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Testicular Cancer
• The most common cancer affecting
young men in their third or fourth
decades of life.
• Relatively rare: 1-1.5% of all cancer in
men
• Highly treatable and usually curable.
• The testicles have several types of
cells, each of which may develop into
one or more types of cancer: they
differ in the treatment and prognosis.
Testicular Cancer
Risk Factors
• Age: commonly found in men between 20 and 45.
• Family history
• Personal history: Men who have had cancer in one
testicle are at increased risk for developing cancer in
the other testicle.
• Race: white men are more likely to be diagnosed.
• Cryptorchidism: men with this condition have an
increased risk of developing testicular cancer.
• Klinefelter's syndrome (extra X chromosom): low
levels of male hormones, infertility, breast
enlargement, small testicles and increases the risk of
developing germ cell tumors.
• Human immunodeficiency virus (HIV) infection.
• Maternal oestrogen exposure
Testicular Cancer
Pathology
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More than 90% of cancers of the testicle develop in germ cells. (cells
that produce sperm).
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Germ cell tumors most commonly start in the testicles but can also
develop in other parts of the body:
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Retroperitoneum
Mediastinum
Lower spine
Pineal gland.
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Two main types of germ cell tumors occur in men:
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Seminomas may be slightly more common.
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Some cancers contain both seminoma and nonseminoma cells. These are
treated as nonseminomas.
– Seminomas
– Non-Seminomas (NSGCT).
Seminomas
• Two main subtypes
– Classical (or typical)
• More than 95% of seminomas
• Between late 30s and early 50s
– Spermatocytic
• Occur in older men (55 year old).
• Tend to grow more slowly and are less likely to
metastasize to other parts of the body than
classical seminomas
SEMINOMAS
Nonseminomas (NSGCT)
• Embryonal carcinoma
– Present in about 40% of testicular tumors.
– Pure embryonal carcinomas occur only 3% to 4% of the time.
– Tends to grow rapidly and metastasize outside the testicle.
• Yolk sac carcinoma
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Cells look like the yolk sac of an early human embryo.
Is the most common form of testicular cancer in children.
Respond very well to chemotherapy
Releases a protein into the bloodstream known as alphafetoprotein (AFP) that helps confirm the diagnosis and is
used to track the patient’s response to treatment.
Nonseminomas (NSGCT)
• Choriocarcinoma
– Very rare and aggressive
– Occurs in adults.
– Is likely to metastasize rapidly to distant organs
of the body: lungs, bone, and brain.
– Pure choriocarcinoma is rare.
– More often, choriocarcinoma cells are present with
other types of nonseminoma cells in a mixed germ
cell tumor.
– Produces a protein, human chorionic gonadotropin
(HCG), which can be used to confirm diagnosis and
to track the patient’s response to treatment.
EMBRYONAL CARCINOMA AND TERATOMA
PREDOMINANTLY TERATOMA, WITH EMBRYONAL
AND SEMINOMA HISTOLOGICALLY
Nonseminomas (NSGCT)
Teratomas
Mature teratomas
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Formed by cells similar to cells of adult tissues.
Rarely spread to nearby tissues and distant parts of the body.
Usually be cured with surgery.
Sometimes deposits of mature teratoma are found after
chemotherapy to treat a mixed NSGC: part of a tumor that was left
behind after chemotherapy but chemotherapy can change other
types of nonseminoma into teratoma.
Immature teratomas
– Cells look like those of an early embryo
– Is more likely to grow into surrounding tissues (invade) and to
metastasize outside the testicle
– Sometimes recur years after treatment.
Teratoma with malignant transformation
– Very rare
– Have some areas that look like mature teratomas but have other
areas where the cells have become a type of cancer that develops
outside of the testicle: muscles, glands of the lungs or intestines, or
the brain.
Carcinoma in situ
• Testicular germ cell cancers may begin as a noninvasive form of
the disease called carcinoma in situ (CIS) or intratubular germ
cell neoplasia.
• CIS may not always progress to cancer
• It is hard to find CIS before it develops into cancer because it
generally causes no symptoms and often does not form a lump
• The only way to diagnose CIS is to have a biopsy: incidentally in
men who have a testicular biopsy for infertility
• Since CIS doesn't always become an invasive cancer observation
(watchful waiting) is the best treatment option.
Stromal Tumors
• They develop in the supportive and
hormone-producing tissues, of the
testicles.
• Less than 4% of adult testicle tumors
but up to 20% of childhood testicular
tumors.
– Leydig cell tumors
– Sertoli cell tumors
Leydig cell tumors
• These tumors develop from the Leydig cells in
the testicle (normally produce androgens)
• Leydig cell tumors develop in both adults
(75% of cases) and children (25% of cases).
• They sometimes produce estrogens
• Most Leydig cell tumors do not metastasize
and are cured with surgery
• If they do metastasize have a poor prognosis
because they do not respond well to
chemotherapy or radiation therapy.
Sertoli cell tumors
• These tumors develop from normal
Sertoli cells, which support the spermproducing germ cells.
• They are usually benign;
• If they spread, they tend to be
resistant to chemotherapy and radiation
therapy.
