2-Tumor markers in diagnosis
3-Morphology of
a)
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Seminomab)
Embryonal carcinoma
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c)
Yolk sac tumor
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4-CryptorchidismTesticular lesion
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? CongenitalAnomalies? RegressiveChanges
? Inflammation (Nonspecific , Specific Inflammations, Granulomatous
(Autoimmune) Orchitis)
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? VascularDisorders(torsion)
? SpermaticCordandParatesticularTumors
? TesticularTumors
INFLAMMATIONS-
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? Inflammation of the testis is termed as orchitis and of epididymis iscalled as epididymitis; the latter being more common
1-Non-specific Epididymitis and Orchitis-
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? may be acute or chronic? common routes of spread are via the vas deferens, or lymphatic and
haematogenous routes
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? caused by urethritis, cystitis, prostatitis and seminal vesiculitis? common infecting organisms in Neisseria gonorrhoeae and Chlamydia
trachomatis
Grossly,
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? acute stage- firm, tense, swollen and congestedmay be multiple abscesses, especially in gonorrhoeal
infection
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? chronic stage- variable degree of atrophy and fibrosisHistological y,
? acute- congestion, oedema and diffuse infiltration by neutrophils, or formation of
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neutrophilic abscesses? Chronic- focal or diffuse chronic inflammation, disappearance of seminiferous
tubules, fibrous scarring and destruction of interstitial Leydig cells
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2-Granulomatous (Autoimmune) Orchitis -Non-tuberculous granulomatous orchitis-
? unilateral, painless testicular enlargement
? may resemble a testicular tumour clinically
? autoimmune basis is suspected
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Gross- enlarged
? Cut section of the testicle is greyish-white to tan-brown
? Histological y, granulomatous reaction(non caseating) is present diffusely
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throughout the testis and is confined to the seminiferous tubules? Peritubular fibrosis
? interstitial lymphocytes and plasma cells
3-Tuberculous Epididymo-orchitis-
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? invariably begins in the epididymis and spreads to the testis? May spread via -tuberculous seminal vesiculitis, prostatitis and renal tuberculosis
? haematogenous spread- from tuberculosis of the lungs
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Grossly, discrete, yellowish, caseous necrotic areas? Microscopical y, numerous tubercles which may coalesce to form large caseous
mass
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? Characteristics of typical tubercles such as epithelioid cells, peripheral mantle oflymphocytes, occasional multinucleate giant cells and central areas of caseation
necrosis are seen
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? AFB positive
4-Spermatic Granuloma(epididymitis nodosa)
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? Spermatic granuloma is the term used for development ofinflammatory lesions due to invasion of spermatozoa into the stroma
MORPHOLOGIC FEATURES-
Grossly,
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? a small nodule, 3 mm to 3 cm in diameter in head of epididymis? firm, white to yellowish-brown
? Histological y, it consists of a granuloma composed of histiocytes,
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epithelioid cells, lymphocytes and some neutrophils
? Characteristical y, the centre of spermatic granuloma contains
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spermatozoa and necrotic debrisVascular disorder
Torsion of Testis
? Twisting of the spermatic cord
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? sudden cessation of venous drainage and arterial supply? usually followed by sudden muscular effort or physical trauma
? Trauma may occure in either in a fully-descended testis or in an
undescended testis
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1-Neonatal torsion-
? occurs either in utero or shortly after birth
? It lacks any associated anatomic defect in testis
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2-"Adult" torsion-
? is typically seen in adolescence and presents with the sudden onset of testicular
pain
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? bel -clapper abnormality -bilateral anatomic defect that leads to increased
mobility of the testes (bel -clapper abnormality)
? Viable- manually untwisted within approximately 6 hours of the
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onset of torsion
MORPHOLOGIC FEATURES-
duration and severity of vascular occlusion
