Prostate Cancer Resource Books

Posted by Pharmaceutical-Stuff on Monday 10 March 2008

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Here is a list of books that contain informations on , i know its such a big list but i had to cover any aspects of the , so this list will include absolute everything, you can start reading.

  1. Albertsen PC, Fryback DG, Storer BE, et al: The impact of co-morbidity on life expectancy among men with localized . J Urol 1996 Jul; 156(1): 127-32[Medline].
  2. Albertsen PC, Fryback DG, Storer BE, et al: Long-term survival among men with conservatively treated localized . JAMA 1995 Aug 23-30; 274(8): 626-31[Medline].
  3. Amling CL, Kane CJ, Riffenburgh RH, et al: Relationship between obesity and race in predicting adverse pathologic variables in patients undergoing radical prostatectomy. Urology 2001 Nov; 58(5): 723-8[Medline].
  4. Berthon P, Valeri A, Cohen-Akenine A, et al: Predisposing gene for -onset , localized on chromosome 1q42.2-43. Am J Hum Genet 1998 Jun; 62(6): 1416-24[Medline].
  5. Bostwick DG: Prostatic intraepithelial neoplasia (PIN): current concepts. J Cell Biochem Suppl 1992; 16H: 10-9[Medline].
  6. Bostwick DG, Qian J: High-grade prostatic intraepithelial neoplasia. Mod Pathol 2004 Mar; 17(3): 360-79[Medline].
  7. Bratt O, Kristoffersson U, Lundgren R, Olsson H: Familial and hereditary in southern Sweden. A population-based case-control study. Eur J 1999 Feb; 35(2): 272-7[Medline].
  8. Carter BS, Bova GS, Beaty TH, et al: Hereditary : epidemiologic and clinical features. J Urol 1993 Sep; 150(3): 797-802[Medline].
  9. Carter HB, Epstein JI, Chan DW, et al: Recommended -specific antigen testing intervals for the detection of curable . JAMA 1997 May 14; 277(18): 1456-60[Medline].
  10. Catalona WJ, Smith DS, Ornstein DK: detection in men with serum concentrations of 2.6 to 4.0 ng/mL and benign examination. Enhancement of specificity with free measurements. JAMA 1997 May 14; 277(18): 1452-5[Medline].
  11. Chodak GW, Thisted RA, Gerber GS, et al: of conservative management of clinically localized . N Engl J Med 1994 Jan 27; 330(4): 242-8[Medline].
  12. Djavan B, Susani M, Bursa B, et al: Predictability and significance of multifocal in the radical prostatectomy specimen. Tech Urol 1999 Sep; 5(3): 139-42[Medline].
  13. Etzioni R, Legler JM, Feuer EJ, et al: surveillance series: interpreting trends in –part III: Quantifying the link between population -specific antigen testing and recent declines in mortality. J Natl Inst 1999 Jun 16; 91(12): 1033-9[Medline].
  14. Feuer EJ, Merrill RM, Hankey BF: surveillance series: interpreting trends in –part II: Cause of death misclassification and the recent rise and fall in mortality. J Natl Inst 1999 Jun 16; 91(12): 1025-32[Medline].
  15. Gleason DF: Histologic grading of : a perspective. Hum Pathol 1992 Mar; 23(3): 273-9[Medline].
  16. Graversen PH, Nielsen KT, Gasser TC, et al: Radical prostatectomy versus expectant primary treatment in stages I and II prostatic . A fifteen-year follow-up. Urology 1990 Dec; 36(6): 493-8[Medline].
  17. Greene FL, Sobin LH: The TNM system: our language for care. J Surg Oncol 2002 Jul; 80(3): 119-20[Medline].
  18. Hoffman RM, Gilliland FD, Eley JW, et al: Racial and ethnic differences in advanced-stage : the Outcomes Study. J Natl Inst 2001 Mar 7; 93(5): 388-95[Medline].
  19. Holmberg L, Bill-Axelson A, Helgesen F, et al: A randomized trial comparing radical prostatectomy with watchful waiting in . N Engl J Med 2002 Sep 12; 347(11): 781-9[Medline].
  20. Hsing AW, Tsao L, Devesa SS: International trends and patterns of incidence and mortality. Int J 2000 Jan 1; 85(1): 60-7[Medline].
  21. Hsing AW, Comstock GW: Serological precursors of : serum hormones and risk of subsequent . Epidemiol Biomarkers Prev 1993 Jan-Feb; 2(1): 27-32[Medline].
  22. Iczkowski KA, Chen HM, Yang XJ, Beach RA: diagnosed after initial biopsy with atypical small acinar proliferation suspicious for malignancy is similar to found on initial biopsy. Urology 2002 Nov; 60(5): 851-4[Medline].
  23. Iczkowski KA, Bassler TJ, Schwob VS, et al: Diagnosis of “suspicious for malignancy” in biopsies: predictive value for . Urology 1998 May; 51(5): 749-57; discussion 757-8[Medline].
