAT3 pathways.

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