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Last update 08 May 2025

PTPRD

Last update 08 May 2025

Basic Info

Synonyms

HPTP, protein tyrosine phosphatase receptor type D, Protein-tyrosine phosphatase delta

+ [4]

Introduction

Can bidirectionally induce pre- and post-synaptic differentiation of neurons by mediating interaction with IL1RAP and IL1RAPL1 trans-synaptically. Involved in pre-synaptic differentiation through interaction with SLITRK2.

Drugs associated with PTPRD

NHB-1109

Target

PTPRD

Mechanism

PTPRD inhibitors

Active Org.

The University of New Mexico [+1]

Originator Org.

University of Maryland School of Medicine

Active Indication

Unspecified drug dependence

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

RD-43

Target

PTPRD

Mechanism

PTPRD inhibitors

Active Org.

Stony Brook University [+1]

Originator Org.

Cold Spring Harbor Laboratory, Inc.

Active Indication

Metastatic breast cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with PTPRD

TCTR20210212002

/ CompletedEarly Phase 1IIT

The effect of RD43 rice yellow noodle consumption on glycemic response and appetite in healthy men subjects

Start Date06 Jan 2020

Sponsor / Collaborator

University of Chulalongkorn

100 Clinical Results associated with PTPRD

100 Translational Medicine associated with PTPRD

0 Patents (Medical) associated with PTPRD

448

Literatures (Medical) associated with PTPRD

01 May 2025·Molecular Psychiatry

Genome-wide copy number variation association study in anorexia nervosa

Article

Author: Chawner, Samuel J R A ; Mitchell, James ; Szatkiewicz, Jin P. ; Fundín, Bengt T. ; Lin, Tian ; Leppä, Virpi M ; Halmi, Katherine A ; Woodside, D. Blake ; Strober, Michael ; Kaplan, Allan S ; Savva, Androula ; Watson, Hunna J. ; Thornton, Laura M ; Crawford, Steven ; Wray, Naomi R. ; Watson, Hunna J ; Wen, Jia ; Pedersen, Nancy L ; Jordan, Jennifer ; Pedersen, Nancy L. ; Berrettini, Wade H. ; McRae, Allan ; Karlsson, Robert ; Sullivan, Patrick F ; Borg, Stina ; Walker, Alicia ; Woodside, D Blake ; Martin, Nicholas G ; Halmi, Katherine A. ; Davies, Helena L. ; Wray, Naomi R ; Sidorenko, Julia ; Sullivan, Patrick F. ; Chawner, Samuel J. R. A. ; Gordon, Scott ; Martin, Nicholas G. ; Kennedy, Martin A. ; Bulik, Cynthia M ; Kaye, Walter H ; Munn-Chernoff, Melissa A ; Baker, Jessica H ; Berrettini, Wade H ; Song, Jie ; Birgegård, Andreas ; Kennedy, Martin A ; Bulik, Cynthia M. ; Thornton, Laura M. ; Fundín, Bengt T ; Szatkiewicz, Jin P ; Baker, Jessica H. ; Munn-Chernoff, Melissa A. ; Landén, Mikael ; Kaye, Walter H. ; Leppä, Virpi M. ; Brandt, Harry ; Kaplan, Allan S. ; Davies, Helena L ; Parker, Richard ; Yilmaz, Zeynep ; Kirov, George

AbstractThis study represents the first large-scale investigation of rare (<1% population frequency) copy number variants (CNVs) in anorexia nervosa (AN). Large, rare CNVs are reported to be causally associated with anthropometric traits, neurodevelopmental disorders, and schizophrenia, yet their role in the genetic basis of AN is unclear. Using genome-wide association study (GWAS) array data from the Anorexia Nervosa Genetics Initiative (ANGI), which included 7414 AN case and 5044 controls, we investigated the association of 67 well-established syndromic CNVs and 178 pleiotropic disease-risk dosage-sensitive CNVs with AN. To identify novel CNV regions (CNVRs) that increase the risk of AN, we conducted genome-wide association studies with a focus on rare CNV-breakpoints (CNV-GWAS). We found no net enrichment of rare CNVs, either deletions or duplications, in AN, and none of the well-established syndromic or pleiotropic CNVs had a significant association with AN status. However, the CNV-GWAS found 21 nominally associated CNVRs that contribute to AN risk, covering protein-coding genes implicated in synaptic function, metabolic/mitochondrial factors, and lipid characteristics, like the CD36 (7q21.11) gene, which transports long-chain fatty acids into cells. CNVRs intersecting genes previously related to neurodevelopmental traits include deletions of NRXN1 intron 5 (2p16.3), IMMP2L (7q31.1), and PTPRD (9p23). Overall, given that our study is well powered to detect the CNV burden level reported for schizophrenia, we can conclude that rare CNVs have a limited role in the etiology of AN, as reported for bipolar disorder. Our nominal associations for the 21 discovered CNVRs are consistent with AN being a metabo-psychiatric trait, as demonstrated by the common genetic architecture of AN, and we provide association results to allow for replication in future research.

