for more information inbox me at mwebazavictor1997@gmail.com

1. M W E B A Z A
VICTOR.J
MBChB 6TH YEAR
UGANDAN
mwebazavictor1997@gmail.com
Kampala international university/
western campus @ Jinja regional
referral hospital site light.
P r o s t a t e c a n c e r
p r e s e n t a t i o n
Surgical department
Supervised by DR. Masereka
JRRHospital
16TH December/2022 @8:00AM

2. S u m m a r y o v e r v i e w
Specialty Oncology, urology
Symptoms, difficulty urinating, blood in the urine,
pain in the pelvis, back, or when urinating
Usual onsetAge > 50
Risk factorsOlder age, family history, race
Diagnostic method Tissue biopsy, medical imaging
Differential diagnosis Benign prostatic hyperplasia
Treatment Active surveillance, surgery, radiation
therapy, hormone therapy, chemotherapy
Prognosis 5-year survival rate 99%
(US)Frequency1.2 million new cases
(2018)Deaths359,000 (2018)
BYMWEBAZA
VICTOR.J
MBCHB6THYR

3. PROSTATE CANCER PRESENTATION
Prostate cancer is the development of cancer in the
prostate, a gland in the male reproductive system.
More common in men over the age of 65
"Prostate Cancer Treatment (PDQ) – Health Professional Version". National Cancer Institute. 2014-04-11.
Archived from the original on 5 July 2014. Retrieved 1 July 2014

4. History
The prostate was first formally identified by Venetian anatomist
Niccolò Massa in Anatomiae libri introductorius (Introduction
to Anatomy) 1536
and illustrated by Flemish anatomist Andreas Vesalius in Tabulae
anatomicae sex (six anatomical tables) in 1538.
Massa described it as a "glandular flesh upon which rests the
neck of the bladder," and Vesalius as a "glandular body". The
first time a word similar to 'prostate' was used to describe the
gland is credited to André du Laurens in 1600, who described
it as a term already in use by anatomists at the time.
The term was however used at least as early as 1549 by French
surgeon Ambroise Pare

5. Nahon, I; Waddington, G; Dorey, G; Adams, R (2011). "The history of urologic surgery: from reeds to robotics". Urologic nursing. 31 (3): 173–80.
PMID 21805756.
Adams J (1853). "The case of scirrhous of the prostate gland with corresponding affliction of the lymphatic glands in the lumbar region and in the
pelvis". Lancet. 1 (1547): 393–94. doi:10.1016/S0140-6736(02)68759-8.
Lytton B (June 2001). "Prostate cancer: a brief history and the discovery of hormonal ablation treatment". The Journal of Urology. 165 (6 Pt 1):
1859–62. doi:10.1016/S0022-5347(05)66228-3. PMID 11371867.

6. Anatomy of the prostate
The prostate is the largest accessory gland in the
male reproductive system.
It secretes proteolytic enzymes into the semen,
which act to break down clotting factors in the
ejaculate.

7. Precursor Endodermic evaginations
of the urethra
Artery Internal pudendal artery,
inferior vesical artery, and middle
rectal artery
Vein Prostatic venous plexus,
pudendal plexus, vesical plexus,
internal iliac vein
Nerve Inferior hypogastric plexus
Lymph internal iliac lymph nodes

8. The prostate lies below the bladder, encompasses the prostatic
urethra.
It is surrounded by a capsule, separated from rectum by
Denonvilliers aponeurosis (fascia)
Blood supply: inferior vesical artery, branch of internal iliac
The capsular branches of inf.vescical aa are a guide to pelvic
plexus arising from the S2-4 and T10-12 nerve roots.
The neurovascular bundle for erectile function lies on either side
of the prostate on the rectum.
"Dorland's Medical Dictionary". Retrieved 2007-12-11.

9. Introduction: Prostate Cancer
1. Prostate cancer is the most common noncutaneous
cancer among males,
2. Diagnosis and staging of this cancer is of great medical
and public interest
3. Prostate cancer is the second most common cause of
cancer death in males, after lung cancer.
4. The American Cancer Society estimated that 26,120
men would die from the disease in 2016.
5. Accounting for almost 10% of cancer-related deaths in
males

10. Epidemiology
An estimated one in six white men and One in five African-
American men Will be diagnosed with prostate cancer in
their lifetime, Risk of prostate cancer increases with age, as
high as 80% by age 80 years.
Prevalence rates of prostate cancer are significantly higher in
African-American men than in white men,

11. Studies have found that young African-American men
have testosterone levels that are 15% higher than in
young white men
Evidence indicates that 5-alpha reductase is active in
African Americans than in whites
In Uganda, prostate cancer is the commonest cancer
among men with an age-standardized incidence rate
for prostate cancer of 39.6 per 100,000 which is one
of the highest rates observed in Africa.

