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testicular cancer
Testicular cancer is a type of cancer that
develops in the testicles, a part of the male reproductive system. In
the United States, about 8,000 to 9,000 diagnoses of testicular cancer
are made each year. Over his lifetime, a man's chance of getting
testicular cancer is roughly 1 in 250 (four tenths of one percent, or
0.4%). It is most common among males aged 15-40 years. Testicular
cancer has one of the highest cure rates of all cancers: in excess of
90%; essentially 100% if it has not spread. Even for the relatively
few cases in which the cancer has spread widely, chemotherapy offers a
cure rate of at least 50%.
Symptoms and early detection
Because testicular cancer is curable (stage I can have a
success rate of >95%) when detected early, experts recommend regular
monthly testicular self-examination after a hot shower or bath, when
the scrotum is looser. Men should examine each testicle, feeling for
pea-shaped lumps. Symptoms may include one or more of the following:
a lump in one testis or a hardening of one of the testicles
pain and tenderness in the testicles
build-up of fluid in the scrotum
a dull ache in the lower abdomen or groin
an increase, or significant decrease, in the size of one testis
blood in semen [1]
Men should report any of these to a doctor as soon as possible.
The extent of testicular cancer and whether the cancer is present are
ascertained by ultrasound (of the testicles), X-rays, and/or CT scans,
which are used to locate tumors. Blood tests are also used to identify
and measure tumor markers that are specific to testicular cancer. A
biopsy should not be performed, as it raises the risk of migrating
cancer cells into the scrotum.
Differential diagnosis
An incorrect diagnosis is made at the initial examination
in up to 25% of patients with testicular tumors and may result in
delay in treatment or a suboptimal surgical approach (scrotal
incision) for exploration.
Epididymitis or epididymoorchitis
Hydrocele
Spermatocele
Granulomatous orchitis
Prevalence and distribution
Testicular cancer is most common among white males and rare
among African Americans. Worldwide incidence has doubled since the
1960s, with the highest rates of prevalence in Scandinavia, Germany,
and New Zealand. Testicular cancer is uncommon in Asia and Africa.
Incidence among African Americans doubled from 1988 to 2001 with a
bias towards seminoma. The lack of any significant increase in the
incidence of early-stage testicular cancer during this timeframe
suggests that the overall increase was not due to heightened awareness
of the disease.
Although testicular cancer is most common among men aged 15-40 years,
it has three peaks: infancy, ages 25-40 years, and age 60 years.
Pathology, staging, and genetics
Testicular cancer can be caused by any type of cell found
in the testes, but more than 95% of all testicular cancers originate
in germ cells. (Germ cells produce sperm. They are not pathogenic;
i.e., they are not to be confused with the "germs" (viruses, bacteria)
that cause illness.) In general, the remainder of this article
discusses germ-cell testicular cancer.
Germ-cell tumors are classified as either seminomas or nonseminomas
(which may be called teratomas in the UK). Seminomas are slow-growing.
Seminomas, when found, tend to be localized (i.e., only in the
testicles), simply because they spread relatively slowly. Nonseminomas,
on the other hand, tend to spread more quickly. Nonseminomas are
further classified into four subtypes; embryonal carcinomas,
choriocarcinomas, yolk sac tumors, teratomas and mixed tumors. Their
appearance under the microscope and also their gene expression is
rather distinguished from each other, their rate of spread varies
somewhat, but they are nevertheless treated similarly. When seminomas
and nonseminomas are both present (which is not unusual), the cancer
is classified as nonseminoma.
Tumor markers
Blood markers for testicular tumors include the beta
subunit of human chorionic gonadotropin (βhCG), lactate dehydrogenase
(LDH), and alpha-fetoprotein (AFP). Seminomatous tumors never present
elevated AFP levels. Placental alkaline phosphatase and other markers
are sometimes used by the pathologist to differentiate between
seminoma and nonseminomatous tumors.
Staging
After removal, a testicular tumor is staged by a
pathologist according to the TNM Classification of Malignant Tumors as
published in the AJCC Cancer Staging Manual. Testicular cancer is
categorized as being in one of three stages (which have
subclassifications). The size of the tumor in the testis is irrelevant
to staging. [2] In broad terms, tesicular cancer is staged as follows:
Stage I: the cancer remains localized to the testis.
Stage II: the cancer involves the testis and metastasis to
retroperitoneal and/or Paraaortic lymph nodes (lymph nodes below the
diaphragm).
