Tumours of the female reproductive system


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tumors of the reproductive systems(male and female).................by urs Dr N.D

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Tumours of the female reproductive system

  1. 1. . Name of the project; tumors system(female &male) Presented by: Dr Barkam Nagaraju M.B.B.S of reproductive
  2. 2. TUMORS OF THE OVARY Ovarian cancer is the fifth most common cancer in US women. It is also the fifth leading cause of cancer death in women.  Three cell types make up the normal ovary: the multipotential surface (coelomic) covering epithelium, the totipotential germ cells, and the multipotntial sex cord/stromal cells. Each of these cell types gives rise to a variety of tumors.  Neoplasms of the surface epithelial origin account for almost 90% of ovarian cancers.  epithelial – 65-70%  stromal – 15-20%  Germ cell tumors – 5-10%  Metastatic tumors – 5%  Surface
  3. 3. TUMORS OF THE OVARY (CONTINUED…)  - - - Pathogenesis: several risk factors for epithelial ovarian cancers have been recognized. Two of the most important are nulliparity and family history. Prolonged use of oral contraceptives reduce the risk somewhat. A majority of hereditary ovarian cancers seem to be caused by mutations in the BRCA1 and BRCA2 ge. K-RAS protein is overexpressed in up to 30% of tumors, mostly mucinous cystadenocarcinoma
  4. 4. SURFACE EPITHELIAL TUMORS all types can be benign, borderline , or malignant, depending upon;    Benign ; - gross: mostly cystic - microscopic; fine papillae, single layer covering (no stratification), no nuclear atypia, no stromal invasion) Borderline ; - gross; cystic / solid foci - microscopic; papillary complexity, stratification, nuclear atypia, no stromal invasion Malignant ; - gross; mostly solid & hemorrhage / necrosis - microscopic; papillary complexity, stratification, nuclear atypia, stromal invasion
  5. 5. SEROUS TUMORS      These are the most frequent of the ovarian tumors. Benign lesions are usually encountered between ages 30 and 40 years, and malignant serous tumors are more commonly seen between 45 and 65 years of age. Serous tumors are the most common malignant ovarian tumors, account for 60% of all ovarian cancers. Grossly, may be small, but most are large, spherical to ovoid, cystic structures. The prognosis for the individual with clearly invasive serous cystadenocarcinoma. Serous Cystadeno ma
  6. 6. SEROUS CYSTADENOMA • single layer of columnar ciliated •Fine papillae
  7. 7. MUCINOUS TUMORS    The differ essentially from serous tumors in that the epithelium consists of mucin-secreting cells simlar to those of the endocervical mucosa. 10% of them are malignant, 10% are of low malignant potential, 80% are benign. The prognosis is of mucinous tumors is better than for the serous counterpart, but the stage is the major determinant of treatment success.
  8. 8. MUCINOUS CYSTADENOMABORDERLINE •Papillary complexity •Nuclear stratification& atypia • No stromal invasion
  9. 9. ENDOMETRIOID TUMORS      They may be solid or cystic, but sometimes they develop as a mass projecting from the wall of a cyst filled with chocolate-colored fluid. Microscopically, formation of tubular glands, similar to those of the endometrium. They are usually malignant tumors, although benign and borderline forms also exist. 15-30% of women with these ovarian tumors have a concomitant endometrial carcinoma. Similar to endometrial cancer, endometrioid carcnoma have mutations in PTEN suppressor gene. Solid / cyst filled by hemorrhage & necrosis
  10. 10. GRANULOSA CELL TUMOR     Hormonally active tumor The most common estrogenic ovarian neoplasm. The adult form occurs mainly in postmenopausal women, associated with endometrial hyperplasia and carcinoma The juvenile type occurs in the first two decades, cause precocious sexual development. •Solid with hemorrhage
  11. 11. BRENNER TUMOR      They are uncommon, most are benign, solid, usually unilateral tumors, consisting of an abundant stroma containing nest of transitionl-like epithelium resembling that of the urinary tract. Occasionally, the nests are cystic and are lined by columnar mucus-secreting cell. They are generally somoothly encapsulated. They may arise from the surface epithelium or from urogenital epithelium trapped within the germinal ridge. Rarely, they are formed as nodules within the wall of a mucinous cystadenoma.
  12. 12. TERATOMAS  Neoplasms of germ-cell origin constitute 15% to 20% of ovarian tumors  However, more than 90% of these germ-cell are benign mature cystic teratomas. The immature malignant variant is rare.