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? may be coagulative necrosis of the testis and epididymis? may be haemorrhagic infarction
Spermatic Cord and Paratesticular Tumors
1-Lipomas
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? common lesions involving the proximal spermatic cord, identified atthe time of inguinal hernia repair
? represent retroperitoneal adipose tissue that has been pulled into the
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inguinal canal along with the hernia sac, rather than a true neoplasm
2-Adenomatoid tumor-
? most common benign paratesticular tumor
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?? typically occurring near the upper pole of the epididymis
? grossly , well circumscribed small nodules
? Microscopically- Proliferation of glandular structures, irregularly lined by cuboidal
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to flattened epithelial cell? Treatmet- local excision
Malignant tumor
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? rhabdomyosarcomas -children
? liposarcomas- adults
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CLASSIFICATION OF TESTICULAR TUMOR? most useful classification of tumors is histogenetic
? Named according to from which tissue they arise and of which they consist
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WHO histological classification of testis tumours
? Germ cell tumours
? Tumours of one histological type (pure forms)
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? Tumours of more than one histological type (mixed forms)? Sex cord/gonadal stromal tumours Pure forms
? Miscellaneous tumours of the testis
? Haematopoietic tumours
? Tumours of collecting ducts and rete
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? Tumours of paratesticular structures? Mesenchymal tumours of the spermatic cord and testicular adnexae
? Secondary tumours of the testis
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Testicular cancer is staged using the TNM system created by the American JointCommittee on Cancer (AJCC)
It's based on 4 key pieces of information:
? T refers to how much the main (primary) tumor has spread to tissues next to the
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testicle
? N describes how much the cancer has spread to regional (nearby) lymph nodes
? M indicates whether the cancer has metastasized (spread to distant lymph nodes
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or other organs of the body)
? S indicates the serum (blood) levels of tumor markers that are made by some
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testicular cancers? Letters or numbers appear after T, N, M, and S to provide more details about
each piece of information.
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? The numbers 0 through 4 indicate increasing severity
? The letters "IS" after the T stand for in situ, which means the tumor is contained
in one place and has not yet penetrated to a deeper layer of tissue.
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? The letter X after T, N, M, or S means "cannot be assessed" because the
information is not known
TNM classification of germ cel tumours of the testis
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pTNM pathological classification
? pTx ?Primary tumour cannot be assessed
? pT0 No evidence of primary tumour (e.g. histologic scar in testis)
? pTis Intratubular germ cell neoplasia (carcinoma in situ)
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? pT1 Tumour limited to testis and epididymis without vascular/lymphaticinvasion; tumour may invade tunica albuginea but not tunica vaginalis
? pT2 Tumour pT1 + involvement of tunica vaginalis
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? pT3 Tumour invades spermatic cord with or without vascular/lymphatic invasion? pT4 Tumour invades scrotum with or without vascular/lymphatic invasion
pN ? Regional lymph nodes
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? pNX Regional lymph nodes cannot be assessed? N0 No regional lymph node metastasis
? pN1 <2 cm or less in greatest dimension and 5 or fewer positive nodes
? pN2 2 to 5 cm in greatest dimension; or more than 5 nodes positive, none more
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than 5 cm; or evidence of extranodal extension of tumour? pN3 Metastasis with a lymph node mass more than 5 cm in greatest dimension
S ? Serum tumour markers
? SX Serum marker studies not available or not performed
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? S0 Serum marker study levels within normal limits? LDH, hCG (mIU/ml) ,AFP (ng/ml)
Serum tumor markers (S)
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For staging, serum (blood) levels of tumor markers are measured after the testiclecontaining the cancer has been removed with surgery
LDH
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HCG
AFP (ng/ml)
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(U/liter)(mIU/ml)
SX Marker studies not available or not done.