  24. Jemal A, Murray T, Samuels A, et al: statistics, 2003. CA J Clin 2003 Jan-Feb; 53(1): 5-26[Medline].
  25. Johansson JE, Andrén O, Andersson SO, et al: Natural history of , localized . JAMA 2004 Jun 9; 291(22): 2713-9[Medline].
  26. Klein EA, Thompson IM, Lippman SM, et al: SELECT: the Selenium and Vitamin E Prevention Trial: rationale and design. Prostatic Dis 2000 Nov; 3(3): 145-151[Medline].
  27. Kolonel LN, Nomura AM, Cooney RV: Dietary fat and : current status. J Natl Inst 1999 Mar 3; 91(5): 414-28[Medline].
  28. Labrie F, Candas B, Dupont A, et al: Screening decreases death: first analysis of the 1988 Quebec prospective randomized controlled trial. 1999 Feb 1; 38(2): 83-91[Medline].
  29. Langer JE, Rovner ES, Coleman BG, et al: Strategy for repeat biopsy of patients with prostatic intraepithelial neoplasia detected by needle biopsy. J Urol 1996 Jan; 155(1): 228-31[Medline].
  30. Lee F, Siders DB, Torp-Pedersen ST, et al: : transrectal ultrasound and pathology comparison. A preliminary study of outer gland (peripheral and central zones) and inner gland (transition zone) . 1991 Feb 15; 67(4 Suppl): 1132-42[Medline].
  31. McCahy PJ, Harris CA, Neal DE: Breast and in the relatives of men with . Br J Urol 1996 Oct; 78(4): 552-6[Medline].
  32. Morgan TO, Jacobsen SJ, McCarthy WF, et al: Age-specific reference ranges for -specific antigen in black men. N Engl J Med 1996 Aug 1; 335(5): 304-10[Medline].
  33. Moyad MA: Soy, disease prevention, and . Semin Urol Oncol 1999 May; 17(2): 97-102[Medline].
  34. Ndubuisi SC, Kofie VY, Andoh JY, Schwartz FM: Black-white differences in the stage at presentation of in the District of Columbia. Urology 1995 Jul; 46(1): 71-7[Medline].
  35. Punglia RS, D’Amico AV, Catalona WJ, et al: Effect of verification bias on screening for by measurement of -specific antigen. N Engl J Med 2003 Jul 24; 349(4): 335-42[Medline].
  36. Rodríguez C, Calle EE, Tatham LM, et al: Family history of breast as a predictor for fatal . Epidemiology 1998 Sep; 9(5): 525-9[Medline].
  37. Ruijter ET, Miller GJ, van de Kaa CA, et al: Molecular analysis of multifocal lesions. J Pathol 1999 Jul; 188(3): 271-7[Medline].
  38. Sellers TA, Potter JD, Rich SS, et al: Familial clustering of breast and cancers and risk of postmenopausal breast . J Natl Inst 1994 Dec 21; 86(24): 1860-5[Medline].
  39. Smith JR, Freije D, Carpten JD, et al: Major susceptibility locus for on chromosome 1 suggested by a genome-wide search. Science 1996 Nov 22; 274(5291): 1371-4[Medline].
  40. Stemmermann GN, Nomura AM, Chyou PH, Yatani R: A prospective comparison of at autopsy and as a clinical event: the Hawaii Japanese experience. Epidemiol Biomarkers Prev 1992 Mar-Apr; 1(3): 189-93[Medline].
  41. Theodorescu D, Broder SR, Boyd JC, et al: p53, bcl-2 and retinoblastoma proteins as long-term prognostic markers in localized carcinoma of the . J Urol 1997 Jul; 158(1): 131-7[Medline].
  42. Theodorescu D, Frierson HF, Sikes RA: Molecular determination of surgical margins using fossa biopsies at radical prostatectomy. J Urol 1999 May; 161(5): 1442-8[Medline].
  43. Thompson IM, Goodman PJ, Tangen CM, et al: The influence of finasteride on the development of . N Engl J Med 2003 Jul 17; 349(3): 215-24[Medline].
  44. Walsh PC, Vaughan ED, Retik AB, Wein A, eds: Campbell’s Urology. Vol 3. 7th ed. Philadelphia, Pa: WB Saunders; 1998: 2487-656.
  45. Weinrich MC, Jacobsen SJ, Weinrich SP, et al: Reference ranges for serum -specific antigen in black and white men without . Urology 1998 Dec; 52(6): 967-73[Medline].
  46. Whitmore WF Jr: Expectant management of clinically localized prostatic . Semin Oncol 1994 Oct; 21(5): 560-8[Medline].
  47. Xu J, Meyers D, Freije D, et al: Evidence for a susceptibility locus on the X chromosome. Nat Genet 1998 Oct; 20(2): 175-9[Medline].
  48. Yatani R, Shiraishi T, Nakakuki K, et al: Trends in frequency of latent carcinoma in Japan from 1965-1979 to 1982-1986. J Natl Inst 1988 Jul 6; 80(9): 683-7[Medline].
  49. Zimmerman SM: Factors influencing Hispanic participation in screening. Oncol Nurs Forum 1997 Apr; 24(3): 499-504[Medline].