  13. 13. BENIGN (MATURE) CYSTIC TERATOMAS       They are marked by differentiation of totipotential germ cells into mature tissues representing all three germ cell layers. Usually there is cysts lined by recognizable epidermis replete. On transection, they are often filled with sebaceous secretion and matted hair, when removed, reveal a hair-bearing epidermal lining. Sometimes teeth protrude from nodular projection. Occasionally, foci of bone and cartilage, nests of bronchial or GIT epithelium, and other recognizable lines of development are also present. Sometimes, they produce infertility for unknown reasons. In about 1% of cases there is malignant transformation, usually taking form of a squamous cell carcinoma.
  14. 14. IMMATURE MALIGNANT TERATOMAS      They are found early in life, the mean age is 18 years. Differ from benign teratomas insofar as they are often bulky, and predominantly solid or near-solid on transection, and are punctuated by areas of necrosis. Uncommonly, one of the cystic foci may contain sebaceous secretion, hair, and other feature similar to those in the mature teratoma. Microscopically, the distinguishing feature is an immature areas of differentiation toward cartilage, bone, muscle, nerve, and other structure. Particularly ominous are foci of neuropithelial differentiation, because they are aggressive and metastasize widely.
  15. 15. SPECIALIZED TERATOMAS Stroma ovarii is composed entirely of mature thyroid tissue that may hyperfunction and produce hyperthyroidism.  They appear as small, solid, unilateral brown ovarian masses.  Stroma ovarii and carcinoid may combined in the same ovary, One of these elements may become malignant.  Specialized teratoma
  16. 16. UTERINE TUMORS Classification: Endometrial tumors: benign-endometrial polyps Malignant-endometrial carcinoma Myometrial tumors: Benign-leiomyoma Malignant-leiomyosarcoma
  17. 17.  Endometrial polyps: sessile, usually hemispheric. Histologically, composed of endometrium resembling the basalis, frequently with small muscular arteries. More often they have cystic dilated glands, but some have normal endometrial architecture. They may occur at any age, but more commonly, they develop at time of menopause. clinical significance: - production of abnormal uterine bleeding. - risk of giving rise to a cancer (rare).
  18. 18. TUMORS  - - (CONTINUED…) Endometrial carcinoma: The most frequent cancer occurring in the female genital tract in the U.S and other Western countries. Appears most frequently between the ages of 55 and 65 years. There are two clinical stettings in which endometrial carcinomas arise: in perimenopausal women with estrogen excess and in older women with endometrial atrophy. (endometroid and serous carcinoma of the endometrium, respectively). Well-defined risk factors for endometroid carcinoma: obesitydiabetes-hypertension-infertility These risk factors poin to increased estrogen stimulation, and it is well recognized that prolonged estrogen replacement therapy and estrogen-secreting tumors increase the risk of this cancer.
  19. 19. TUMORS ENDOMETRIAL CARCINOMA: (CONTINUED…) - 1. 2. Many of these risk factors are the same as those for endometrial hyperplasia, and endometrial carcinoma frequently arises on a background of endometrial hyperplasia. These tumors are termed endometrioid because of their similarity to normal endometrial gland. Two familial cancer syndromes that have an increased risk of the endometrioid type of endometrial carcinoma: hereditary nonpolyposis colon cancer syndrome. Cowden‟s syndrome (carries an increased risk of carcinoma of the breast, thyroid, and endometrium, have mutations in PTEN, a tumor suppressor gene).
  20. 20. TUMORS ENDOMETRIAL CARCINOMA: (CONTINUED…) - - - Serous carcinoma of the endometrium typically arises in a background of atrophy, sometimes in the setting of an endometrial polyps. Mutations in DNA mismatch repair genes and PTEN are rare in serous carcinoma; however, nearly all cases have mutations in the p53 tumor suppressor gene. Marked leukorrhea and irregular bleeding are the fist clinical indication of all endometrial carcinoma. With progression, uterus may be palpably enlarged, and in time it becomes fixed to surrounding structures by extension of the cancer beyond the uterus. Fortunately, these are usually late-metastasizing neoplasms, but dissemination eventually occurs.
  21. 21. TUMORS (CONTINUED…)  - - Leiomyoma: The most common benign tumor in females and are found in 30% to 50% of women during reproductive life. More frequent in blacks than in whites. They are often referred to as fibroids because they are firm. Estrogens and oral contraceptives stimulate their growth; conversely, they shrink postmenopausally. They may be entirely asymptomatic, discovered on routine pelvic examination. The most frequent manifestation, when present, is menorrrhagia, with or without metrorrhagia. They may become palpable to the woman or may produce a dragging sensation. They rarely transform into sarcomas.