12. Risk factors
The primary risk factors are obesity, age, and
family history. Obese men have been found to
have a 34% greater death rate from prostate
cancer than those with normal weight.
Prostate cancer is uncommon in men younger
than 45, but becomes more common with
advancing age.
"Chapter 5.11". World Cancer Report. World Health Organization. 2014. ISBN 978-9283204299

13. Men with high blood pressure are more
likely to develop prostate cancer. A
small increase in risk is associated
with lack of exercise. Elevated blood
testosterone levels may increase risk.
Friedenreich CM, Neilson HK, Lynch BM (September 2010). "State of the epidemiological evidence on physical
activity and cancer prevention". European Journal of Cancer. 46 (14): 2593–604. doi:10.1016/j.ejca.2010.07.028.
PMID 20843488.

14. Genetics
Many genes are involved in prostate cancer. Mutations in
BRCA1 and BRCA2 (important risk factors for ovarian
cancer and breast cancer in women) have been
implicated. Other linked genes include hereditary
prostate cancer gene 1 (HPC1), the androgen receptor,
and the vitamin D receptor. TMPRSS2-ETS gene family
fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4
promotes cancer cell growth. These fusions can arise
via complex rearrangement chains called chromoplexy.
Gallagher RP, Fleshner N (October 1998). "Prostate cancer: 3. Individual risk factors" (PDF). CMAJ. 159 (7): 807–
13. PMC 1232741. PMID 9805030. Archived (PDF) from the original on 2009-12-29.
Struewing JP, Hartge P, Wacholder S, Baker SM, Berlin M, McAdams M, et al. (May 1997). "The risk of cancer associated with
specific mutations of BRCA1 and BRCA2 among Ashkenazi Jews". The New England Journal of Medicine. 336 (20): 1401–8.
doi:10.1056/NEJM199705153362001. PMID 9145676.

15. Two large genome-wide association studies linked
single-nucleotide polymorphisms (SNPs) to prostate
cancer in 2008.
These studies identified several relevant SNPs. For
example, individuals with TT allele pair at SNP
rs10993994 were reported to be at 1.6 times higher
risk than those with the CC allele pair
Eeles RA, Kote-Jarai Z, Giles GG, Olama AA, Guy M, Jugurnauth SK, et al. (March 2008). "Multiple newly
identified loci associated with prostate cancer susceptibility". Nature Genetics. 40 (3): 316–21. doi:10.1038/ng.90.
PMID 18264097.

16. This SNP explains part of the increased risk faced by
African-Americans. The C allele is much more
prevalent in the latter; this SNP is located in the
promoter region of the MSMB gene, thus affects
the amount of MSMB protein synthesized and
secreted by epithelial cells of the prostate.
Thomas G, Jacobs KB, Yeager M, Kraft P, Wacholder S, Orr N, et al. (March 2008). "Multiple loci identified in a
genome-wide association study of prostate cancer". Nature Genetics. 40 (3): 310–5. doi:10.1038/ng.91.
PMID 18264096. Archived from the original on 2020-08-06. Retrieved 2020-08-08.
Whitaker HC, Kote-Jarai Z, Ross-Adams H, Warren AY, Burge J, George A, et al. (October 2010). Vickers A (ed.).
"The rs10993994 risk allele for prostate cancer results in clinically relevant changes in microseminoprotein-beta
expression in tissue and urine". PLOS ONE. 5 (10): e13363. Bibcode:2010PLoSO...513363W.
doi:10.1371/journal.pone.0013363. PMC 2954177. PMID 20967219.

17. Dietary
Consuming fruits and vegetables has been found to
be of little preventive benefit. Evidence supports
little role for dietary fruits and vegetables. Red meat
and processed meat appear to have little effect.
Some studies reported that higher meat
consumption was associated with higher risk.
Lower blood levels of vitamin D may increase risks.
One study found no effect of folic acid supplements
on risk
Qin X, Cui Y, Shen L, Sun N, Zhang Y, Li J, et al. (September 2013). "Folic acid supplementation and cancer risk: a meta-analysis of
randomized controlled trials". International Journal of Cancer. 133 (5): 1033–41. doi:10.1002/ijc.28038. PMID 23338728.

18. Medication exposure
Some links have been established between
prostate cancer and medications, medical
procedures, and medical conditions. Statins may
also decrease risk.
NOTE 5α-reductase inhibitors appear to decrease low-grade cancer
risk, they do not affect high-grade cancer risk and thus are not
recommended for prevention. Supplementation with vitamins or
minerals does not appear to affect the risk.
Shannon J, Tewoderos S, Garzotto M, Beer TM, Derenick R, Palma A, Farris PE (August 2005). "Statins and
prostate cancer risk: a case-control study". American Journal of Epidemiology. 162 (4): 318–25.
doi:10.1093/aje/kwi203. PMID 16014776.