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S0 Normal
Normal
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NormalS1 <1.5 x
<5,000
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<1,000
*
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NormalS2 1.5 - 10 x
5,000 -
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1,000 -
+
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Normal50,000
10,000
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S3 >10 x
>50,000
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>10,000+
Normal
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Cryptorchidism? Cryptorchidism is a complete or partial failure of the intra-abdominal testes to
descend into the scrotal sac
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associated with? testicular dysfunction
? an increased risk of testicular cancer
? In 70% of cases, the undescended testis lies in the inguinal ring
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? in 25% in the abdomenETIOLOGY. exact etiology is not known in majority of cases
1. Mechanical factors-
? short spermatic cord
? narrow inguinal canal
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? adhesions to the peritoneum? problems with development of the gubernaculum
? a patent processus vaginalis, or impaired intra-abdominal pressure have also
been hypothesized to contribute to cryptorchidism
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2. Genetic factors-
? up to 23% of cases suggesting an underlying genetic mutation
? Mutations in insulin-like factor 3 and its receptor, LGR8, have been
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demonstrated in a small number of cases? trisomy 13
3. Hormonal factor- cryptorchidism is only rarely associated with a well-defined
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hormonal disorder? deficient androgenic secretions
? mullerian inhibiting substance
? insulin-like 3 hormone
4. Neuromuscular- abnormalities of the genitofemoral nerve's calcitonin gene-
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related peptide or the cremasteric nucleus have been postulated to cause
cryptorchidism
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Miscellaneous-? Maternal alcohol consumption, analgesic consumption, and smoking have also
been associated with an increased risk
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? Gestational diabetes has been shown to be related to the development ofcryptorchidism
MORPHOLOGIC FEATURES. Cryptorchidism is unilateral in 80% cases
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Grossly, the cryptorchid testis is small in size, firm and fibroticHistology-
1-Seminiferous tubules
? tubular basement membrane is thickened
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? hyalinised tubules with a few Sertoli cells? foci of spermatogenesis are discernible in 10% of cases
2. Interstitial stroma: usual y increase in the interstitial fibrovascular stroma and
conspicuous presence of Leydig cells, seen singly or in small clusters
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? CLINICAL FEATURES. asymptomatic and is discovered only on physical
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examination1. Sterility-infertility. Bilateral cryptorchidism is associated with sterility while
unilateral disease may result in infertility
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2. Inguinal hernia. A concomitant inguinal hernia is frequently present along withcryptorchidism
3-Malignancy. Cryptorchid testis is at 30-50 times increased risk of developing
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testicular malignancy
? most commonly seminoma and embryonal carcinoma, than a normally
descended testis
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? risk of malignancy is greater in intraabdominal testis than in testis in the inguinal
canal
? current recommendations are for correction at 6 to 12 months of age
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? carcinoma arises from foci of intratubular germ cell neoplasia within the atrophictubules
? Orchiopexy reduces the risk of sterility and cancer
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Tumour marker
Tumour markers- Germ cell tumours of the testis secrete polypeptide hormones
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and certain enzymes which can be detected in the bloodThere are two principal serum tumour markers
? alpha fetoprotein (AFP) and
? beta subunit of human chorionic gonadotropin (shCG)
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? In addition, carcinoembryonic antigen (CEA), human placental lactogen (HPL),placental alkaline phosphatase, testosterone, oestrogen and luteinising hormone
may also be elevated
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AFP-? synthesized by fetal yolk sac and also the liver and intestine
? elevated in 50-70% of testicular germ cell tumours
? Markedly elevated in yolk sac tumor
? a serum half life of 4.5 days
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? However, elevated serum AFP levels are also found in liver cell carcinomahCG-
? secreted by placental trophoblastic cells
? elevated in non-seminomatous germ cell tumours of the testis (e.g. in
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choriocarcinoma, yolk sac tumour and embryonal carcinoma)
? elevated in 50% of patients with germ cell tumours
? elevation in seminoma in 10-25% of cases
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Lactate dehydrogenase (LDH)-
? may also be elevated
? direct relationship between LDH and tumour burden
? However, this test is nonspecific although its degree of elevation correlates with
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bulk of disease
Applications-
? In the evaluation of testicular masses
? In the staging of testicular germ cell tumors. For example, after orchiectomy,
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persistent elevation of HCG or AFP concentrations indicates stage II disease even
if the lymph nodes appear of normal size by imaging studies
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? In assessing tumor burden? In monitoring the respons to therapy. After eradication of tumors there is a
rapid fall in serum AFP and HCG. With serial measurements it is often possible to
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predict recurrence before the patients become symptomatic or develop any otherclinical signs of relapse
TESTICULAR TUMOR
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Testicular tumor? Most germ cell tumours occur between the ages of 20 and 50 years
? Before puberty, seminoma is extremely uncommon
? usual germ cell tumours , yolk sac tumour and the better differentiated types of
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teratoma
? Spermatocytic seminoma and malignant lymphoma usually occur in older
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patients? incidence increases shortly after the onset of puberty and reaches a maximum in
men in the late twenties and thirties
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ETIOLOGIC FACTORS
? Cryptorchidism
? Other developmental disorders- Dysgenetic gonads associated with endocrine
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abnormalities such as androgen insensitivity syndrome? Genetic factors-high incidence in first-degree family members, twins
? Other factors. A few less common factors
?Orchitis
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?Trauma?Carcinogens. LSD, hormonal therapy for sterility, copper, zinc etc
Prenatal risk factors ?
