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Pangen (collagen, Fournier / Pangen)

✓ Approved

AbbVie, Inc. · therapeutic agent

What is Pangen?

Pangen is a therapeutic agent developed by AbbVie, Inc.. It is approved for therapeutic indications.

Drug Profile

Brand Namescollagen, Fournier, Pangen
CompanyAbbVie, Inc.
StatusApproved
Sources: ClinicalTrials.gov, AbbVie, Inc.

Therapeutic Indications

Pangen is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
General disorders and administration site conditionsImpaired healing✓ Approved
Vascular disordersThrombosis✓ Approved

Related Research Articles

PubMedNPJ precision oncology2025-04-05

The tandem duplicator phenotype may be a novel targetable subgroup in pancreatic cancer.

Farooq Abdul R AR, Zhang Amy X AX, Chan-Seng-Yue Michelle M, Topham James T JT et al.

Tandem duplicator phenotype (TDP) consists of distinct genomic rearrangements where tandem duplications are randomly distributed. In this study, we characterized the prevalence and outcomes of TDP in a large series of prospectively sequenced tumors from patients with pancreatic ductal adenocarcinomas (PDAC). Whole-genome sequencing (WGS) was performed in 530 PDAC cases from the PanCuRx Initiative, COMPASS and PanGen/POG trials in Canada. Of 530 cases, 52 were identified as TDP (9.8%; 13 resected, 39 advanced). Etiological subgroups of TDP included BRCA1 (n = 9), CCNE1 (n = 4), and unknown (n = 39). Presence of TDP was not prognostic in resected specimens (p = 0.77) compared with non-HRD and non-TDP cases, described as typicals. In advanced cases, when stratified for only classical subtype cases, platinum therapy was correlated with longer response in non-BRCA1 TDP vs. typicals (p = 0.0036). There was no difference in overall survival between TDP and typicals (p = 0.5).TDP represents a potential novel targetable subgroup for chemotherapy selection in PDAC.

PMID 40185871
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PubMedDatabase : the journal of biological databases and curation2024-07-24

PANGEN: an online platform for the comparison and creation of diagnostic gene panels.

Isakov Ofer O, Marek-Yagel Dina D, Greenberg Rotem R, Naftali Michal M et al.

Targeted gene panel sequencing is used to limit the search for causative genetic variants solely to genes with an established association with the phenotype. The design of gene panels is challenging due to the lack of consensus regarding phenotypic associations for some genes, which results in high variation in gene composition for the same panel offered by different laboratories. We developed PANGEN, a platform that provides a centralized resource for gene panel information, with the ability to compare and generate new intelligent diagnostic panels. Gene-phenotype associations were collected from 12 public and commercial sources (Blueprint, Cegat, Centogene, ClinGen, Fulgent, GeneDx, Health in Code, Human Phenotype Ontology, Invitae, PanelApp, Prevention genetics, and Pronto diagnostics). Gene-phenotype associations are categorized into tiers according to categories derived from the original source panel. Pairwise panel similarity was calculated by dividing the number of common genes by the total number of genes in both panels. Regions with extreme guanine-cytosine (GC) content were collected from the Genome in a Bottle stratifications dataset, and putative genomic duplications were retrieved from the University of Santa Cruz database. Overall, 1533 panels, 9759 phenotypes, and 6979 genes were collected. The platform provides an interface to (i) explore and compare collected panels, (ii) find similar panels, (iii) identify genes with high GC content or duplication levels, (iv) generate gene panels by combining panels from various sources, and (v) stratify a generated panel into genes with a strong phenotype association ('core') and those with a weaker association ('extended'). The presented platform represents a unique resource for gene panel exploration and comparison that facilitates the generation of tailored diagnostic panels through a public online web server. Database URL: https://c-gc.shinyapps.io/PANGEN/.

PMID 39043627
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PubMedNature communications2022-10-09

Integrative analysis of KRAS wildtype metastatic pancreatic ductal adenocarcinoma reveals mutation and expression-based similarities to cholangiocarcinoma.

Topham James T JT, Tsang Erica S ES, Karasinska Joanna M JM, Metcalfe Andrew A et al.

Oncogenic KRAS mutations are absent in approximately 10% of patients with metastatic pancreatic ductal adenocarcinoma (mPDAC) and may represent a subgroup of mPDAC with therapeutic options beyond standard-of-care cytotoxic chemotherapy. While distinct gene fusions have been implicated in KRAS wildtype mPDAC, information regarding other types of mutations remain limited, and gene expression patterns associated with KRAS wildtype mPDAC have not been reported. Here, we leverage sequencing data from the PanGen trial to perform comprehensive characterization of the molecular landscape of KRAS wildtype mPDAC and reveal increased frequency of chr1q amplification encompassing transcription factors PROX1 and NR5A2. By leveraging data from colorectal adenocarcinoma and cholangiocarcinoma samples, we highlight similarities between cholangiocarcinoma and KRAS wildtype mPDAC involving both mutation and expression-based signatures and validate these findings using an independent dataset. These data further establish KRAS wildtype mPDAC as a unique molecular entity, with therapeutic opportunities extending beyond gene fusion events.

