Last update 01 Nov 2024

CDH16

Last update 01 Nov 2024

Basic Info

Synonyms

cadherin 16, Cadherin-16, CDH16

+ [2]

Introduction

Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types.

Drugs associated with CDH16

Anti-CD33-KSPi ADC (Vincerx Pharma)

Target

CD33 x CDH16

Mechanism

CD33 inhibitors [+1]

Active Org.

Vincerx Pharma, Inc.

Originator Org.

Vincerx Pharma, Inc.

Active Indication

Leukemia [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CDH16

100 Translational Medicine associated with CDH16

0 Patents (Medical) associated with CDH16

219

Literatures (Medical) associated with CDH16

08 Oct 2024·Proceedings of the National Academy of Sciences

Toward a CRISPR-based mouse model of Vhl -deficient clear cell kidney cancer: Initial experience and lessons learned

Article

Author: He, Lixia ; Yun, Changhong ; Morgan, Tamara ; Pignon, Jean-Christophe ; James, Amy ; Zhao, Yongmei ; Ricketts, Christopher J. ; Pinheiro, Elaine M. ; Turan, Sevilay ; Ileva, Lilia ; Schmidt, Laura S. ; Bi, Kevin ; Difilippantonio, Simone ; Van Allen, Eliezer M. ; Vigeant, Sean M. ; Morris, Nicole ; Tran, Bao ; Karim, Baktiar ; Unite, Joanne ; Choudhari, Sulbha ; Dhandapani, Sripriya ; Linn, Douglas E. ; Sticco-Ivins, Maura ; Gao, Wenhua ; Kalen, Joseph D. ; Stransky, Laura A. ; Kaelin, William G. ; Linehan, W. Marston ; Parab, Vaishali ; Signoretti, Sabina ; Ramesh, Vijyendra ; Warner, Andrew C. ; Jeon, Albert

CRISPR is revolutionizing the ability to do somatic gene editing in mice for the purpose of creating new cancer models. Inactivation of the VHL tumor suppressor gene is the signature initiating event in the most common form of kidney cancer, clear cell renal cell carcinoma (ccRCC). Such tumors are usually driven by the excessive HIF2 activity that arises when the VHL gene product, pVHL, is defective. Given the pressing need for a robust immunocompetent mouse model of human ccRCC, we directly injected adenovirus-associated viruses (AAVs) encoding sgRNAs against VHL and other known/suspected ccRCC tumor suppressor genes into the kidneys of C57BL/6 mice under conditions where Cas9 was under the control of one of two different kidney-specific promoters ( Cdh16 or Pax 8) to induce kidney tumors. An AAV targeting Vhl, Pbrm1, Keap1 , and Tsc1 reproducibly caused macroscopic ccRCCs that partially resembled human ccRCC tumors with respect to transcriptome and cell of origin and responded to a ccRCC standard-of-care agent, axitinib. Unfortunately, these tumors, like those produced by earlier genetically engineered mouse ccRCCs, are HIF2 independent.

01 Sep 2024·Asian Pacific Journal of Cancer Prevention

Effect of Crocin and Crocetin Compared to Cyclophosphamide on the Expression Level of miRNA-16-1 in a B Cell Transformed with EBV Virus Cell Line

Article

Author: Sotoodeh Jahromi, Abdolreza ; Erfanian, Saeideh ; Kargar, Mohammad ; Rahmanian, Karamatollah ; Moradzadeh, Malihe ; Haghshenas, Mohammad Reza ; Hojjat-Farsangi, Mohammad

INTRODUCTIONCrocin and Crocetin are compounds that have shown promising therapeutic potentials in various medical contexts. To date, the effect of crocin and crocetin on the expression level of miRNA-16-1 in Epstein Barr Virus (EBV)-induced lymphoma has not been investigated. This research delved into a comparative analysis of the cytotoxic effects of crocin and crocetin compared to cyclophosphamide, the main drug used in the treatment of lymphoma and PTLD, on B-cell lymphoma infected with EBV (cell line CO 88BV59-1). Additionally, the study examines the changes in miRNA-16-1 expression following these treatments in this cell line.MATERIALS AND METHODSCO 88BV59-1 LCL cells were treated with crocin, crocetin (0.2 to 200 μM), and cyclophosphamide (0.05 to 50 μM) for 72 hours. Cell viability and apoptosis were assessed using resazurin and Annexin V/PI techniques, respectively. Additionally, the expression of miRNA-16-1-3p and miRNA-16-1-5p was determined using the Real-Time PCR method. The data were analyzed using one-way analysis of variance (ANOVA) with Tukey's multiple comparisons post-hoc test.RESULTSCrocin and crocetin inhibited the proliferation and apoptosis caused by EBV-infected cells in a dose- and time-dependent manner (P<0.05). The expression levels of miRNA-16-1-3p and miRNA-16-1-5p remained unchanged in cells treated with crocin and crocetin.CONCLUSIONThe study found that the cytotoxic effect of Crocin, Crocetin, and Cyclophosphamide on CO 88BV59-1 LCL is independent of the expression level of miRNA-16-1. The results showed a reduction in cell survival and an increase in cell death.

01 Sep 2024·Virchows Archiv

PAX8 expression in cancerous and non-neoplastic tissue: a tissue microarray study on more than 17,000 tumors from 149 different tumor entities

Article

Author: Burandt, Eike ; Minner, Sarah ; Kluth, Martina ; Hinsch, Andrea ; Steurer, Stefan ; Lebok, Patrick ; Sauter, Guido ; Luebke, Andreas M ; Baltruschat, Sarah ; Fraune, Christoph ; Clauditz, Till S ; Hube-Magg, Claudia ; Gorbokon, Natalia ; Lennartz, Maximilian ; Simon, Ronald ; Krech, Till ; Bernreuther, Christian ; Höflmayer, Doris ; Jacobsen, Frank ; Marx, Andreas H

AbstractPAX8 plays a role in development of the thyroid, kidney, and the Wolffian and Mullerian tract. In surgical pathology, PAX8 immunohistochemistry is used to determine tumors of renal and ovarian origin, but data on its expression in other tumors are conflicting. To evaluate PAX8 expression in normal and tumor tissues, a tissue microarray containing 17,386 samples from 149 different tumor types and 608 samples of 76 different normal tissue types was analyzed by immunohistochemistry. PAX8 results were compared with previously collected data on cadherin 16 (CDH16). PAX8 positivity was found in 40 different tumor types. The highest rate of PAX8 positivity was found in thyroidal neoplasms of follicular origin (98.6–100%), gynecological carcinomas (up to 100%), renal tumors (82.6–97.8%), and urothelial neoplasms (2.3–23.7%). Important tumors with near complete absence of PAX8 staining (< 1%) included all subtypes of breast cancers, hepatocellular carcinomas, gastric, prostatic, pancreatic, and pulmonary adenocarcinomas, neuroendocrine neoplasms, small cell carcinomas of various sites, and lymphomas. High PAX8 expression was associated with low tumor grade in 365 non-invasive papillary urothelial carcinomas (p < 0.0001) but unrelated to patient outcome and/or tumor phenotype in clear cell renal cell carcinoma, high-grade serous ovarian cancer, and endometrioid endometrial carcinoma. For determining a renal tumor origin, sensitivity was 88.1% and specificity 87.2% for PAX8, while sensitivity was 85.3% and specificity 95.7% for CDH16. The combination of PAX8 and CDH16 increased specificity to 96.8%. In conclusion, PAX8 immunohistochemistry is a suitable diagnostic tool. The combination of PAX8 and CDH16 positivity has high specificity for renal cell carcinoma.

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CDH16

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