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Novel therapeutic targets for pancreatic cancer
Shing-Chun Tang1, Yang-Chao Chen1
1Shing-Chun Tang, Yang-Chao Chen, School of Biomedical Sciences, Faculty of Medicine, the Chinese University of Hong Kong, Hong Kong, China.
Abstract:
Pancreatic cancer has become the fourth leading cause of cancer death in the last two decades. Only 3%-15% of patients diagnosed with pancreatic cancer had 5 year survival rate. Drug resistance, high metastasis, poor prognosis and tumour relapse contributed to the malignancies and difficulties in treating pancreatic cancer. The current standard chemotherapy for pancreatic cancer is gemcitabine, however its efficacy is far from satisfactory, one of the reasons is due to the complex tumour microenvironment which decreases effective drug delivery to target cancer cell. Studies of the molecular pathology of pancreatic cancer have revealed that activation of KRAS, overexpression of cyclooxygenase-2, inactivation of p16(INK4A) and loss of p53 activities occurred in pancreatic cancer. Co-administration of gemcitabine and targeting the molecular pathological events happened in pancreatic cancer has brought an enhanced therapeutic effectiveness of gemcitabine. Therefore, studies looking for novel targets in hindering pancreatic tumour growth are emerging rapidly. In order to give a better understanding of the current findings and to seek the direction in future pancreatic cancer research; in this review we will focus on targets suppressing tumour metastatsis and progression, KRAS activated downstream effectors, the relationship of Notch signaling and Nodal/Activin signaling with pancreatic cancer cells, the current findings of non-coding RNAs in inhibiting pancreatic cancer cell proliferation, brief discussion in transcription remodeling by epigenetic modifiers (e.g., HDAC, BMI1, EZH2) and the plausible therapeutic applications of cancer stem cell and hyaluronan in tumour environment.
Insights
Pancreatic cancer research explores novel therapeutic targets to overcome drug resistance and improve survival rates. This review highlights strategies including targeting molecular pathways, non-coding RNAs, and the tumor microenvironment for enhanced treatment effectiveness.
Area of Science:
- Oncology
- Molecular Pathology
- Cancer Therapeutics
Background:
- Pancreatic cancer is a leading cause of cancer death with a low 5-year survival rate (3%-15%).
- Current chemotherapy (gemcitabine) efficacy is limited by drug resistance, metastasis, and the tumor microenvironment.
- Key molecular alterations include KRAS activation, cyclooxygenase-2 overexpression, and p16(INK4A)/p53 inactivation.
Purpose of the Study:
- To review current findings on novel therapeutic targets for pancreatic cancer.
- To explore strategies for suppressing tumor metastasis and progression.
- To discuss the role of signaling pathways, non-coding RNAs, and epigenetic modifiers in pancreatic cancer.
Main Methods:
- Literature review focusing on molecular pathology and therapeutic targets in pancreatic cancer.
- Analysis of studies investigating KRAS downstream effectors, Notch, and Nodal/Activin signaling.
- Examination of research on non-coding RNAs, epigenetic modifiers (HDAC, BMI1, EZH2), cancer stem cells, and hyaluronan.
Main Results:
- Targeting molecular pathological events alongside gemcitabine enhances therapeutic effectiveness.
- Emerging research focuses on novel targets to hinder tumor growth, metastasis, and progression.
- Non-coding RNAs and epigenetic modifications show potential in inhibiting pancreatic cancer cell proliferation.
Conclusions:
- Novel therapeutic strategies targeting molecular pathways, signaling, and the tumor microenvironment are crucial for improving pancreatic cancer treatment.
- Further research into non-coding RNAs, epigenetic modifiers, cancer stem cells, and hyaluronan holds promise for future therapies.
- Understanding these targets can guide future research directions and enhance gemcitabine's therapeutic effectiveness.
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