The public health burden of prostate cancer is substantial. A total of 220,800 new cases of prostate cancer and 27,540 deaths from the disease are anticipated in the United States in 2015, making it the most frequent nondermatologic cancer among U.S. males. A man’s lifetime risk of prostate cancer is one in seven. Prostate cancer is the second leading cause of cancer death in men, exceeded only by lung cancer.
Some men with prostate cancer remain asymptomatic and die from unrelated causes rather than as a result of the cancer itself. This may be due to the advanced age of many men at the time of diagnosis, slow tumor growth, or response to therapy. The estimated number of men with latent prostate carcinoma (i.e., prostate cancer that is present in the prostate gland but never detected or diagnosed during a patient’s life) is greater than the number of men with clinically detected disease. A better understanding is needed of the genetic and biologic mechanisms that determine why some prostate carcinomas remain clinically silent, while others cause serious, even life-threatening illness.
Prostate cancer exhibits tremendous differences in incidence among populations worldwide; the ratio of countries with high and low rates of prostate cancer ranges from 60-fold to 100-fold. Asian men typically have a very low incidence of prostate cancer, with age-adjusted incidence rates ranging from 2 to 10 cases per 100,000 men. Higher incidence rates are generally observed in northern European countries. African American men, however, have the highest incidence of prostate cancer in the world; within the United States, African American men have a 60% higher incidence rate than white men. African American men have been reported to have approximately twice the rate of prostate cancer–specific death compared with non-Hispanic white men. Differences in race-specific prostate cancer survival estimates may be narrowing over time.
These differences may be due to the interplay of genetic, environmental, and social influences (such as access to health care), which may affect the development and progression of the disease. Differences in screening practices have also had a substantial influence on prostate cancer incidence, by permitting prostate cancer to be diagnosed in some patients before symptoms develop or before abnormalities on physical examination are detectable. An analysis of population-based data from Sweden suggested that a diagnosis of prostate cancer in one brother leads to an early diagnosis in a second brother using prostate-specific antigen (PSA) screening. This may account for an increase in prostate cancer diagnosed in younger men that was evident in nationwide incidence data. A genetic contribution to prostate cancer risk has been documented, and there is increasing knowledge of the molecular genetics of the disease, although much of what is known is not yet clinically actionable. Malignant transformation of prostate epithelial cells and progression of prostate carcinoma are likely to result from a complex series of initiation and promotional events under both genetic and environmental influences.
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الصحة العامة عبء الإصابة بسرطان البروستاتا كبيرة. ويتوقع إجمالي 220,800 حالة جديدة من سرطان البروستاتا و 27,540 من الوفيات الناجمة عن هذا المرض في الولايات المتحدة بحلول عام 2015، مما يجعل من سرطان نونديرماتولوجيك الأكثر شيوعاً بين الذكور في الولايات المتحدة. خطر في رجل الإصابة بسرطان البروستاتا هو واحد من بين كل سبعة. سرطان البروستاتا هو السبب الرئيسي الثاني للوفاة السرطان في الرجال، تجاوزت فقط بسرطان الرئة.تبقى أعراض بعض الرجال المصابين بسرطان البروستاتا ويموت من أسباب غير ذات صلة وليس نتيجة السرطان نفسها. قد يكون هذا بسبب سن متقدمة لكثير من الرجال في وقت التشخيص، وورم بطيء النمو، أو استجابة للعلاج. العدد المقدر للرجال المصابين بسرطان البروستاتا الكامن (أي سرطان البروستاتا التي هي موجودة في غدة البروستات ولكن ابدأ الكشف عن أو تشخيصها أثناء حياة المريض) أكبر من عدد الرجال المصابين بالمرض المكتشفة سريرياً. من الضروري فهم الآليات البيولوجية والوراثية التي تحدد لماذا بعض سرطانات البروستاتا تظل صامتة سريرياً، بينما البعض الآخر يسبب أمراض خطيرة، وحتى مهددة للحياة. Prostate cancer exhibits tremendous differences in incidence among populations worldwide; the ratio of countries with high and low rates of prostate cancer ranges from 60-fold to 100-fold. Asian men typically have a very low incidence of prostate cancer, with age-adjusted incidence rates ranging from 2 to 10 cases per 100,000 men. Higher incidence rates are generally observed in northern European countries. African American men, however, have the highest incidence of prostate cancer in the world; within the United States, African American men have a 60% higher incidence rate than white men. African American men have been reported to have approximately twice the rate of prostate cancer–specific death compared with non-Hispanic white men. Differences in race-specific prostate cancer survival estimates may be narrowing over time.These differences may be due to the interplay of genetic, environmental, and social influences (such as access to health care), which may affect the development and progression of the disease. Differences in screening practices have also had a substantial influence on prostate cancer incidence, by permitting prostate cancer to be diagnosed in some patients before symptoms develop or before abnormalities on physical examination are detectable. An analysis of population-based data from Sweden suggested that a diagnosis of prostate cancer in one brother leads to an early diagnosis in a second brother using prostate-specific antigen (PSA) screening. This may account for an increase in prostate cancer diagnosed in younger men that was evident in nationwide incidence data. A genetic contribution to prostate cancer risk has been documented, and there is increasing knowledge of the molecular genetics of the disease, although much of what is known is not yet clinically actionable. Malignant transformation of prostate epithelial cells and progression of prostate carcinoma are likely to result from a complex series of initiation and promotional events under both genetic and environmental influences.
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