Stage III: the cancer involves the testis and metastasis beyond the
retroperitoneal and Paraaortic lymph nodes. Stage III is further
subdivided into nonbulky stage III and bulky stage III. [3]
Genetics
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Most germ cell tumors have a chromosome count in the hypo to hyper
triploid range (i.e. 60-70 chromosomes per cell nucleus in stead of
the normal 46). About 80 % of these tumors also have a specific marker
chromosome called isochromosome 12p. This is a chromosome where the
shortest "arm" of chromosome 12 (12p) is present on both sides of the
same centromer. Among germ cell tumors not having the isochromosome
12p, almost all have increased DNA copy number of 12p through other
means. Thus, in tumors with unknown origin, increased DNA copy number
of 12p is used as a marker for germ cell origin. The general gene
expression patterns are clearly distinguishing the various
histological subtypes of germ cell tumors. For example, in embryonal
carcinomas, the same genes are overexpressed as are found highly
expressed in embryonic stem cells. Further, AFP is a gene specifically
expressed from yolk sac tumor, and CGB (encoding HCG) and other
"pregnancy related genes" are specifically expressed from
choriocarcinomas.
Germ cell tumors of the testis and their rates of
occurrence
Seminoma (35%)
Embryonal carcinoma (20%)
Teratoma (5%)
Choriocarcinoma (<1%)
Mixed Cell Type (40%)
Carcinoma in Situ [4]
Non-germ cell tumors of the testis
Leydig cell tumors
Sertoli cell tumors
Gonadoblastomas [5]
Secondary tumors of the testis
Lymphoma
Leukemic infiltration of the testis
Metastatic tumors [6]
Treatment
The three basic types of treatment are surgery, radiation
therapy, and chemotherapy.
Surgery is performed by urologists; radiation therapy is administered
by radiation oncologists; and chemotherapy is the work of medical
oncologists.
Surgery
Orchiectomy
While it may be possible, in some cases, to remove
testicular cancer tumors from a testis while leaving the testis
functional, this is almost never done, as more than 95% of testicular
tumors are malignant. Since only one testis is typically required to
maintain fertility, hormone production, and other male functions, the
afflicted testis is almost always removed completely in a procedure
called inguinal orchiectomy. (The testicle is almost never removed
through the scrotum; an incision is made beneath the belt line in the
inguinal area.) Most notably, since removing the tumor alone does not
eliminate the precancerous cells that exist in the testis, it is
usually better in the long run to remove the entire testis to prevent
another tumor. A plausible exception could be in the case of the
second testis later developing cancer as well.
RPLND
In the case of nonseminomas that appear to be stage I,
surgery may be done on the retroperitoneal/Paraaortic lymph nodes (in
a separate operation) to accurately determine whether the cancer is in
stage I or stage II and to reduce the risk that malignant testicular
cancer calls that may have metastasised to lymph nodes in the lower
abdomen. This surgery is called Retroperitoneal Lymph Node Dissection
(RPLND). However, this approach, while standard in many places,
especially the United States, is falling out of favor due to costs and
the high level of expertise required to perform the surgery.
Many patients are instead choosing surveillance, where no further
surgery is performed unless tests indicate that the cancer has
returned. This approach maintains a high cure rate because of the
growing accuracy of surveillance techniques.
Lymph node surgery may also be performed after chemotherapy to remove
masses left behind, particularly in the cases of advanced initial
cancer or large nonseminomas.
Radiation therapy
Radiation may be used to treat stage II seminoma cancers,
or as adjuvant (preventative) therapy in the case of stage I seminomas,
to minimize the likelihood that tiny, non-detectable tumors exist and
will spread (in the inguinal and para-aortic lymph nodes). Radiation
is never used as a primary therapy for nonseminoma because a much
higher dose is required and chemotherapy is far more effective in that
setting.
Chemotherapy
As an adjuvant treatment, use of chemotherapy as an
alternative to radiation therapy is increasing, because radiation
therapy appears to have more significant long-term side effects (for
example, internal scarring, increased risks of secondary malignancies,
etc.). Two doses of carboplatin, typically delivered three weeks
apart, is proving to be a successful adjuvant treatment, with
recurrence rates in the same ranges as those of radiotherapy.
