Chemical treatment of pancreatic cancer

By | April 23, 2012

Pancreatic cancer chemotherapy, clinical pancreatic cancer diagnosis, most have reached the late stage, unresectable, pancreatic cancer chemotherapy can reduce symptoms, remission of disease, chemotherapy can also be made part of the surgical treatment of patients with access to opportunities. Pancreatic low sensitivity to chemotherapeutic drugs, effective drugs are known to few drugs are sensitive to gemcitabine ,5-Fu, adriamycin, epirubicin (EPI) and streptozocin (chain gill ADM), among which, gemcitabine has a good effect on pancreatic cancer, pancreatic cancer patients can improve quality of life and prolong survival. We found that lipid metabolism in pancreatic cancer cell growth and angiogenesis. Arachidonic acid can promote the growth of pancreatic cancer cells, while COX-2CCQX-2) is a specific inhibitor of pancreatic cancer cells and inhibit the growth of implanted tumor, peroxisome proliferator-activated receptor CPPAR) after activation of the growth of pancreatic cancer showed a negative regulatory role, PPAR activation by up-regulating pro-apoptotic gene bak, bax, decreased anti-apoptotic gene bel-xl, Survivi expression, which induced apoptosis in pancreatic cancer cells, suggesting pancreatic cancer cell proliferation in the process of abnormal lipid metabolism, adjust the disorder of lipid metabolism during pancreatic cancer may be pancreatic cancer, a new direction.
Pancreatic cancer chemotherapy, recent studies have shown that the regulation of cell proliferation and differentiation of changes in signal transduction pathways in cancer plays a key role, in which growth factors in pancreatic cancer development, invasion and metastasis received wide attention . Many growth factor receptors are tyrosine kinase C tyrosine kinase, TK) activity, through phosphorylation of proteins within the cell stage, thereby regulating and tumor proliferation, differentiation, invasion and metastasis of signal transduction pathways. Growth factor for targeted therapy has become a new direction for the treatment of pancreatic cancer, which inhibit the growth factor receptor TK activity is to study the hot spot, has synthesized a variety of TK inhibitors, and is the line pre-clinical or clinical experiments. TK inhibitor is a synthetic small molecule compounds, the interaction with ATP and (or) competition of the enzyme ATP binding site, thereby inhibiting the TK phosphorylation, blocking its activation occurred after a series of signal transduction cascade. TK inhibitor because of its small molecular weight, more into the tumor, and its preparation is generally oral, patient compliance is good, a good clinical application.
Currently there are common following several TK inhibitors: epidermal growth factor receptor tyrosine kinase inhibitors, with Tarceva (erlotinib, OSI-774), Iressa (gefitinib, ZD1839), PD153035, PK ~ 166, GW572016, PD158780, EKB-569, PD169414, PD168393 and CI-I033, etc., Tarceva through reversible competitive inhibition of ATP binding site of EGF receptor TK activity, and its anti-tumor effect is induced cell cycle arrest and apoptosis of tumor cells.
At present, many countries have conducted Tarceva and gemcitabine treatment of advanced pancreatic cancer clinical trials Tian. Iressa is an oral cha stare Lin, drugs, and its anti-tumor mechanisms, including induction of cell cycle arrest, promote apoptosis and inhibit tumor angiogenesis, a large number of pre-clinical data indicate that Iressa alone or in combination with other chemotherapy drugs can effectively inhibit tumor cell growth, I phase of clinical trials showed that Iressa, including a variety of solid tumors, including pancreatic cancer have a good effect. PKI-166 was inhibited slightly abnormal Anhui adjacent oral drugs, the chemical structure of 4-R-phenyl ammonia -6– (from) phenyl-7H-11 2.3-dJ-than slightly slightly anything, but the study proved to be effective inhibition of pancreatic cancer growth. TK inhibitor of VEGF receptors are SU5416, SU6668 and PTK787, etc., SU6668 significantly inhibited the CFPAC human pancreatic cancer cells and growth of tumor blood flow and increase the survival rate of tumor-bearing mice, PTK787 also significantly reduce the bare rat orthotopic pancreatic cancer tumor volume to grow 34%, while the combination of PTK787 and PKI166 will enable further reduced tumor volume, PTK787 also reduce the growing tumor and liver metastasis of regional lymph node metastasis occurs, combined with PKI166, the transfer rate further reduced, platelet-derived growth factor receptor tyrosine kinase inhibitors, there are Gleevec (emitinib, STI57l), study found, Gleevec dose-dependent inhibition of pancreatic cancer cell growth.
The chemical treatment of pancreatic cancer, chemotherapy has generally adopted a single-agent chemotherapy and combination chemotherapy in two ways. Single-agent chemotherapy drugs used in chemotherapy of choice for the gemcitabine or 5-Fu. Combination chemotherapy, the traditional program using F-can 4 or SMF, chemotherapy response rate was 28%, evaluation of survival is only 5-7 months, more than failure of chemotherapy and drug resistance. In addition to systemic administration of intravenous drug delivery, but can still exercise, K infusion administration to increase the local drug concentration, and reduce systemic side effects of drugs.

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