Dr. Weeks’ Comment: The trick for surviving cancer is to understand that cancer is a process – a cytosolic metabolic disease and not an “it” – meaning you can’t cut “it” out. The “it” you see or feel is a symptom of the cancer process and not the cancer itself. Confused? Consider with me the big mushroom growing off a tree – the shelf mushroom which is flat on the top and you could put your coffee mug on it – well, if I took a sledge hammer and knocked this shelf fungus off the tree would you believe that I thereby “cured” the tree of cancer? No. Of course not. So why do you think cutting a great off will cure your body of the cancer process operating within? Strike the root of cancer – all cancers – correct your metabolism and correct the cancer process so your metabolism becomes healthy again. Corrective Cancer Care™ corrects imbalances and allows your metabolism to become more cancer free. It also remedies the cancer STEM cell and shuts down the method the cancer process uses to metastasize – inflammation. Watch this lecture to learn how to strike the root of cancer.
Identification of Pik3caMutation as a Genetic Driver of Prostate Cancer That Cooperates with PtenLoss to Accelerate Progression and Castration-Resistant Growth
Cancer Discov; 8(6); 764–79. ©2018 AACR.
Helen B. Pearson, et al
Abstract
Genetic alterations that potentiate PI3K signaling are frequent in prostate cancer, yet how different genetic drivers of the PI3K cascade contribute to prostate cancer is unclear. Here, we report PIK3CAmutation/amplification correlates with poor survival of patients with prostate cancer. To interrogate the requirement of different PI3K genetic drivers in prostate cancer, we employed a genetic approach to mutate Pik3cain mouse prostate epithelium. We show Pik3caH1047Rmutation causes p110α-dependent invasive prostate carcinoma in vivo. Furthermore, we report that PIK3CAmutation and PTENloss coexist in patients with prostate cancer and can cooperatein vivoto accelerate disease progression via AKT–mTORC1/2 hyperactivation. Contrasting single mutants that slowly acquire castration-resistant prostate cancer (CRPC), concomitant Pik3camutation and Ptenloss caused de novoCRPC. Thus, Pik3camutation and Ptendeletion are not functionally redundant. Our findings indicate that PIK3CAmutation is an attractive prognostic indicator for prostate cancer that may cooperate with PTENloss to facilitate CRPC in patients.
Significance: We show PIK3CAmutation correlates with poor prostate cancer prognosis and causes prostate cancer in mice. Moreover, PIK3CAmutation and PTENloss coexist in prostate cancer and can cooperate in vivoto accelerate tumorigenesis and facilitate CRPC. Delineating this synergistic relationship may present new therapeutic/prognostic approaches to overcome castration/PI3K–AKT–mTORC1/2 inhibitor resistance.
Discovering the mechanisms that underlie prostate cancer
July 12, 2018 by Julia Short, Cardiff University
New research has uncovered insights into the mechanisms that underlie prostate cancer, providing potential targets for new cancer therapies.
Prostate cancer is the third most common cause of cancer-related deaths in the UK, and researchers from Cardiff University have identified a genetic alteration that is linked to poor prognosis for patients with the disease.
Advanced prostate cancer patients initially respond well to hormonal therapies but nearly all will eventually develop an aggressive form of the disease called castrate-resistant prostate cancer.
Previously, genetic mutations in a tumour suppression gene, PTEN, have been shown to activate the cell signalling pathway, PI3K, which gives prostate cancer cells their ability to grow uncontrollably.
The new research has uncovered the role of another genetic mutation in prostate cancer, which influences the aggressive nature of the disease.
Dr. Helen Pearson, Cardiff University’s European Cancer Stem Cell Research Institute, said: “We’ve identified a new genetic mutation that may drive the growth of prostate cancer cells. In our research, we found that when prostate cells were given a mutation in the PIK3CA gene, they rapidly formed tumours that developed resistance to hormone therapy.
“Our findings indicate that people who are carrying a PIK3CA genetic alteration are highly likely to develop resistance to hormonal cancer treatments and have a poor treatment outcome.
“We also found that both PTEN and PIK3CA genetic alterations are present in prostate cancer, and that they can work together via potentially independent mechanisms to accelerate the development of the tumour, as well as causing the cancer to become resistant to hormone therapy.
“Survival of patients with castrate-resistant prostate cancer is poor, so it is vital to develop novel and targeted treatments for this aggressive disease.”
Professor Wayne Phillips, from the Peter MacCallum Cancer Centre, Melbourne, Australia, added: “This research gives a new insight into the development of prostate cancer, and provides a foundation for new targeted therapeutic approaches to tackle this disease.”
The research was the result of an international collaboration between Dr. Helen Pearson from Cardiff University and Professor Wayne Phillips at the Peter MacCallum Cancer Centre, Melbourne, Australia.
The article ‘Identification of Pik3ca mutation as a genetic driver of prostate cancer that cooperates with Pten loss to accelerate progression and castration-resistant growth’ is published in Cancer Discovery.
Explore further: Study paves the way for better treatment of prostate cancer
More information: Helen B. Pearson et al. Identification of Pik3ca Mutation as a Genetic Driver of Prostate Cancer That Cooperates with Pten Loss to Accelerate Progression and Castration-Resistant Growth, Cancer Discovery (2018). DOI: 10.1158/2159-8290.CD-17-0867