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    "Do not look where you fell, but where you slipped." - African Proverb No symptoms…does it matter? Low PSA…does it mean no cancer? Big prostate…means cancer? Small prostate means no cancer? Surgery better than radiation? Proton better than regular “ole” radiation? Age over 75-is surgery best? Do you have a higher incidence of impotence with cryosurgery? Why do they only do Proton on the well-mod prostate cancer in terms of the “favorability” of prostate cancer? High PSA means prostate cancer? You have a biopsy of your prostate cancer because of a high PSA…and it is negative…was the biopsy unnecessary? Can you die of prostate cancer? Can you have it before the age of 50? Are all urologists the same? Are all surgeons the same? Will surgeons only recommend surgery? What is the Gleason’s score? If the guy at your church had seeds for his cancer is that the best treatment for you? Are all prostate biopsies that have cancer the same? Are all prostate cancers the same? Does everyone that has surgery become impotent? Does everyone that has radiation preserve their potency? What is HIFU? What is NanoKnife? If you have trouble voiding does that mean you have prostate cancer? When do you think the male should begin having PSAs and rectal exams? Is prostate cancer hereditary? Do blacks have prostate cancer more or less often than others?\ Does Avodart cause cancer of the prostate? Can a dog smell prostate cancer in a man’s urine? What is a Free PSA? How can you use it in the treatment decision-making? If your friend had a particular treatment and did well, if you have the same treatment by the same doctor does that mean you will do well? Is it smart to have anything other than prostate removal for prostate cancer if you are 50 or so and in good health? Hint: Think years at risk. Why is years at risk, your physiologic age important in your decision? What is the Partin table? If there is cancer in your lymph nodes can you be cured with radiation or surgery? What is the Prostatic Acid Phosphatase and how can it help you and your doctor? If your Free PSA is very high indicating that you have a low likelihood of prostate cancer..does that mean you won’t have prostate cancer on biopsy? Why do men get infections after a prostate biopsy? What is the difference in a “autopsy evaluation of the prostate” and “twelve cores taken at the time of a prostate biopsy?” Do you have others? I am tired for now but have probably hundred others that I will add from time to time. Comment won’t you? Mr. Cass…I bet you have a few to add. From my book, “What was thought to be a simple disease of old men becomes after diagnosis  a potentially lethal disease with a very difficult treatment decision scenario for the newly diagnosed prostate cancer patient to consider.”theprostatedecision.wordpress.com


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    Recurrent gene fusions involving ETS family genes are a distinguishing feature of human prostate cancers, with TMPRSS2–ERG fusions representing the most common subtype. The TMPRSS2–ERG fusion transcript and its splice variants are well characterized in prostate cancers; however, not much is known about the levels and regulation of wild-type ERG. By employing an integrative approach, we show that the TMPRSS2–ERG gene fusion product binds to the ERG locus and drives the overexpression of wild-type ERG in prostate cancers. Knockdown of TMPRSS2–ERG in VCaP cells resulted in the downregulation of wild-type ERG transcription, whereas stable overexpression of TMPRSS2–ERG in the gene fusion-negative PC3 cells was associated with the upregulation of wild-type ERG transcript. Further, androgen signaling-mediated upregulation of TMPRSS2–ERG resulted in the concomitant upregulation of wild-type ERG transcription in VCaP cells. The loss of wild-type ERG expression was associated with a decrease in the invasive potential of VCaP cells. Importantly, 38% of clinically localized prostate cancers and 27% of metastatic prostate cancers harboring the TMPRSS2–ERG gene fusions exhibited overexpression of wild-type ERG. Taken together, these results provide novel insights into the regulation of ERG in human prostate cancers. Cancer Res; 71(16); 5387–92. ©2011 AACR. cancerres.aacrjournals.org


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    An international team of researchers led by Fred Hutchinson Cancer Research Center has identified five inherited genetic variants that are strongly associated with aggressive, lethal prostate cancer. The discovery ultimately could lead to the development of a simple blood test that could be given upon diagnosis to determine which men should receive aggressive treatment versus a more conservative "watchful waiting" approach.
    www.physorg.com   ...Read On

    Recurrent gene fusions involving ETS family genes are a distinguishing feature of human prostate cancers, with TMPRSS2–ERG fusions representing the most common subtype. The TMPRSS2–ERG fusion transcript and its splice variants are well characterized in prostate cancers; however, not much is known about the levels and regulation of wild-type ERG. By employing an integrative approach, we show that the TMPRSS2–ERG gene fusion product binds to the ERG locus and drives the overexpression of wild-type ERG in prostate cancers. Knockdown of TMPRSS2–ERG in VCaP cells resulted in the downregulation of wild-type ERG transcription, whereas stable overexpression of TMPRSS2–ERG in the gene fusion-negative PC3 cells was associated with the upregulation of wild-type ERG transcript. Further, androgen signaling-mediated upregulation of TMPRSS2–ERG resulted in the concomitant upregulation of wild-type ERG transcription in VCaP cells. The loss of wild-type ERG expression was associated with a decrease in the invasive potential of VCaP cells. Importantly, 38% of clinically localized prostate cancers and 27% of metastatic prostate cancers harboring the TMPRSS2–ERG gene fusions exhibited overexpression of wild-type ERG. Taken together, these results provide novel insights into the regulation of ERG in human prostate cancers. Cancer Res; 71(16); 5387–92. ©2011 AACR.
    cancerres.aacrjournals.org   ...Read On

    The insulin-like growth factor binding protein IGFBP-3 is a proapoptotic and antiangiogenic protein in prostate cancer (CaP). Epidemiologic studies suggest that low IGFBP-3 is associated with greater risk of aggressive, metastatic prostate cancers, but in vivo functional data are lacking. Here we show that mice that are genetically deficient in IGFBP-3 exhibit weaker growth of primary prostate tumors but higher incidence of metastatic disease. Prostates in IGFBP-3 knockout mice (IGFBP-3KO mice) failed to undergo apoptosis after castration. Spontaneous prostate tumors did not develop in IGFBP-3KO mice, but splenic lymphomas occurred in 23% of female IGFBP-3KO mice by 80 weeks of age. To assess the effects of IGFBP-3 deficiency on prostate cancer development, we crossed IGFBP-3KO mice with a c-Myc–driven model of CaP that develops slow-growing, nonmetastatic tumors. By 24 weeks of age, well-differentiated prostate cancers were observed in all mice regardless of IGFBP-3 status. However, by 80 weeks of age IGFBP-3KO mice tended to exhibit larger prostate tumors than control mice. More strikingly, lung metastases were observed at this time in 55% of the IGFBP-3KO mice but none in the control animals. Cell lines established from IGFBP-3KO:Myc tumors displayed more aggressive phenotypes in proliferation, invasion, and colony formation assays, relative to control Myc tumor cell lines. In addition, Myc:IGFBP-3KO cells exhibited evidence of epithelial–mesenchymal transition. Our findings established a function for IGFBP-3 in suppressing metastasis in prostate cancer, and they also offered the first reported transgenic model of spontaneous metastatic prostate cancer for studies of this advanced stage of disease. Cancer Res; 71(15); 5154–63. ©2011 AACR.
    cancerres.aacrjournals.org   ...Read On


    		   
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