GSK3βhigh/NFATc1high subtype targeting overcomes therapy resistance in pancreatic cancer through transcriptional induction of homologous recombination repair - Scorecard - MDSpire
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Targeting the GSK3βhigh/NFATc1high Subtype to Overcome Therapy Resistance in Pancreatic Cancer via Induction of Homologous Recombination Repair Mechanisms

  • By

  • Muhammad Umair Latif

  • Xueang Liu

  • Aiko Bockelmann

  • Laura Huhnold

  • Geske Elisabeth Schmidt

  • Lukas Klein

  • Xueyuan Zhao

  • Lena-Christin Conradi

  • Karly Conrads

  • Anna Lena Weber

  • Sercan Mercan

  • Kristina Reutlinger

  • Atmika Paul

  • Zeynab Najafova

  • Steven A Johnsen

  • Zuriñe Bonilla Del Rio

  • Frederike Penz

  • Jovan Todorovic

  • Holger Bastians

  • Tim Beissbarth

  • Ulrich Sax

  • Ramy Ashry

  • Oliver H Krämer

  • Elisabeth Hessmann

  • Günter Schneider

  • Philipp Stroebel

  • Ivan Bogeski

  • Shiv K Singh

  • Volker Ellenrieder

  • August 1, 2026

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Clinical Scorecard: Targeting the GSK3βhigh/NFATc1high Subtype to Overcome Therapy Resistance in Pancreatic Cancer via Induction of Homologous Recombination Repair Mechanisms

At a Glance

CategoryDetail
ConditionPancreatic ductal adenocarcinoma (PDAC)
Key MechanismsNuclear GSK3β promotes growth and DNA repair by activating NFATc1-dependent transcription of homologous recombination repair genes.
Target PopulationPatients with GSK3βhigh/NFATc1high subtype PDAC.
Care SettingClinical oncology and research settings focusing on PDAC treatment.

Key Highlights

  • GSK3βhigh/NFATc1high subtype predicts early recurrence and poor survival after surgery.
  • Inactivation of GSK3β-NFATc1 signalling enhances efficacy of cisplatin.
  • Tumours with HR repair defects show increased sensitivity to platinum-based therapy.

Guideline-Based Recommendations

Diagnosis

  • Identify GSK3βhigh/NFATc1high subtype in PDAC for prognosis.

Management

  • Consider pharmacological inhibition of GSK3β-NFATc1 axis in treatment strategies.

Monitoring & Follow-up

  • Monitor for early recurrence in patients with GSK3βhigh/NFATc1high subtype.

Risks

  • High levels of GSK3β correlate with poor patient survival.

Patient & Prescribing Data

Patients with resected PDAC and GSK3βhigh/NFATc1high subtype.

Tailored inhibition of GSK3β may improve outcomes with platinum-based chemotherapy.

Clinical Best Practices

  • Stratification-based clinical trials are necessary for GSK3βhigh/NFATc1high subtype.
  • Utilize HR repair gene status to guide treatment decisions.

Related Resources & Content

Original Source(s)

GSK3βhigh/NFATc1high subtype targeting overcomes therapy resistance in pancreatic cancer through transcriptional induction of homologous recombination repair

  • by Muhammad Umair Latif, Xueang Liu, Aiko Bockelmann, Laura Huhnold, Geske Elisabeth Schmidt, Lukas Klein, Xueyuan Zhao, Lena-Christin Conradi, Karly Conrads, Anna Lena Weber, Sercan Mercan, Kristina Reutlinger, Atmika Paul, Zeynab Najafova, Steven A Johnsen, Zuriñe Bonilla Del Rio, Frederike Penz, Jovan Todorovic, Holger Bastians, Tim Beissbarth, Ulrich Sax, Ramy Ashry, Oliver H Krämer, Elisabeth Hessmann, Günter Schneider, Philipp Stroebel, Ivan Bogeski, Shiv K Singh, Volker Ellenrieder

  • August 1, 2026

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