  22. 22. Leiomyosacrcoma A uterine leiomyosarcoma is a rare malignant (cancerous) tumor that arises from the smooth muscle lining the walls of the uterus (myometrium). Smooth muscles react involuntarily in response to various stimuli. For example, the myometrium stretches during pregnancy Leiomyosarcoma is classified as a soft tissue sarcoma. Sarcomas are malignant tumors that arise from the connective tissue ELECTRON MICROSCOPY: The nuclei of the tumor cells are round, oval or spindle with high pleomorphism and condensed chromatin and occasional prominent nucleoli.
  23. 23. UTERINE TUBE(FALLOPIAN TUBE) Primary neoplasia  Epithelial:  Adenoma  Adenocarcinoma  Mesenchymal:  Leiomyoma  Mixed tumours:  Fibroadenoma  Adenomyoma  metastatic granulosa cell tumor 
  24. 24.   Adenocarcinoma is a cancer of an epithelium that originates in glandular tissue. Epithelial tissue includes, but is not limited to, the surface layer of skin, glands and a variety of other tissue that lines the cavities and organs of the body. Epithelium can be derived embryologically from ectoderm, endoderm or mesoderm. To be classified as Adenocarcinoma Leiomyoma of the fallopian tube is extremely rare. Most cases are asymptomatic and found incidentally at autopsy or unrelated operation. These leiomyomas tend to be singular, small, and unilateral, with a resultant rare preoperative diagnosis
  25. 25.    Fibroadenomas are round, firm, rubbery masses that arise from excess growth of glandular and connective tissue. These masses can grow to the size of a small plum, but they're benign and usually painless. If you have a fibroadenoma, it may bounce or move slightly when you press the area. fibroadenoma. Mammography and ultrasound may help with the diagnosis, but the only way to be certain of a fibroadenoma is to take a sample of tissue for lab analysis (biopsy). Your doctor may also recommend surgery to remove the lump completely. Gross examination of the fallopian tubes revealed no masses or lesions; however, 2 small foci of granulosa cells were identified microscopically within one of the fallopian tubes. These foci were suspicious for granulosa cell tumor metastases. The patient subsequently underwent a bilateral oophorectomy, which revealed no primary granulosa cell tumor
  26. 26. TUMORS OF THE CERVIX Cervical carcinoma is one of the major causes of cancer-related deaths in women, despite improvements in early diagnosis and treatment.  Since introduction of the Papanicolaou (Pap) smear 50 years ago, the incidence of cervical cancer has plummeted.  The pap smear remains the most successful cancer screening test ever developed.  Over the same period, the incidence precursor cervical intraepithelial neoplasia (CIN) has increased to more than 50,000 cases annually. It is important to know that nearly all invasive cervical squamous cell carcinoma arise from epithelial changes CIN. 
  27. 27. CERVICAL INTRAEPITHELIAL NEOPLASIA    Cytologic examination can detect epithelial changes (CIN) before the development of an overt cancer by many years. However, only a fraction of cases of CIN progress to invasive carcinoma. The peak incidence of CIN is about 30 years, whereas that of invasive carcinoma is about 45 years. Risk factors for the development of CIN and invasive carcinoma are: -Early age at first intercourse -Multiple sexual partners -Male partner with multiple previous sexual partners -persistent infection by „„High-risk‟‟ HPV They point to the likelihood of sexual transmission of a causative agent, in this case HPV.
  28. 28. HPV (ADDITIONAL INFORMATION)     High-risk HPV types: 16, 18, 45, and 31, account for the majority of carcinomas, smaller contributions by HPV33, 35, 39, 45, 52, 56, 58, and 59. The viral DNA integrates into the host genome and express E6 and E7 proteins which inactivate tumor suppressor genes p53 and RB, respectively. Low-risk HPV types: 6, 11, 42, 44 which produce condylomas; the viral DNA does not integrate into the host genome. The recently introduced HPV vaccine is very effective in preventing HPV infections and cervical cancers. Many women harbor these viruses, only few develop cancer, suggesting other influences like cigarette smoking and exogenous or endogenous immunodeficiency.