? consistent associations of testicular cancer with low birth weight
Exposures in adulthood
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? Possible etiological clues, however, include a low level of physical activity andhigh socioeconomic class
qPATHOGENESIS-vast majority of these tumours originate from germ cells
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1-Developmental disorders- contribute to the pathogenesis2-Molecular genetic features-common molecular pathogenesis of all germ cell
tumours:
? Hyperdiploidy is almost a constant feature
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? isochromosome of short arm of chromosome 12? Telomerase activity is present in all germ cell tumours of the testis
? Other mutations include p53, cyclin E and FAS gene
3-Intratubular germ cel neoplasia (ITGCN) or carcinoma insitu-
Most testicular germ cell tumors originate from a precursor lesion called
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intratubular germ cell neoplasia (ITGCN)exceptions to this rule are
? pediatric yolk sac tumors
? Teratomas
? adult spermatocytic seminoma
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4-Three hit' process. Germ cells in seminiferous tubules undergo
a. first hit-activate the cell
b. second hit- occure in CIS cell and further activate
c. third hit- via some epigenetic phenomena cell become invasive
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this sequential tumorigenesis explains the development of seminomatous tumoursCLINICAL FEATURES AND DIAGNOSIS
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? gradual gonadal enlargement and a dragging sensation in the testis? secondary symptoms such as pain, lymphadenopathy, haemoptsis and urinary
obstruction (Metastatic involvement )
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SPREAD-? Lymphatic spread- retroperitoneal para-aortic lymph nodes, mediastinal lymph
nodes and supraclavicular lymph nodes
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? Haematogenous spread -primarily occurs to the lungs, liver, brain and bones1-Intratubular germ cel neoplasia, unclassified type (IGCNU)
? Also called carcinoma in situ (CIS) stage of germ cell tumours
? preinvasive stage of germ cell tumours
? intratubular seminoma and intratubular embryonal carcinoma are common
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? 2-4% of cryptorchidism pt show? Clinical features - atrophic testis, infertility, maldescended testis, and intersex
features
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? gross- no grossly visible lesion? Histopathology - Germ cells with abundant vacuolated cytoplasm, large, irregular
nuclei and prominent nucleoli located within the seminiferous tubules
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? restricted to the seminiferous tubules without evident invasion into theinterstitium
? Immunoprofile- PLAP can be demonstrated in 83-99% of intratubular germ cell
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neoplasia of the unclassified type (IGCNU) cases and is widely used for diagnosis
Comparison of morphological features of normal seminiferous tubules (left part) and intratubular
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germ cel neoplasia (IGCNU) in seminiferous tubules (right part).
Seminoma
? Seminomas are the most common type of germ cell tumor, making up about
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(50%)
? peak incidence is the third decade and they almost never occur in infants
? An identical tumor arises in the ovary, where it is called dysgerminoma
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.
