The rational behind this is:
HER and EGFR are major stimulatory components in a cell that cause the cell to divide and survive (among other things). This also helps to send out signals that cause angiogenesis. Blocking these pathways helps but the cell doesn't always die and can become resistant to inhibition of these inhibitors.

HDAC inhibitors work on proteins that are abnormally high in cancer cells. The idea is that cancer makes these proteins in order to turn off other pathways. These pathways are sometimes normal pathways that should be turned on when a cell is functioning properly. Once these pathways are turned back on the hope is that it will help turn these cells back into a more normal phenotype and allow the immune system recognize the cancer cells. So you have two inhibitors of cell growth and one inhibitor of gene repression (which will actually help cause gene activation, to make it into a more normal functioning cell type). HDAC's are a ubiquitous class of proteins and it remains to be seen how toxic it will be.



Interrupting HER1/EGFR growth signaling

HER receptors play a key role in mediating cell survival, differentiation, and proliferation, and have been implicated in the development of a variety of cancers.1,2 In preclinical models, dysregulation of HER1/EGFR, in particular, has been implicated in multiple tumor types.3
http://www.biooncology.com/bioonc/approach/HERPathway.m?s_cid=0003&s_src=googleppc
[img]http://www.biooncology.com/bioonc/approach/HER1_image.m[/img]


HDAC info

Despite US marketing approval for the first histone deacetylase inhibitor, these prolific agents still have a lot to prove.
Introduction

The approval by the US Food and Drug Administration (FDA) of the first histone deacetylase (HDAC) inhibitor in October went largely unnoticed. "A quiet event," Daniel Von Hoff, head of translational research at the Translational Genomics Research Institute in Phoenix, Arizona called it. As a new drug class, "they've been under the radar screen a little bit," he says.

One reason for the low profile is that Zolinza (vorinostat; suberoylanilide hydroxamic acid, SAHA), from Merck in Whitehouse Station, New Jersey won approval to treat a rare cancer, cutaneous T-cell lymphoma (CTCL). But there is an aggressive development effort by industry and the National Cancer Institute (NCI) in Bethesda, Maryland, to bring HDAC inhibitors to market for every major tumor type, both solid and hematologic. At least 80 clinical trials are underway, testing ten different agents in everything from rare leukemias and lymphomas to breast, prostate and ovarian cancer. That's because the drugs, directly or indirectly, attack virtually all the hallmarks of cancer. "HDAC inhibitors [work on] cell cycle, apoptosis, angiogenesis, cellular differentiation and cellular transformation," says Mitchell Keegan, director of drug development for Gloucester Pharmaceuticals in Cambridge, Massachusetts. "They have the potential to work in multiple tumor types, through different mechanisms."

Yet HDAC inhibitors may never realize that potential. So far, little clinical evidence exists that HDAC inhibitors work well against solid tumors, although most trials are in early stages. A paucity of knowledge of HDAC biology and the role of individual HDACs in cancer has led to an empirical approach to testing HDAC inhibitors, which threatens to slow the field's progress. Finally, HDAC inhibitors suffer from a history of heart-related side effects. Most of these effects seem to be medically insignificant, but they've already led to one HDAC inhibitor being dropped and may create a perception problem unless the drugs soon prove their worth against common cancers.

http://www.nature.com/nbt/journal/v25/n1/full/nbt0107-17.html (click for more info)

IND was filed 5/12/08 and expected to start phase I in early July of 08

HSP90 might be partnered or started in 2H09



http://www.curis.com/Curis_CorporatePresentation_2008.pdf

[quote="hedgehog"]The rational behind this is:
HER and EGFR are major stimulatory components in a cell that cause the cell to divide and survive (among other things). This also helps to send out signals that cause angiogenesis. Blocking these pathways helps but the cell doesn't always die and can become resistant to inhibition of these inhibitors.

HDAC inhibitors work on proteins that are abnormally high in cancer cells. The idea is that cancer makes these proteins in order to turn off other pathways. These pathways are sometimes normal pathways that should be turned on when a cell is functioning properly. Once these pathways are turned back on the hope is that it will help turn these cells back into a more normal phenotype and allow the immune system recognize the cancer cells. So you have two inhibitors of cell growth and one inhibitor of gene repression (which will actually help cause gene activation, to make it into a more normal functioning cell type). HDAC's are a ubiquitous class of proteins and it remains to be seen how toxic it will be.



Interrupting HER1/EGFR growth signaling

HER receptors play a key role in mediating cell survival, differentiation, and proliferation, and have been implicated in the development of a variety of cancers.1,2 In preclinical models, dysregulation of HER1/EGFR, in particular, has been implicated in multiple tumor types.3
http://www.biooncology.com/bioonc/approach/HERPathway.m?s_cid=0003&s_src=googleppc
[img]http://www.biooncology.com/bioonc/approach/HER1_image.m[/img]


HDAC info

Despite US marketing approval for the first histone deacetylase inhibitor, these prolific agents still have a lot to prove.
Introduction

The approval by the US Food and Drug Administration (FDA) of the first histone deacetylase (HDAC) inhibitor in October went largely unnoticed. "A quiet event," Daniel Von Hoff, head of translational research at the Translational Genomics Research Institute in Phoenix, Arizona called it. As a new drug class, "they've been under the radar screen a little bit," he says.

One reason for the low profile is that Zolinza (vorinostat; suberoylanilide hydroxamic acid, SAHA), from Merck in Whitehouse Station, New Jersey won approval to treat a rare cancer, cutaneous T-cell lymphoma (CTCL). But there is an aggressive development effort by industry and the National Cancer Institute (NCI) in Bethesda, Maryland, to bring HDAC inhibitors to market for every major tumor type, both solid and hematologic. At least 80 clinical trials are underway, testing ten different agents in everything from rare leukemias and lymphomas to breast, prostate and ovarian cancer. That's because the drugs, directly or indirectly, attack virtually all the hallmarks of cancer. "HDAC inhibitors [work on] cell cycle, apoptosis, angiogenesis, cellular differentiation and cellular transformation," says Mitchell Keegan, director of drug development for Gloucester Pharmaceuticals in Cambridge, Massachusetts. "They have the potential to work in multiple tumor types, through different mechanisms."

Yet HDAC inhibitors may never realize that potential. So far, little clinical evidence exists that HDAC inhibitors work well against solid tumors, although most trials are in early stages. A paucity of knowledge of HDAC biology and the role of individual HDACs in cancer has led to an empirical approach to testing HDAC inhibitors, which threatens to slow the field's progress. Finally, HDAC inhibitors suffer from a history of heart-related side effects. Most of these effects seem to be medically insignificant, but they've already led to one HDAC inhibitor being dropped and may create a perception problem unless the drugs soon prove their worth against common cancers.

http://www.nature.com/nbt/journal/v25/n1/full/nbt0107-17.html (click for more info)[/quote]the information is apt but the worries i have are these 'How can cancer be explained to somebody who will not understand the language of the biologist'
'Can natural supplements reduce the rate of cancer attack ?'