  29. 29. INVASIVE CARCINOMA OF THE CERVIX    The most common cervical carcinoma are sqamous cell carcinoma 75%, adenocarcinoma and adenosquamous carcinoma 20%, and small cell neuro-ednocrine carcinoma 5%. In some individual with aggressive intraepithelial changes, the time interval may be considerably shorter, whereas in other women CIN precursors may persist for life. The only reliable way to monitor the course of the disease is with careful follow-up and repeat biopsies. The relative proportion of adenocarcinoma has been increasing in recent decades; glandular lesions are not detected well by Pap smear.
  30. 30. INVASIVE CARCINOMA OF THE CERVIX (CONTINUED…)    advanced cases of cervical cancer are invariably seen in women who either have never had a Pap smear or have waited many years since the prior smear. Such tomors may be symptomatic, called to attention by unexpected vaginal bleeding, leukorrhea, painful coitus, and dysuria. Detection of precursors by cytologic examination and their eradication by laser vaporization or cone biopsy is the most effective method of cancer prevention. Invasive carcinomas range from microscopic foci of early stromal invasion to grossly conspicuous tumors encircling the os. Tumors encircling the cervix and penetrate into the stroma produce a “barrel cervix”, which can be identified by direct palpation.
  31. 31. VULVA TUMORS  - - Condylomas and low-grade vulvar intraepithelial Neoplasian (VIN) Condylomas fall into two distinctive biologic forms: Condylomata lata: (not commonly seen today), are flat, moist, minimally elevated lesions that occur in secondary syphilis Condylomata accuminata: (more common) may be papillary and distinctly elevated. They occur anywhere on the anogenital surface. Significant characteristic cellular morphology is: perinuclear cytoplasim vacuolization. Vulvar cndylomas are not pre-cancerous but coexist with foci of intraepithelial neoplasia in vulva (VIN grade 1) and cervix.
  32. 32. CONDYLOMAS Giant condyloma accuminata A vulva chancre and condylomata
  33. 33. TUMORS (CONTINUED …)  - - - High-grade vulvar intraepithelial neoplasia and carcinoma of the vuvla Carinoma of vulva represent about 3% of all genital tract cancers in women. 90% of vulvar carcinomas are squamous cell carcinomas; and 90% of them are HPV related, and most common seen in relatively younger patients. Non-HPV-related vulvar squamous cell carcinoma occrus in older women; It is well differentiated and unifocal, and is associated with lichen sclerosus or other inflammatory conditions.
  34. 34. VAGINAL INTRAEPITHELIAL NEOPLAISA AND SQUAMOUS CELL CARCINOMA      Extremely uncommon, usually occur in women older than age 60 years. Risk factors are similar to those for carcinoma of the cervix (discussed later). Associated with HPV infection in most cases. Vaginal clear cell adenocarcinoma, usually encountered in young women in their late teens whose mothers took diethylstilbestrol during pregnancy; overall risk is 1 per 1000 of those exposed in utero. Vaginal adenosis, are small glandular or microcystic inclusions appear in vaginal mucosa, appear as red glandular foci lined by mucus-secreting cell; from such inclusions rare clear cell adenocarciona arises.
  35. 35. TUMORS OF THE BREAST  Fibroadenoma  It is the most common benign neoplasms of the female breast. They almost never become malignant. Usually appear in young women; the peak incidence is in the third decade of life.  An increase in estrogen activity is thought to contribute to its development.  Similar lesions may appear with fibrocystic changes.  They usually present as solitary, discrete, movable mass. They may enlarge late in the menstrual cycle and during pregnancy.
  36. 36. PHYLLODES TUMOR        They are much less common than fibroadenomas. Arise from the periductal stroma and from preexisting fibroadenomas. They may be small or grow to large massive size, distending the breast. Some become lobulated and cystic; on gross section they exhibit leaflike clefts and sliits, that is why they called phylodes tumors. In the past they had the name cystosarcoma phyllodes, an unfortunate name because they are benign. The most ominous change is the appearance of increased stromal cellularity with anaplasia and high mitotic activity, accompanied by rapid increase in size, and invasion of adjacent breast tissue by malignant stroma. they remain localized and are cured by excision;even malignant tumors also tend to remain localized. Only the most malignant (15% of cases) metastasize to distant sites.
  37. 37. INTRADUCTAL PAPILLOMA It is a neoplastic papillary growth within a duct.  Most are solitary, found within the principal lactiferous ducts or sinuses.  Present clinically as a result of - Appearance of serous or blody nipple discharge - Precence of small subareolar tumor - Nipple retraction (rare).  In some cases there are multiple papillomas in several ducts (intraductal papillomatosis). These lesion sometimes become malginant, wherease the solitary papilloma almost always remain benign. 