PMID 36209277
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PubMedClinical cancer research : an official journal of the American Association for Cancer Research2019-09-05

Altered Gene Expression along the Glycolysis-Cholesterol Synthesis Axis Is Associated with Outcome in Pancreatic Cancer.

Karasinska Joanna M JM, Topham James T JT, Kalloger Steve E SE, Jang Gun Ho GH et al.

Identification of clinically actionable molecular subtypes of pancreatic ductal adenocarcinoma (PDAC) is key to improving patient outcome. Intertumoral metabolic heterogeneity contributes to cancer survival and the balance between distinct metabolic pathways may influence PDAC outcome. We hypothesized that PDAC can be stratified into prognostic metabolic subgroups based on alterations in the expression of genes involved in glycolysis and cholesterol synthesis. We performed bioinformatics analysis of genomic, transcriptomic, and clinical data in an integrated cohort of 325 resectable and nonresectable PDAC. The resectable datasets included retrospective The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC) cohorts. The nonresectable PDAC cohort studies included prospective COMPASS, PanGen, and BC Cancer Personalized OncoGenomics program (POG). On the basis of the median normalized expression of glycolytic and cholesterogenic genes, four subgroups were identified: quiescent, glycolytic, cholesterogenic, and mixed. Glycolytic tumors were associated with the shortest median survival in resectable (log-rank test P = 0.018) and metastatic settings (log-rank test P = 0.027). Patients with cholesterogenic tumors had the longest median survival. KRAS and MYC-amplified tumors had higher expression of glycolytic genes than tumors with normal or lost copies of the oncogenes (Wilcoxon rank sum test P = 0.015). Glycolytic tumors had the lowest expression of mitochondrial pyruvate carriers MPC1 and MPC2. Glycolytic and cholesterogenic gene expression correlated with the expression of prognostic PDAC subtype classifier genes. Metabolic classification specific to glycolytic and cholesterogenic pathways provides novel biological insight into previously established PDAC subtypes and may help develop personalized therapies targeting unique tumor metabolic profiles.See related commentary by Mehla and Singh, p. 6.

PMID 31481506
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PubMedInternational journal of cancer2018-09-20

Pancreatic cancer and autoimmune diseases: An association sustained by computational and epidemiological case-control approaches.

Gomez-Rubio Paulina P, Piñero Janet J, Molina-Montes Esther E, Gutiérrez-Sacristán Alba A et al.

Deciphering the underlying genetic basis behind pancreatic cancer (PC) and its associated multimorbidities will enhance our knowledge toward PC control. The study investigated the common genetic background of PC and different morbidities through a computational approach and further evaluated the less explored association between PC and autoimmune diseases (AIDs) through an epidemiological analysis. Gene-disease associations (GDAs) of 26 morbidities of interest and PC were obtained using the DisGeNET public discovery platform. The association between AIDs and PC pointed by the computational analysis was confirmed through multivariable logistic regression models in the PanGen European case-control study population of 1,705 PC cases and 1,084 controls. Fifteen morbidities shared at least one gene with PC in the DisGeNET database. Based on common genes, several AIDs were genetically associated with PC pointing to a potential link between them. An epidemiologic analysis confirmed that having any of the nine AIDs studied was significantly associated with a reduced risk of PC (Odds Ratio (OR) = 0.74, 95% confidence interval (CI) 0.58-0.93) which decreased in subjects having ≥2 AIDs (OR = 0.39, 95%CI 0.21-0.73). In independent analyses, polymyalgia rheumatica, and rheumatoid arthritis were significantly associated with low PC risk (OR = 0.40, 95%CI 0.19-0.89, and OR = 0.73, 95%CI 0.53-1.00, respectively). Several inflammatory-related morbidities shared a common genetic component with PC based on public databases. These molecular links could shed light into the molecular mechanisms underlying PC development and simultaneously generate novel hypotheses. In our study, we report sound findings pointing to an association between AIDs and a reduced risk of PC.

PMID 30229903
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PubMedAdvances in genetics2018-07-25

In Search of Darwin's Imaginary Gemmules.

Liu Yongsheng Y

Darwin's gemmules were supposed to be "thrown off" by cells and were "inconceivably minute and numerous as the stars in heaven." They were capable of self-propagation and diffusion from cell to cell, and circulation through the system. The word "gene" coined by Wilhelm Johannsen, was derived from de Vries's term "pangen," itself a substitute for "gemmule" in Darwin's Pangenesis. Johannsen resisted the "morphological" conception of genes as particles with a certain structure. Morgan's genes were considered to be stable entities arranged in an orderly linear pattern on chromosomes, like beads on a string. In the late 1940s, McClintock challenged the concept of the stability of the gene when she discovered that some genes could move within a chromosome and between chromosomes. In 1948, Mandel and Metais reported the presence of cell-free nucleic acids in human blood for the first time. Over the past several decades, it has been universally accepted that almost all types of cells not only shed molecules such as cell-free DNA (including genomic DNA, tumor DNA and fetal DNA), RNAs (including mRNA and small RNAs) and prions, but also release into the extracellular environment diverse types of membrane vesicles (known as extracellular vesicles) containing DNA, RNA and proteins. Thus Darwin's speculative gemmules of the 19th century have become the experimentally demonstrated circulating cell-free DNA, mobile RNAs, prions and extracellular vesicles.

PMID 30037394
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