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Targeted therapies in pancreatic cancer: Promises and failures
Matineh Barati Bagherabad1, Fahimeh Afzaljavan1, Soodabeh ShahidSales2
1Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract:
Pancreatic ductal adenocarcinoma (PDAC) is an incidence rate nearly equal to its mortality rate. The poor prognosis of the disease can be explained by the absence of effective biomarkers for screening and early detection, together with the aggressive behavior and resistance to the currently available chemotherapy. The therapeutic failure can also be attributed to the inter-/intratumor genetic heterogeneity and the abundance of tumor stroma that occupies the majority of the tumor mass. Gemcitabine is used in the treatment of PDAC; however, the response rate is less than 12%. A recent phase III trial revealed that the combination of oxaliplatin, irinotecan, fluorouracil, and leucovorin could be an option for the treatment of metastatic PDAC patients with good performance status, although these approaches can result in high toxicity level. Further investigations are required to develop innovative anticancer agents that either improve gemcitabine activity, within novel combinatorial approaches or acts with a better efficacy than gemcitabine. The aim of the current review is to give an overview of preclinical and clinical studies targeting key dysregulated signaling pathways in PDAC.
Insights
Pancreatic ductal adenocarcinoma (PDAC) remains deadly due to late detection and treatment resistance. This review examines novel therapeutic strategies targeting key signaling pathways to improve outcomes for this challenging cancer.
Area of Science:
- Oncology
- Cancer Biology
- Translational Medicine
Background:
- Pancreatic ductal adenocarcinoma (PDAC) presents a significant clinical challenge with high mortality and limited effective treatments.
- Current therapies like gemcitabine show poor response rates (<12%), and combination therapies can cause severe toxicity.
- Tumor heterogeneity and abundant stroma further complicate treatment efficacy.
Purpose of the Study:
- To provide a comprehensive overview of preclinical and clinical research.
- To highlight studies focusing on key dysregulated signaling pathways in PDAC.
- To identify potential novel therapeutic targets and strategies for PDAC treatment.
Main Methods:
- Review of preclinical studies investigating novel agents and combinations.
- Analysis of clinical trials targeting specific molecular pathways in PDAC.
- Synthesis of data on therapeutic efficacy and toxicity.
Main Results:
- Identification of several promising signaling pathways implicated in PDAC progression and resistance.
- Evaluation of novel agents and combinatorial approaches showing potential to overcome current treatment limitations.
- Assessment of the efficacy and toxicity profiles of emerging therapies.
Conclusions:
- Targeting specific signaling pathways holds promise for improving PDAC treatment outcomes.
- Further research is crucial for developing innovative therapies that enhance gemcitabine activity or offer superior efficacy.
- Novel therapeutic strategies are needed to address the challenges posed by PDAC's aggressive nature and treatment resistance.
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