  38. 38. CARCINOMA      Despite advances in diagnosis and treatment, almost onefourth of women who develop these neoplasms will die of the disease. 75% of women with breast cancer are older than age 50. only 5% are younger than the age 40. Oral contraceptives: they have been suspected of increasing the risk of breast cancer. Ionizing radiation to the chest increases the risk of breast cancer. Only women irradiated before age 30, seem to be affected. 20% to 30% of women irradiated for Hodgkin lymphoma in their teens and 20s develop breast cancer, but the risk for women treated later in life is not elevated. Other less well-established risk factors: obesity, alchohol consumption, and a diet high in fat.
  39. 39. CARCINOMA (CONTINUED…) Pathogenesis: as with all cancers, the cause of breast cancer remain unknown. however, three set of influences seem to be important:  Genetic change:  Hormonal influences  Enviornmental variables  Genetic change - Mutations affecting proto-oncogenes and tumor supressor genes in breast epithelium contribute to the oncogenic transformation process. .
  40. 40. CARCINOMA (CONTINUED…) A large number of genes including the estrogen receptor may be inactivated by promoter hypermethylation. - Most likely, multiple acquired genetic alterations are involved in the sequential transormation of a normal epithelial cell into a cacerous cell.  Hormonal influences: - Endogenous estrogen excess or hormonal imbalance has a significant role. Many risk factors (mentioned before) imply increased exposure to estrogen peaks during the menstrual cycle. Enviornmental variables: - They are suggested by the variable incidence of breast cancer in genetically homogeneous groups and the geographic differences in prevalence. Important environmental variables include irradiation and exogenous estrogens. -
  41. 41. CARCINOMA (CONTINUED…) Spread of breast cancer:       Occurs through lymphatic and hematogenous channels. Lymph node metastasis are present in about 40% of cancers presenting as a palpable masses. Outer quadrant and centrally located lesions typically spread to the axillary nodes. Those in the inner quadrants often involve the lymph node along the internal mammary arteries. The supraclavicular nodes are sometimes the primary site of spread, but they become involved only after the axillary and internal mammary nodes are affected. Metastatic involvement maybe to any organ, such as lungs, skeleton, liver, adrenals brain, spleen, and pituitary. Matastases may appear many years after apparent therapeutic control of the primary lesion, sometimes 15 years later.
  42. 42. CARCINOMA  1. 2. 3. 4. (CONTINUED…) Prognosis is influenced by the following variables: The size of the primary carcinoma. Invasive carcinoma smaller than 1cm have an excellent prognosis in the absence of lymph node metastases. Lymph node involvement and the number of lymph nodes involved by metastases. Distant metastases. Patient who develop hematogenous spread are rarely curable. The grade of the carcinoma. The most common grading system for breast cancer evaluates tubule formation, nuclear grade, and mitotic rate to divide carcinomas in to three groups.
  43. 43. CARCINOMA 5. 6. 7. 8. 9. (CONTINUED…) The histologic type of carcinoma. All specialized types of breast carcinoma (tubular, medullary, cribriform, adenoid cystic, and mucinous) have a better prognosis than carcinomas of no special type (ductal carcinoma). The presence or absence of estrogen or progesterone receptors. The reason for determining their presence is to predict the response to anti-estrogen therapy. The proliferation rate of the cancer. High proliferative rates are associated with a poorer prognosis. Aneuploidy. Carcinoma with an abnormal DNA content have a slightly worse prognosis. Overexpression of HER2/NEU. Ovexpression is associated with poorer prognosis. However, the importance of evaluating HER2/NEU is to predict resposne to monoclonal antibody “Herceptin” to the gene product.
  44. 44. CARCINOMA  - - - - (CONTINUED…) The major prognostic factors are used by the American Joint Committee on Cancer to devide breast cancer into clinical stages as follows: Stage 0. DCIS or LCIS (5-year survival rate: 92%) Stage 1. invasive carcinoma 2cm, without nodal involvement (5-year survival rate: 87%) Stage 2. invasive carcinoma 5cm, with up to 3 involved axillary nodes (5-year survival rate: 75%) Stage 3. invasive carcinoma 5cm with four or more involved axillary nodes. (5-year survival rate: 43%) Stage 4. breast cancer with distant metastases (5-year survival rate: 13%)
  45. 45. MALE BREAST    Only two disorders occur in male breast with sufficient frequency. Gynecomastia: male breast are also subject to hormonal influences, but they are less sensitive than are female breasts. Gynecomastica may occur in response to estrogen excess. The most important cause is cirrhosis of the liver, with consequent inability of the liver to metabolize estrogens. Other causes include Klinefelter syndrome, estrogen-secreting tumors, estrogen therapy, digitalis therapy. Physiologic gynecomastia occurs in puberty and in old age. Morphologic features are simlar to intraductal hyperplasia. Carcinoma: frequency ratio to breast cancer in the female of 1:125. It occurs in advanced age. Because of scant amount of breast substance in males, the tumor rapidly infiltrates the skin and underlying thoracic wall. They resemble invasive carcinoma in females both morphologically and biologically.
