Cancer stem cells are one of the main reasons why cancers are able to survive surgery, chemotherapy, and radiation. They are able to hide from those therapies and, at a future date, emerge and spread the cancer in the body once again.
Jionglia Cheng, PhD., the lead author of a new CIRM-funded study, says that’s one of the reasons why pancreatic cancer has proved so difficult to treat.
Pancreatic cancer is the most common cause of cancer‑related death. Most patients resist current therapies, making effective treatment difficult.
Dr. Cheng, a researcher at ChemRegen Inc., worked with John Cashman at the Human BioMolecular Research Institute to identify a compound that blocks cancer stem cells.
In earlier studies, the compound—PAWI‑2—blocked breast, prostate, and colon cancer. In lab tests, PAWI‑2 killed pancreatic cancer stem cells, including drug‑resistant ones.
When combined with erlotinib (Tarceva), a common pancreatic cancer drug, PAWI‑2 was even more effective than erlotinib alone.
In a news release, Dr. Cheng said: “This molecule could be used alone or with chemotherapy at lower doses as a new treatment for pancreatic cancer. This may greatly reduce toxicity for patients.”
The study is published in the journal Scientific Reports.
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I am so sorry to hear about your granddaughter. That must be so awful for you to watch and for her to have to live with. I am afraid that I don’t know of any stem cell therapies that would be appropriate for her. It seems she has so many problems and I don’ know of a clinical trial underway right now that would be helpful. I’m sorry I can’t be of more help but wish you and your granddaughter all the best.
The genotype and phenotype of cancer stem cells are not stable, they are heterogeneous. For instance, normal melanocytes require multiple growth factors whereas primary melanoma require less growth factors to growth. In contrary, the metastatic cells are independent of growth factors, they have ability to produce abundant of various growth factors to support autocrine growth. The progression of cancer stem cells from primary to metastatic cancers are varying between cell types and individual’s immune system. For instance, melanoma, prostate, breast and bladder cancer are less maglinancy than pancreas and lung cancers which can develop into highly metastatic.
The early study showed that PAWI-2 was able to kill pancreatic cancer stem cells (PCSCs) and drug (erlotinib) -resistant PCSCs. The study proof that PAWI-2 inhibited β3-KRAS signaling by targeting downstream TBKL phosphorylation. The phenotype and genotype of PCSCs are heterogeneous, the cancer stem cells are not stable . The existence of PAWI-2 and erlotinib either alone or combination may trigger the cancer stem cells to become resistant over time. At the begining of chemotherapy, patients may show promising improvement of clinical results, but patients may relapse over time. None of the drug can completely eradicate 100% of PCSCs instantly. This may provide room of opportunity for a small number of cancer stem cells to become growth advantage and develop drug-resisitant. They change their genotype and phenotype to become more aggressive and metastatic. The individual mmune systems play roles to delay the progression of PCSCs. The strong immunity suppresses the outgrowth of PCSCs whereas poor immunity accelerate the cancer stem cells to become more metastatic. The progression of cancer stem cells from one stage to the other is usually followed by altering the existence signaling network or newly development of intracellular signaling network. Therefore, the discovery of new drug may repeat the cycle of developing a new dominant and growth advantage cancer stem cell.