01 May 2025·American Journal of Surgical Pathology

Clinicopathologic and Molecular Characterization of Gynecologic Carcinosarcomas With a Mesonephric-Like Carcinomatous Component

Article

Author: Mendoza, Rachelle P. ; Tjota, Melisa Y. ; Lastra, Ricardo R. ; Chapel, David B. ; Xing, Deyin ; Euscher, Elizabeth D. ; Bakkar, Rania ; Afkhami, Michelle ; Barroeta, Julieta E. ; Kolin, David L. ; Choi, Donghyuk N. ; Numan, Tricia A.

Carcinosarcoma with a mesonephric-like carcinomatous component (MLCS) is a rare subtype of gynecologic malignancy recently described in the literature. This study aims to expand the genomic characterization of MLCS by performing independent molecular analysis of the carcinomatous and sarcomatous components in a series of MLCS. Eight cases of gynecologic MLCS (endometrial, lower uterine segment, and ovarian) were identified and underwent clinicopathologic evaluation. Genomic DNA extraction and next-generation sequencing (NGS) were performed separately from the carcinomatous and sarcomatous components of 4 tumors, while 2 tumors underwent NGS of combined carcinomatous and sarcomatous components. The average age at diagnosis was 65.6 years (range 50 to 83 years). MLCS patients were diagnosed at FIGO stage I (n=3), stage II (n=2), stage III (n=2), and stage IV (n=1). The carcinomatous and sarcomatous components were observed to harbor the same single nucleotide variations. All cases had less than 10 mutations/Mb and were microsatellites stable. All cases (6/6, 100%) harbored KRAS point mutations in codon 12, including the following variants: p.G12D (n=2), p.G12A (n=2), and p.G12V (n=2). Five cases showed additional alterations in ARID1A (case 1), PTEN (case 2), PIK3CA (case 4), SPOP (case 6), TET1 (case 6), BUB1 (case 7), LYN (case 7) and PTPRD (case 7). The presence of both KRAS and PTEN/PIK3CA alterations suggests a combined endometrioid and mesonephric differentiation in MLCS.

01 May 2025·Computers in Biology and Medicine

Discovery of mutations predictive of survival benefit from immunotherapy in first-line NSCLC: A retrospective machine learning study of IMpower150 liquid biopsy data

Article

Author: Ding, Haolun ; Yang, Yaning ; Xu, Xu Steven ; Feng, Wei ; Yuan, Min

Predictive biomarker identification in cancer treatment has traditionally relied on pre-defined analyses, limiting discoveries to expected biomarkers and potentially overlooking novel ones predictive of therapy response. In this work, we develop a novel machine-learning approach capable of exploring full landscape of mutations and combinations and identify potentially new predictive biomarkers for chemoimmunotherapy. Utilizing the liquid biopsy dataset from 313 non-small cell lung cancer (NSCLC) patients in the Phase 3 Impower150 trial (NCT02366143), we developed the HRdiffRF algorithm with a novel hazard ratio-splitting criterion. Predictive mutations and combinations were identified for overall survival (OS) improvement with atezolizumab plus bevacizumab plus carboplatin and paclitaxel (ABCP) compared to bevacizumab plus carboplatin and paclitaxel (BCP). Our analysis confirms the predictive role of KRAS mutations and reveals the predictive value of PTPRD and SMARCA4 mutations in chemoimmunotherapy efficacy. Unlike other KRAS wild-type NSCLC patients, NSCLC patients with KRAS wild-type status and mutations in FAT1, ERBB2, or PTPRD may benefit from chemoimmunotherapy, while NTRK3 and GNAS mutations could negatively impact survival. Patients harboring concurrent KRAS and KEAP1 mutations may not benefit from chemoimmunotherapy. These findings highlight the complex genetic factors influencing treatment response for chemoimmunotherapy in NSCLC. In summary, the proposed machine-learning tool identified potential predictive biomarkers for first-line chemoimmunotherapy in NSCLC and can be readily applied to other tumor types and studies. It can also be extended to explore predictive biomarkers beyond mutations.

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PTPRD

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