  50. 50. Immature Teratoma With Embryonal
  51. 51. TESTICULAR TUMORS  Most are malignant Excellent results with treatment.  Must look for „markers‟ before removal   Germ line (actual reproductive cells) Seminoma  Embryonal  Choriocarcinoma  Mixed pattern   Non-germ line  Specialized supportive cells  Leydig, may be hormonally active
  52. 52. TUMOR MARKERS  Some tumors produce agents measurable in the blood. Embryonic tissue markers  Beta-HCG  Placental marker  We measure this in pregnancy tests   Alpha-feto protein  Marker associated with embryonic gut
  53. 53. SEMINOMA  Most common type  Curable  Arises from sperm producing cells  Several histologic types.  Lymphocytes
  54. 54. SEMINOMA  Little fried egg looking cells.  Lymphocytes  No production of Bet-HCG or Alpha-fetoprotein
  55. 55. EMBRYONAL CARCINOMA  Aggressive  Areas tumor of hemorrhage and necrosis  Two histologically distinct cell types  Lance Armstrong
  56. 56. EMBRYONAL CA  Two   tissue types Stroma Glands  Metastasizes widely
  57. 57. CHORIOCARCINOMA  Placental   elements Synciotrophoblasts Make Beta-HCG  Typically part of a „mixed lineage‟ tumor.  Highly aggressive  This element spreads early.
  58. 58. TERATOMA  Aggressively malignant  Three germ lines Ectoderm  Endoderm  Mesoderm 
  59. 59. LEYDIG CELL TUMOR  One of several so-called „specialized stromal tumors.  Non-germ line Benign generally  Hormonally active  Androgens  Estrogens    Gynecomastia Sometimes even corticosteroids
  60. 60. HYDROCELE
  61. 61. HYDROCELE  Fluid filled scrotal cyst.  Benign  Often with inguinal hernia  Transilluminates  Fluid will recollect if aspirated.  Can be large
  62. 62. GERM CELL TUMOURS OF THE TESTIS mainly 15-40 yrs  more common in undescended testes & in testicular dysgenesis (Klinefelter‟s syndrome)  usually presents as painless mass  almost always malignant  seminoma and “non-seminoma” are two main types  precursor lesion = ITGCN 
  63. 63. INTRATUBULAR GERM CELL NEOPLASIA  like CIS in other organs  seen adjacent to most tumours  also often seen where germ cell tumours may arise, e.g. cryptorchidism, Klinefelter‟s syndrome  progresses to invasive tumour in ~ 50% cases over ~ 5 years  may be bilateral  important to follow up/treat (e.g. radiotherapy)
  64. 64. GERM CALL TUMOURS - SEMINOMA  most common type  (seminoma = ovarian dysgerminoma)  (rarely arise elsewhere - mediastinum, pineal, retroperitoneum)  can metastasise– especially nodes and bone  radiosensitive - 95% cure in early stages  pathology    pale homogenous tumour big cells, lymphocytes, few mitoses contain PLAP (placental alkaline phosphatase)
  65. 65. BENIGN PROSTATIC HYPERPLASIA    Nodular growth pattern Some chronic inflammation Glands always have a double layer of epithelium Columnar &  Reserve layer 
  66. 66. PROSTATE CANCER  Very    common Blacks & Whites Rare in Asians  Incidence increases with age.  Peripheral zone  PSA  Family history
  67. 67. PROSTATE CANCER  Adenocarcinoma  Single layer of epithelium  Gland-within-gland  LN and Bone mets   Osteoblastic & Osteolytic  Treatment Surgery &  Hormone manipulation 
  68. 68. PENILE TUMORS  Papillomas  HPV   Some are dangerous serotypes. Cause unregulated epithelial growth
  69. 69. PAPILLOMA
  70. 70. SQUAMOUS CARCINOMA  In situ  Invasive  Ulcerative  HPV   16 18  Regional lymph nodes.  Metatasizes widely.
  72. 72. ` `