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so glad I chose such a chill career path, so gr8 not having time for anything else 🙏
How cancer hijacks healthy cell circuits to stay alive
Fundamentally, cancer is a disease of cell growth and function run amok. Frequently, the culprit is mutations in the proteins that regulate growth, such as epidermal growth factor receptor or EGFR, which has been implicated in a variety of cancers.
Among these is glioblastoma multiforme (GBM), a highly malignant brain cancer that has thus far defied satisfactory remedy. More than 9,000 new cases of GBM are diagnosed each year in the United States and effective treatments are limited. GBM tumors are aggressive and resistant to current therapies, such as surgery, radiation and chemotherapy. The median survival rate for newly diagnosed GBM patients is just 14 months.
Drugs devised to block mutant growth signals in GBM have so far proven only temporarily effective. Eventually, cancer cells adapt and overcome. Most current research has focused on how mutations in other proteins in cancer cells allow them to become drug resistant.
In a new paper, published in Cancer Discovery, a team of scientists co-led by Paul Mischel, MD, a principal investigator at the Ludwig Institute for Cancer at the University of California, San Diego and a professor of pathology in the UC San Diego School of Medicine, identify a unique mechanism that allows GBM cells to develop resistance to drugs targeting EGFR signaling.
The feat, according to Mischel and co-leader Steven Bensinger, VMD, PhD, at UCLA, is accomplished not through mutation, but by hijacking the signaling of a normal cell surface protein called platelet-derived growth factor receptor-beta or PDGFR-beta.
“It’s almost like a game of whack-a-mole,” said Mischel. “You use a drug to suppress a choice target and something else pops up to take its place and keep the cells alive—in this case a growth factor receptor that is perfectly normal in physiological terms.”
When scientists targeted both EGFR and PDGFR-beta in GBM tumors in animal models, the tumors were suppressed and drug resistance prevented. The next step is to develop clinical trials of treatments that target both involved proteins. And while this study focused on glioblastomas, Mischel and Bensinger believe the findings are relevant to other forms of cancer.
You can read the full Ludwig news release here.
Almost eight years, I do not think another song could take it’s place.
The old Lie: Dulce et decorum est, pro patria mori.
In short, Mademoiselle, I have lived, and I know the world; why not amuse yourself and invite each passenger to tell his story; if you find a single one of them who has not repeatedly cursed his existence, who has not repeatedly told himself that he is the unhappiest man alive, then you may throw me into the sea head first.
Chronic lymphocytic leukemia cells
Researchers at the University of California, San Diego Moores Cancer Center have identified a humanized monoclonal antibody that targets and directly kills chronic lymphocytic leukemia (CLL) cells.
The findings, published in the online Early Edition of the Proceedings of the National Academy of Sciences on March 25, 2013 represent a potential new therapy for treating at least some patients with CLL, the most common type of blood cancer in the United States.
CLL cells express high levels of a cell-surface glycoprotein receptor called CD44. Principal investigator Thomas Kipps, MD, PhD, Evelyn and Edwin Tasch Chair in Cancer Research, and colleagues identified a monoclonal antibody called RG7356 that specifically targeted CD44 and was directly toxic to cancer cells, but had little effect on normal B cells.
Moreover, they found RG7356 induced CLL cells that expressed the protein ZAP-70 to undergo apoptosis or programmed cell death. Roughly half of CLL patients have leukemia cells that express ZAP-70. Such patients typically have a more aggressive form of the disease than patients with CLL cells that do not express that specific protein.
Previous research by Kipps and others has shown that CLL cells routinely undergo spontaneous or drug-induced cell death when removed from the body and cultured in the laboratory. They found that CLL cells receive survival signals from surrounding non-tumor cells that are present in the lymph nodes and bone marrow of patients with CLL. One of these survival signals appears to be transmitted through CD44. However, when CD44 is bound by the RG7356 monoclonal antibody, it seems to instead convey a death signal to the leukemia cell.
“By targeting CD44, it may be possible to kill CLL cells regardless of whether there are sufficient numbers of so-called ‘effector cells,’ which ordinarily are required by other monoclonal antibodies to kill tumor cells,” said Kipps. “We plan to initiate clinical trials using this humanized anti-CD44 monoclonal antibody in the not-too-distant future.”
Words do not express thoughts very well. They always become a little different immediately they are expressed, a little distorted, a little foolish. And yet it also pleases me and seems right that what is of value and wisdom to one man seems nonsense to another.
Wildin out with @rosalouiseltw @lukexschwartz
& he said, I have never been as happy as I am today