New Delhi (PTI): Anti-cancer treatments may have an opposite effect on the cancareous cells increasing the small population of cancer stem cells believed to drive the disease, according to a latest research.

The research was undertaken by Vasyl Vasko, alongwith scientists from the CRTRC Institute for Drug Development in San Antonio and Johns Hopkins University after questions were raised on efficacy of some therapies used in treating cancer.

"Our experiments suggest that some treatments could be producing more cancer stem cells that then are capable of metastasizing, because these cells are trying to find a way to survive the therapy," said Vasko.

Vasko and his team measured both stem cells markers and tumor volume before and after treatment on mouse.

The stem cell markers contribute to stem cells' defining ability to renew themselves and differentiate into different cell types.

The researchers selected a rare form of cancer, Mesenchymal Chondrosarcoma (MCS), to study the expression of stem cell markers in metastasizing tumors and primary tumors.

They applied various therapies in mice implanted with human MSC, and analysed the effects on tumors.

Analysis of stem cell expression before and after treatment revealed that even as some anti-cancer treatments shrank tumors, they increased expression of stem cell markers.

"These treatments were not enough to completely inhibit tumour growth," Vasko said adding "the small number of cells that survived the treatment could then generate another tumor that metastasizes".

"Dying cells could secrete a lot of factors that induce expression of stem cell markers in other cancer cells," he said.

Meanwhile, according to another report published in "Cell" an ancient mechanism for coping with environmental stresses -- induction of heat-shock proteins (HSPs) -- also helps cancerous tumors survive.

These proteins under the control of a small family of heat-shock factors (HSFs) guard against the abnormal activity of other proteins in the face of stressors such as heat and oxygen starvation, said Susan Lindquist, an investigator at the Whitehead Institute for Biomedical Research.

Researchers used a common mouse model of skin cancer and found that the mice unable to switch on the heat-shock response were "far more resistant" to tumor formation than normal mice.

"The mutant mice were less likely to develop cancer and, when they did, had fewer and smaller tumors," she said adding "the HSF1-deficient mice also lived longer."

The researchers next examined mice predisposed to develop cancer. Again, they found, the shock factor-deficient animals lived tumor-free for dramatically longer.

Through studies on cultured mouse cells, they found further evidence that shock factors supports the transformation to cancer by orchestrating a variety of basic cell functions.