MORPHOLOGY- cut surface has a homogeneous, graywhite, lobulated, usually
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devoid of hemorrhage or necrosis
Generally the tunica albuginea is not penetrated
but occasionally extension to the epididymis, spermatic cord, or scrotal sac occurs
Microscopy- typical seminoma is composed of sheets of uniform cells divided
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into poorly demarcated lobules by delicate fibrous septa containing a lymphocytic
infiltrate
Tumor cell-
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cell is large and round to polyhedral and has a distinct cell membrane; clear orwatery-appearing cytoplasm; and a large, central nucleus with one or two
prominent nucleoli
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Stroma-
? delicate fibrous tissue which divides the tumour into lobules
? characteristic lymphocytic infiltration, indicative of immunologic response of the
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host to the tumourVariable features-
? tumor giant cells and greater mitotic activity
? 15% of seminomas contain syncytiotrophoblasts
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? ill-defined granulomatous reaction (20%)Special stain-Cytoplasm contains variable amount of glycogen that stains positively
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with PAS reactionIHC- seminoma cells stain positively for KIT, (regardless of KIT mutational status),
OCT4, and placental alkaline phosphatase (PLAP)
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Prognosis-? better than other germ cell tumours
? tumour is highly radiosensitive
Spermatocytic Seminoma-
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? Spermatocytic seminoma is both clinically and morphologically a distinctivetumour from classic seminoma
? Incidence of about 5% of all germ cell tumours
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? older patients? generally in 6th decade of life
? bilateral in 10% of patients
? Grossly, spermatocytic seminoma is homogeneous, larger, softer and
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more yellowish and gelatinous than the classic seminoma? Histological y, the distinctive features are as under:
1. Tumour cells. lymphocyte-like to huge mononucleate or multinucleate giant
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cells. Majority of cells are, however, of intermediate size. Mitoses are oftenfrequent.
2. Stroma. stroma lacks lymphocytic and granulomatous reaction seen in classic
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seminoma.? prognosis of spermatocytic seminoma is excellent
? slow-growing and rarely metastasises
? tumour is radiosensitive
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Embryonal Carcinoma-? 30% of germ cell tumours more common
? 2nd to 3rd decades of life
? 90% cases are associated with elevation of AFP or hCG or both
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Grossly,- a small tumour in the testis
? distorts the contour of the testis as it frequently invades the tunica and the
epididymis
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? Cut surface- greywhite, soft with areas of haemorrhages and necrosis
Microscopy-
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1. tumour cells are arranged in a variety of patterns-- glandular, tubular, papillaryand solid
2.tumour cells are highly anaplastic carcinomatous cells having large size, indistinct
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cell borders, amphophilic cytoplasm and prominent hyperchromatic nucleiYolk Sac Tumour (Synonyms: Endodermal Sinus Tumour,
Orchioblastoma, Infantile Embryonal Carcinoma)
? most common testicular tumour of infants and young children upto the age of 4
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year
? may be present as the major component in 40% of germ cell tumours
? AFP levels are elevated in 100% cases of yolk sac tumours
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? Grossly, the tumour is generally soft, yellow-white, mucoid with areas of necrosis
and haemorrhages
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Microscopical y, yolk sac tumour has the following features1. patterns--loose reticular network, papil ary, tubular and solid arrangement
2. flattened to cuboid epithelial cells with clear vacuolated cytoplasm
3.A pathognomonic feature is Schil er -Duvel body
a central vessel surrounded by tumor cells in a cystic space often lined by flattened
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tumor cells
4. presence of both intracellular and extracellular PAS-positive hyaline globules
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Choriocarcinoma? highly malignant tumour composed of syncytiotrophoblast and cytotrophoblast
? 2nd decade of life
? serum and urinary levels of hCG are greatly elevated in 100% cases
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? Grossly, the tumour is usually small and may appear as a soft, haemorrhagic
and necrotic mass
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? Microscopical y, the characteristic feature is syncytiotrophoblast andcytotrophoblast without formation of definite placental-type vil i
Teratoma-
? Teratomas are complex tumours composed of tissues derived from more than
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one of the three germ cell layers--endoderm, mesoderm and ectoderm
? more common in infants and children and constitute ( 40%)
? in adults they comprise 5% of all germ cell tumours
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MORPHOLOGIC FEATURES. Testicular teratomas are classified into 3 types:
1. Mature (differentiated) teratoma
2. Immature teratoma
3. Teratoma with malignant transformation
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Gross-
? large, grey-white masses enlarging testis
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? Cut surface shows characteristic variegated appearance--grey-white solid areas,cystic and honey-combed areas, and foci of cartilage and bone
Germ cell layer derivatives
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Microscopicy-? three categories of teratomas show different appearances:
1-Mature (differentiated) teratoma. Well differentiated structures such as
cartilage, smooth muscle, intestinal and respiratory epithelium, mucus glands, cysts
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lined by squamous and transitional epithelium, neural tissue, fat and bone
2-Immature teratoma.
