A newly released study by scientists, mostly from Penn State University, outlines their technique of penetrating cancer cells and editing them to make them more vulnerable to cancer therapies.
The proof-of-concept study was published July 4 in Nature Biotechnology.
The scientists “devised an approach to edit cancer cells, delivering two new ‘switches’ into them. The first switch enables modified cells to outgrow the rest of the cancer cell population. Then, the second switch allows these cells to unleash a toxic drug onto the remaining tumor,” Kristel Tiandra wrote in LiveScience.
Tiandra explained that the scientists inserted two “suicide genes” into non-small cell lung cancer cells (NSCLC); one gene, aided by the cancer drug erlotinib — which usually stops a protein called EGFR from being activated — allowed the cancer cells to become resistant to erlotinib, thus permitting the team to control whether the cancer cells proliferated.
The modified cancer cells grew faster than the unmodified cells that resisted the drug. Once more of the modified cells were added, the scientists stopped using erlotinib, and the growing cells stopped.
“Once their trap was set, the scientists activated the second suicide gene using a harmless molecule called 5-FC. Cleverly, the second gene codes for an enzyme that helps cells transform 5-FC into a toxin, called 5-FU, that kills cancer. The 5-FU ultimately kills both the modified cancer cells and the cells surrounding them,” Tiandra explained.
The team found that after 20 days of treatment, the modified cancer cells had outgrown the unmodified cells; by roughly 14 weeks after the initial treatment, the tumor’s volume had dwindled to zero.
“We see this as something beyond the treatment of lung cancer,” lead study author Scott Leighow said. “We see this as a generalizable platform for delivering therapeutic genes in cancer and using those to create therapeutic opportunities that might lead to cures in the future.”
Aaron Goldman, a cancer pharmacologist at the Brigham and Women’s Hospital, told LiveScience, “I’ve not seen anything like this.”
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A newly released study by scientists, mostly from Penn State University, outlines their technique of penetrating cancer cells and editing them to make them more vulnerable to cancer therapies.
The proof-of-concept study was published July 4 in Nature Biotechnology.
The scientists “devised an approach to edit cancer cells, delivering two new ‘switches’ into them. The first switch enables modified cells to outgrow the rest of the cancer cell population. Then, the second switch allows these cells to unleash a toxic drug onto the remaining tumor,” Kristel Tiandra wrote in LiveScience.
Tiandra explained that the scientists inserted two “suicide genes” into non-small cell lung cancer cells (NSCLC); one gene, aided by the cancer drug erlotinib — which usually stops a protein called EGFR from being activated — allowed the cancer cells to become resistant to erlotinib, thus permitting the team to control whether the cancer cells proliferated.
The modified cancer cells grew faster than the unmodified cells that resisted the drug. Once more of the modified cells were added, the scientists stopped using erlotinib, and the growing cells stopped.
“Once their trap was set, the scientists activated the second suicide gene using a harmless molecule called 5-FC. Cleverly, the second gene codes for an enzyme that helps cells transform 5-FC into a toxin, called 5-FU, that kills cancer. The 5-FU ultimately kills both the modified cancer cells and the cells surrounding them,” Tiandra explained.
The team found that after 20 days of treatment, the modified cancer cells had outgrown the unmodified cells; by roughly 14 weeks after the initial treatment, the tumor’s volume had dwindled to zero.
“We see this as something beyond the treatment of lung cancer,” lead study author Scott Leighow said. “We see this as a generalizable platform for delivering therapeutic genes in cancer and using those to create therapeutic opportunities that might lead to cures in the future.”
Aaron Goldman, a cancer pharmacologist at the Brigham and Women’s Hospital, told LiveScience, “I’ve not seen anything like this.”
“}]]