Chemotherapy is the standard treatment, with or without radiation,
when the cancer has spread to other parts of the body (that is, stage
II or III). The standard chemotherapy protocol is three to four rounds
of Bleomycin-Etoposide-Cisplatin (BEP). This treatment was developed
by Dr. Lawrence Einhorn at Indiana University. An alternative, equally
effective treatment involves the use of four cycles of
Etoposide-Cisplatin (EP).
While treatment success depends on the stage, the average survival
rate after five years is around 95%, and stage I cancers cases (if
monitored properly) have essentially a 100% survival rate (which is
why prompt action, when testicular cancer is a possibility, is
extremely important).
Actions after treatment
Surveillance
For stage I cancers that have not had any adjuvant
(preventive) therapy, close monitoring for at least a year is
important, and should include blood tests (in cases of nonseminomas)
and CT-scans (in all cases), to ascertain whether the cancer has
metastasized (spread to other parts of the body). For other stages,
and for those cases in which radiation therapy or chemotherapy was
administered, the extent of monitoring (tests) will vary on the basis
of the circumstances, but normally should be done for five years (with
decreasing intensity).
Fertility
A man with one remaining testis can lead a normal life,
because the remaining testis takes up the burden of testerone
production and will generally have adequate fertility.[7] However, it
is worth the (minor) expense of measuring hormone levels before
removal of a testicle, and sperm banking may be appropriate for
younger men who still plan to have children, since fertility may be
lessened by removal of one testicle[citation needed], and can be
severely affected if extensive chemotherapy and/or radiotherapy is
done.
Less than five percent of those who have testicular cancer will have
it again in the remaining testis. A man who loses both testicles will
normally have to take hormone supplements (in particular,
testosterone, which is created in the testicles), and will be
infertile, but can lead an otherwise normal life.
Famous survivors
Decorated cyclist Lance Armstrong
American actor Richard Belzer
Canadian comedian Tom Green was diagnosed with testicular cancer in
2000 and made a widely acclaimed documentary about his treatment.
In 1997, figure-skater Scott Hamilton survived a bout with testicular
cancer.
Four English footballers (soccer players): England's World Cup winning
captain Bobby Moore was treated for testicular cancer in 1962, soon
after his international debut. More recently, Alan Stubbs, Jason Cundy,
and Neil Harris have also survived the condition.
Jos Francisco Molina , Spanish football goalkeeper from Real Club
Deportivo de la Corua, in 2001, UEFA player page
Bulgarian footballer Luboslav Penev, from Valencia, in 1994
English Snooker player Jimmy White
British drummer Philly Morris survived testicular cancer in 2003.
Afterwards, he created checkemlads.com, Europe's biggest testicular
cancer web site, with Mick Riley and Tim Stollery.
Former Major League Baseball player John Kruk, who played for the
Philadelphia Phillies when they won the 1993 National League Pennant,
but lost to the Toronto Blue Jays in the World Series. Kruk was
diagnosed during spring training in 1994.
Steve Scott, an American miler who currently holds the American Mile
Record (3:47.69). He also attempted to be the first cancer survivor to
run a sub 4:00 after completing treatment; however, his best time
following treatment was a 4:02.
Mike Lowell, Boston Red Sox third baseman was diagnosed during spring
training of his rookie year.
Christopher Arena, National Basketball Association and co-founder of
ArenaTilton Golf
Australian politician Mark Latham
Former Hereford United Exeter City and Shrewsbury Town physiotherapist
and television actor Simon Shakeshaft
American rapper Postaboy, completing his recovery in late 2005/early
2006 and back on the hip hop scene as of May 2006.
Hockey player Phil Kessel of the Boston Bruins, diagnosed during his
rookie season in 2006-07
Famous victims
Brian Piccolo, an American football player in the late
1960s with the Chicago Bears, died of a germ cell tumor that was not
detected until it had metastasized into his lungs. Piccolo would be a
major subject of teammate and friend Gale Sayers's autobiography, I Am
Third; Sayers's story of their friendship and of Piccolo's struggle
with cancer was adapted into the legendary TV movie Brian's Song.
Peter Crimmins, an Australian rules football player in the 1970s with
the Hawthorn Hawks, suffering from the cancer was forced to stand down
as captain in 1976. An emotional coach inspired the team to do it for
the little feller, with the Hawks taking out the 1976 VFL premiership
for the courageous small rover. Crimmins died just a few days after
the victory. [8]
Sean Kimerling, born on April 17, 1966, a New York sports anchor for
The WB, died of testicular cancer at the age of 37 on September 9,
2003.
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