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Pancreatic Cancer Symptoms

Posted by Pharmaceutical-Stuff on Saturday 8 March 2008

Symptoms:

The main symptoms of include the following:

  • Pain in the abdomen, the back, or both
  • Weight loss, often associated with the following:
  • Loss of appetite (anorexia)
  • Bloating
  • Diarrhea or fatty bowel movements that float in water (steatorrhea)
  • Rarely may present with new diabetes in a person with weight loss and nausea
  • Jaundice (yellowing of the skin)

The symptoms of are generally vague and can easily be attributed to other less serious and more common conditions. This lack of specific symptoms explains the high number of people who have a more advanced stage of disease when is discovered.

Symptoms

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Prostate Cancer - Pathophysiology and Natural History (part3)

Posted by Pharmaceutical-Stuff on Saturday 1 March 2008


develops when the rates of cell division and cell death are no longer equal, leading to uncontrolled tumor growth. Following the initial transformation event, further mutations of a multitude of genes, including the genes for p53 and retinoblastoma, can lead to tumor progression and metastasis. Most cancers are adenocarcinomas (95%).

Approximately 4% of cases of have transitional cell morphology and are thought to arise from the urothelial lining of the prostatic urethra. Few cases have neuroendocrine morphology. When present, they are believed to arise from the neuroendocrine stem cells normally present in the or from aberrant differentiation programs during cell transformation.

Of cases of , 70% arise in the peripheral zone, 15-20% arise in the central zone, and 10-15% arise in the transitional zone. Most cancers are multifocal, with synchronous involvement of multiple zones of the , which may be due to clonal and nonclonal tumors.

Natural history
The natural history is still relatively unknown, and many aspects of progression are poorly understood. Symptoms or abnormal DRE findings in the pre- era only brought 40-50% of patients with to medical attention, and these patients usually had locally advanced disease. The advent of testing has helped identify patients with less-advanced, organ-confined disease.

Evidence suggests that most cancers are multifocal and heterogeneous. Cancers can start in the transitional zone or, more commonly, the peripheral zone. When these cancers are locally invasive, the transitional zone tumors spread to the bladder neck, while the peripheral zone tumors extend into the ejaculatory ducts and seminal vesicles. Penetration through the prostatic capsule and along the perineural or vascular spaces is a relatively late event.

The mechanism for distant metastasis is poorly understood. The spreads to bone , occasionally without significant lymphadenopathy. Currently, 2 predominant theories have been proposed for spread, the mechanical theory and the seed-and-soil theory.

The mechanical theory involves direct spread through the lymphatics and venous spaces into the lower lumbar spine. Advocates of the seed-and-soil theory believe tissue factors must be present that allow for preferential growth in certain tissues, such as the bone. Lung, liver, and adrenal metastases have also been documented. Specific tissue growth factors and extracellular matrices are possible examples.

The doubling time in -stage disease is as slow as 2-4 years, but this changes as the tumor grows and becomes more aggressive. Larger tumors usually have a higher Gleason grade and a faster doubling time.
Taken together, these data suggest that although most cancers diagnosed at an stage have an indolent course, local tumor progression and aggressive disease may develop in the long term. In addition, these findings would support radical treatment, notably among patients with an estimated life expectancy exceeding 15 years.

- and Natural History

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Prostate Cancer - Introduction (part1)

Posted by Pharmaceutical-Stuff on Wednesday 27 February 2008

is the most common noncutaneous among males. Lung and bronchial account for 37% of male deaths, and and colon account for another 10% each. The diagnosis and treatment of continue to evolve. With the development of -specific antigen () screening, more men are identified earlier as having . While can be a slow-growing , thousands of men die of the disease each year. Education is important to help men understand the risk of progression and the various treatment options. This article provides a current overview of the biology, pathology, diagnostic techniques, natural history, and screening for this disorder.

Incidental findings
In the modern era, most patients present because of abnormalities in a screening level or digital rectal examination (DRE) and not because of symptoms (see -Specific Antigen). However, can be an incidental pathologic finding when tissue is removed at the time of transurethral resection for obstructive prostatic symptoms.