? incompletely differentiated and primitive or embryonic tissues
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? along with some mature elements present are poorly-formed cartilage,mesenchyme, neural tissues, abortive eye, intestinal and respiratory tissue
elements etc
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? Mitoses are usual y frequent
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Immature stroma
3-Teratoma with malignant transformation-
? extremely rare form of teratoma
? one or more of the tissue elements show malignant transformation
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? Transformation may take the form of a squamous cell carcinoma, mucin-secreting adenocarcinoma, sarcoma, or other cancers.
? importance of recognizing a non?germ cell malignancy arising in a teratoma is
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that these secondary tumors are chemoresistant
Mixed Germ Cell Tumours
? About 60% of germ cel tumours have more than one of the above
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histologic types (except spermatocytic seminoma) and are cal ed mixed
germ cel tumours
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most common combinations of mixed germ cel tumours are as under:1. Teratoma, embryonal carcinoma, yolk sac tumour and syncytiotrophoblast
2. Embryonal carcinoma and teratoma (teratocarcinoma)
3. Seminoma and embryonal carcinoma
? SEX CORD-STROMAL TUMOURS-Tumours arising from specialised gonadal
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stroma
primitive mesenchyme>>>
? specialised stroma of gonads in either sex gives rise to theca, granulosa and lutein
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cells in the female
? Sertoli and interstitial Leydig cells in the male
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vLeydig (Interstitial) Cell Tumour-? 20 to 50 yr,
? secrete androgen, or both androgen and oestrogen
Grossly, as a small, well-demarcated and lobulated nodule. Cut surface is
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homogeneously yellowish or brownHistological y, the tumour is composed of sheets and cords of normal-looking
Leydig cells
These cells contain abundant eosinophilic cytoplasm and Reinke's crystals and a
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small central nucleus
vSertoli Cell Tumours (Androblastoma)-
? infants and children
? Oestrogen or androgen
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? gynaecomastia in an adult? precocious sexual development in a child
? Grossly, the tumour is large, firm, round, and well circumscribed. Cut surface is
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yellowish or yellow-grey? Microscopical y, Sertoli cell tumour is composed of benign Sertoli cells arranged
in well-defined tubules
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MIXED GERM CELL-SEX CORD STROMAL TUMOURS-? Gonadoblastoma- secrete androgen
? Grossly, the tumour is of variable size, yellowish-white and soft
? Microscopical y, gonadoblastoma is composed of 2 principal cell types--large
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germ cells resembling seminoma cells, and small cells resembling immatureSertoli, Leydig and granulosa cells
OTHER TUMOURS
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Malignant Lymphoma-? comprises 5% of testicular malignancies
? most common testicular tumour in the elderly
? Bilaterality is seen in half the cases
? Most common are large cell non-Hodgkin's lymphoma of B cell type
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Must know1-classification
2-Tumor markers in diagnosis
3-Morphology of
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a)Seminoma
b)
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Embryonal carcinoma
c)
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Yolk sac tumor4-Cryporchidism