Poliovirus therapy activates immune response against cancer

An investigational therapy using modified poliovirus to attack cancer tumors appears to unleash the body's own capacity to fight malignancies by activating an inflammation process that prevent cancer cells to evade the immune system.

Glioblastoma is a lethal form of brain cancer. The research team elucidated how the poliovirus works not only to attack cancer cells directly, but also activates longer-lasting immune response that appears to inhibit regrowth of the tumor.

Using human melanoma and breast cancer cell lines, and then validating the findings in mouse models, the researchers found that the modified poliovirus therapy starts by attaching to malignant cells, which have an abundance of CD155 protein.

The CD155 protein is a poliovirus receptor. The modified virus then begins to attack the tumor cells, directly killing many, but not all. This releases tumor antigens. The second phase of assault is more complicated, by killing the cancer cells, the modified poliovirus triggers an alarm within the immune system, alerting the body's defenses to attack.

This appears to occur when the modified poliovirus infects dendritic cells and macrophages. Dendritic cells then present tumor to T cells to launch an immune response. Once the immune system is activated against the poliovirus-infected tumor, the cancer cells can no longer hide and they remain vulnerable to ongoing immune attack.

Poliovirus killed tumor cells and infected the antigen-presenting cells, which allows them to function in such a way that they can raise a T-cell response that can recognize and infiltrate a tumor. Poliovirus stimulates an innate inflammatory response.
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Zika kills brain cancer stem cells

Zika virus is a mosquito-borne infection known for causing birth defects in unborn fetuses. Latest research discovered that it is possible to use the virus to target tumor cells in adult brains. Combining Zika virus with chemotherapy and radiation can be use to remove brain tumors.

Glioblastoma is the most common and deadly forms of brain cancer with patients dying within two years of diagnosis. The growth and development of glioblastomas is driven by stem cells that proliferate and give rise to other tumor cells.

Stem cells of the cancer are hard to kill because they avoid body's immune system and are resistant to chemotherapy and radiation. Killing these cells is very important to prevent new tumors from recurring after the original tumor has been surgically removed.

 Glioblastoma can occur in any part of the brain, when glioblastoma is diagnosed, microfibers can spread to the rest of the brain which magnetic resonance imaging MRI would not detect. It is common in men between the age of 50 and 60, and there is no link between developing glioblastoma and having a previous cancer history.

Intense exposure to radiation increases the risk of brain cancer. Zika virus disrupts fetal brain development targeting neural stem and progenitor cells, however the virus' effects on adult brains are less severe.

 The preference of Zika virus for neural precursor cells could be leveraged against glioblastoma stem cells, researchers found the virus infected and killed patient-derived glioblastoma stem cells compared with other glioblastoma cell types or normal neural cells.

When mice with aggressive glioblastoma were injected with a mouse-adapted strain of Zika virus, the virus slowed tumor growth and significantly extended the animals' lifespan.

Researchers also tested a mutated strain of Zika on body's immune response, which was more effective when combined with a chemotherapy drug, temozolomide, that usually has little effect on these cells. Zika virus can kill the kind of glioblastoma cells that tend to be resistant to current treatments.
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Better cancer treatment

Cancer patients can now have better and safer treatment by the use of less toxic drug for cancer treatment.
 Synthetic lethal interactions could inhibit the growth of tumors in mesenchymal cells, cells that develop into connective tissue such as those found in bones, soft tissues, and the central nervous system.

Presently, chemotherapy is the only available treatment for persistent cancers known as alternative lengthening telomere ALT cancers.
In healthy stem cell reproduction, the enzyme telomerase prevents the shortening of linear DNA ends called telomeres with each replication.

 The enzyme can also be re-activated to promote genetic stability and immortality in many cancer cells. While many cancers that multiple through telomerase re-activation may be treated with therapies other than chemotherapy, ALT cancer cells lack telomerase and few treatment options have been developed to inhibit their proliferation.

 ALT cancer cells account for fifteen percent of cancer cases, these incidences include some of the most deadly cancers like glioblastoma.

Researchers investigated three human genes associated with cancer development: FANCM mutations of which are associated with blood cancers), BRCA1 (mutations of which are commonly found in patients with breast and ovarian cancers), and BLM (mutations of which cause a variety of cancers).

FANCM, known to repair DNA damage where two DNA strands have been incorrectly linked, was removed from cells also deficient of BRCA1 or BLM. As a result, the team found that simultaneous inactivation of BLM and FANCM or of BRCA1 and FANCM resulted in dramatic increases of unrepaired DNA damages, preventing the cancerous cells from further reproducing.

 Their discoveries suggest that if drugs are developed to simultaneously inhibit BLM and FANCM, or BRCA1 and FANCM, they should kill the ALT cancers without posing the same toxic effects as the conventional chemotherapy drugs.
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