Elevated level
is a single-chain glycoprotein that has chymotrypsinlike properties. slowly hydrolyzes peptide bonds, thereby liquifying semen. The upper limit of normal for is 4 ng/mL. Some advocate age-related cutoffs, such as 2.5 ng/mL for the fifth decade of life, 3.5 ng/mL for the sixth decade of life, and 4.5 ng/mL for the seventh decade of life. Others advocate race-specific reference ranges. Using recent data from screening studies, some have advocated upper limits of normal of 2.5 ng/mL instead of 4 ng/mL.

Percent of free
A recent development, the measurement of bound and free can help discriminate between patients with mildly elevated levels from and those with benign prostatic hyperplasia. The lower the ratio of free-to-total , the higher the likelihood of . Free is reported as a percent. Using 25% as the cutoff, 95% of cancers can be detected in both African Americans and whites. A cutoff of 22% maximizes detection and minimizes unnecessary biopsies. Generally, these percents are useful in patients who have a level in the range of 4-10 ng/mL.

This information is most useful in men with very large glands or in men who have already had one negative biopsy result. If the man is healthy and has a level of 4-10 ng/mL, many recommend biopsy directly, without the additional free- test, or consider a trial of antibiotic therapy for 4-6 weeks before repeating the test. If antibiotic therapy lowers the to normal levels in a short time, is less likely to have caused the prior elevation, and the test should be repeated in a few months.

Abnormal DRE findings
Various factors are taken into consideration when performing a DRE. A nodule is important, but findings such as asymmetry, difference in texture, and bogginess are important clues to the patient’s condition and should be considered in conjunction with the level. Change in texture over time can offer important clues about the need for intervention. Cysts or stones cannot be accurately differentiated from based on DRE findings alone; therefore, maintain a high index of suspicion if the DRE are abnormal. In addition, if is detected, the DRE findings form the basis of clinical staging of the primary tumor (ie, T stage in the TNM staging system). In current practice, most patients diagnosed with have normal DRE but abnormal readings.

Local symptoms
In the pre- era, patients with commonly presented with local symptoms. Urinary retention occurred in 20-25%, back or leg pain occurred in 20-40%, and hematuria occurred in 10-15%. Currently, with screening, patients report urinary frequency (38%), decreased urine stream (23%), urinary urgency (10%), and hematuria (1.4%). However, none of these complaints is unique to and each could arise from a variety of other ailments. Forty-seven percent of patients are asymptomatic.

symptoms
symptoms include weight loss and loss of appetite; bone pain, with or without pathologic fracture (because , when , has a strong predilection for bone); and lower extremity pain and edema from nodal metastasis obstructing venous and lymphatic tributaries. Uremic symptoms can occur from ureteral obstruction caused by local growth or retroperitoneal adenopathy secondary to nodal metastasis.

Frequency
With the advent of screening, a greater number of men require education about and how it is diagnosed, staged, and treated in order to select the most appropriate treatment.

According to recent figures from the American Society, 220,900 new cases were diagnosed in 2003 and 28,900 men will die of . is rarely diagnosed in men younger than 40 years, and it is uncommon in men younger than 50 years.

Prevalence rates of remain significantly higher in African American men than in white men, while the prevalence in Hispanic men is similar to that of non-Hispanic white men. Hispanic men and African American men present with more advanced disease, most likely related to external (eg, income, education, insurance status) and cultural factors. In addition, African American men generally have higher levels of testosterone, which may contribute to the higher incidence of carcinoma.

Between 1989 and 1992, incidence rates of increased dramatically, probably because of earlier diagnoses in asymptomatic men as a result of the increased use of serum testing. In fact, the incidence of organ-confined disease at diagnosis has increased because both testing and standard DRE are performed. incidence rates are currently declining, with peak rates in 1992 among white men and in 1993 among African American men.

During 1992-1996, mortality rates for declined significantly, approximately 2.5% per year . Although mortality rates are continuing to decline among white and African American men, mortality rates in African American men remain 2.3 times as high as rates in white men based on 2003 American Society projections.

is also found during autopsies performed following other causes of death. The rate of this latent or autopsy is much greater than that of clinical . In fact, it may be as high as 80% by age 80 years.

The prevalence of clinical varies regionally, and these differences may be due to some of the genetic, hormonal, and dietary factors discussed in the next section. High rates are reported in northern Europe and North America, intermediate rates are reported in southern Europe and Central and South America, and low rates are reported in eastern Europe and Asia.

Interestingly, the prevalence of the latent or autopsy form of the disease is similar worldwide. Together with migration studies, this suggests that environmental factors, such as diet, may play a significant promoting role in the development of a clinical from a latent precursor.

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