Secondary Testicular Tumors
• Testicular lymphoma
– The most common secondary testicular cancer in
men older than 50.
– Prognosis depends on the type and stage of
lymphoma
– The usual treatment is surgical removal, followed
by radiation and/or chemotherapy.
• In children with acute leukemia, the leukemia
cells can sometimes form a tumor in the
testicle.
• Cancers of the prostate, lung, skin
(melanoma), kidney, also can spread to the
testicles.
• Treatment depends on the specific type of
cancer
Testicular Cancer
• Metastatic spread
– Para aortic nodes,
lung, brain and bone
– Retroperitoneal
nodes
• Why diagnosis
delayed?
– Failure to self
examine
– Failure to visit
– Delay in diagnosis
Testicular Cancer
• PRESENTATION
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• DD
Painless lump in testicle
Can “appear” after trauma
Can be painful
Noticed by partner
Breast tenderness or growth
Metastasis (back pain, Chest
pain, dyspnoea)
– Hydrocoele, spermatocoele,
calcification of scrotal
cysts, infections (orchitis,
epididymitis), injury
Self-Examination of the Testes
Testicular Cancer
Guidelines for the diagnosis and staging
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Physical examination
Testis ultrasound
Serum Markers: AFP, hCG and LDH
Pathological examination
– Biopsy: rarely done
– Radical inguinal orchiectomy
• Abdomen and chest CT scan: assessment of
retroperitoneal, mediastinal and supraclavicolar
nodes and visceral state
• Retroperitineal Lymph Node Dissection (RPLND)
Cancer Stage Grouping
• Stage 0. Carcinoma in situ
• Stage I. Cancer is limited to the testis
• Stage II. Cancer has spread to the
lymph nodes in the abdomen
• Stage III. Cancer has spread to other
parts of the body: lungs, liver, brain and
bones .
Advanced Testicular Cancer
Risk Group Classification
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Good-Risk
Intermediate-Risk
Poor-Risk
This is based on the ability to
successfully treat patients with this
disease.
• Patients with poor-risk disease still
have about a 50% chance of successful
treatment.
Testicular Cancer
Prognosis and Treatment Options
The prognosis and treatment options depend on
the following:
• Stage of the cancer (whether it is in or near
the testicle or has spread to other places in
the body, and blood levels of AFP, β-hCG, and
LDH).
• Type of cancer
• Size of the tumor
• Number and size of retroperitoneal lymph
nodes
Guidelines for the treatment
Stage I
• Seminoma
– Para-aortic prophylactic radiotherapy (20 Gy)
– Surveillance
– Carboplatin-based chemotherapy
• NSGCT
– Clinical Stage IA (no vascular invasion)
• Surveillance
• Nerve-sparing RPLND or primary chemotherapy
• If RPLND reveals lymph node disease, adjuvant chemotherapy (2
course of PEB) should be considered
– Clinical Stage IB (vascular invasion-high risk)
• Primary adjuvant chemotherapy (2 course of PEB) is
recommended
• If chemotherapy is not feasible, nerve-sparing RPLND or
surveillance with treatment at relapse (in 50% of patients) are
alternative options
Guidelines for the treatment
Stage II
• Seminoma
– Low volume: radioterapy (30-36 Gy); when
necessary chemotherapy can be used as salvage
therapy
– High volume: 3 cycles of BEP. residual tumor
resection is usually not necessary
• NSGCT
– Low volume with-out serum markers elevation:
surveillance or nerve-sparing RPLND
– Low volume with elevated serum markers:
chemotherapy (3 cycles of BEP)
Guidelines for the treatment:
Metastatic NSGCT
• Good prognosis NSGCT
– BEP x 3
• Intermediate and poor prognosis
– BEP x 4
• Residual mass >1cm with tumor markers
normal
– Surgical resection
Side Effects of Cancer and
Cancer Treatment
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Anemia
Diarrhea
Hormone deprivation symptoms in men
Infection
Nervous system disturbances
Sexual dysfunction
Skin problems
Long-term side effects
– Effects of bleomycin on lungs
– Effects of chemotherapy on kidneys
– Effects of chemotherapy on blood vessels and risk factors for heart
disease
– Effects of cisplatin on nerves and hearing
– Secondary malignancies
– Fertility
– Effects on testosterone level
– Chemobrain
Testicular Cancer
Follow-up
• Regular follow-up is vital
• Follow-up schedules depend on the
histology, stage and post-orchiectomy
treatment option chosen
• The aim is to detect relapse as early as
possible, to avoid unnecessary
treatment and to detect asynchronous
tumor in the controlateral testis
Testicular Cancer
Follow-up
• Every one-three months for one-two years.
• In each follow-up visit: physical examination, chest x-ray
and blood tests for tumor markers
• CT scan of abdomen, pelvis and chest are performed
once a year.
• Treatment of recurrent disease will depend on the stage
and extent of the reoccurred disease: experimental
chemotherapy schedules
• Radiation therapy may be helpful in managing painful or
symptomatic areas
• For patients with advanced disease, where most
treatments have failed, one could consider assistance
from hospice