19. Infection
Prostatitis (infection or inflammation) may increase
risk. In particular, infection with the sexually
transmitted infections Chlamydia, gonorrhea, or
syphilis seems to increase risk.
Papilloma virus has been proposed in several studies
to have a potential role, but as of 2015, the evidence
was inconclusive. A 2018 review suggested possible
increased risk, but was still debatable.
Heidegger I, Borena W, Pichler R (May 2015). "The role of human papilloma virus in urological malignancies".
Anticancer Research. 35 (5): 2513–9. PMID 25964524.

20. Pathophysiology
Most prostate cancers are classified as
adenocarcinomas, or glandular cancers, that
begin when semen-secreting gland cells
mutate into cancer cells. The region of the
prostate gland where the adenocarcinoma is
most common is the peripheral zone. Initially,
small clumps of cancer cells remain within
otherwise normal prostate glands, a condition
known as carcinoma in situ or prostatic
intraepithelial neoplasia (PIN).

21. Although Over time, these cells multiply and spread
to the surrounding prostate tissue (the stroma)
forming a tumor. Eventually, the tumor may grow
large enough to invade nearby organs such as the
seminal vesicles or the rectum, or tumor cells may
develop the ability to travel in the bloodstream and
lymphatic system.
Prostate cancer most commonly metastasizes to the bones and
lymph nodes, and may invade the rectum, bladder, and lower
ureters after local progression. The route of metastasis to bone is
thought to be venous, as the prostatic venous plexus draining the
prostate connects with the vertebral veins.

22. Molecular Pathophysiology
The prostate is a zinc-accumulating, citrate-producing
organ. Transport protein ZIP1 is responsible for the
transport of zinc into prostate cells. One of zinc's
important roles is to change the cell's metabolism to
produce citrate, an important semen component.
Prostate cancer cells are generally devoid of zinc. Prostate
cancer cells save energy by not making citrate, and use
the conserved energy to grow, reproduce and spread.
The absence of zinc is thought to occur via silencing the
gene that produces ZIP1. It is called a tumor suppressor
gene product for the gene SLC39A1. The cause of the
epigenetic silencing is unknown.
Sharma, Ankur; Yeow, Wen-Shuz; Ertel, Adam; Coleman, Ilsa; Clegg, Nigel; Thangavel, Chellappagounder; Morrissey, Colm; Zhang, Xiaotun;
Comstock, Clay E. S.; Witkiewicz, Agnieszka K.; Gomella, Leonard (2010-12-01). "The retinoblastoma tumor suppressor controls androgen signaling
and human prostate cancer progression". The Journal of Clinical Investigation. 120 (12): 4478–4492. doi:10.1172/JCI44239. ISSN 0021-9738.
PMC 2993601. PMID 21099110.

23. Loss of cancer suppressor genes, early in prostatic
carcinogenesis, have been localized to
chromosomes 8p, 10q, 13q, and 16q. P53 mutations
in the primary prostate cancer are relatively low
and are more frequently seen in metastatic settings,
hence, p53 mutations are a late event in the
pathology.
Other tumor suppressor genes that are thought to
play a role include PTEN and KAI1.
"Scientists Discover Anti-Cancer Mechanism that Arrests Early Prostate Cancer". August 4, 2005. Archived from the original on May
19, 2008.

24. The androgen receptor helps cancer cells to survive.
Prostate-specific membrane antigen (PSMA) or PSA
stimulates cancer development by increasing folate
levels, helping the cancer cells to survive and grow;
it increases available folates for use by hydrolyzing
glutamated folates.
Yao V, Berkman CE, Choi JK, O'Keefe DS, Bacich DJ (February 2010). "Expression of prostate-specific membrane antigen (PSMA), increases cell
folate uptake and proliferation and suggests a novel role for PSMA in the uptake of the non-polyglutamated folate, folic acid". The Prostate. 70 (3): 305–
16. doi:10.1002/pros.21065. PMID 19830782.

25. Signs and symptoms
Early prostate cancer usually has no clear symptoms.
When they do appear, they are often similar to those of
benign prostatic hyperplasia. These include
1. frequent urination.
2. nocturia (increased urination at night).
3. difficulty starting and maintaining a steady stream of
urine.
4. hematuria (blood in the urine).
5. dysuria (painful urination).
Miller DC, Hafez KS, Stewart A, Montie JE, Wei JT (September 2003). "Prostate carcinoma presentation, diagnosis, and staging: an update form
the National Cancer Data Base" (PDF). Cancer. 98 (6): 1169–78. doi:10.1002/cncr.11635. hdl:2027.42/34379. PMID 12973840. Archived from
the original on 2021-04-17. Retrieved 2020-08-08.

26. Prostate cancer is associated with urinary dysfunction
as the prostate gland surrounds the prostatic
urethra.
Metastatic prostate cancer can cause additional
symptoms. The most common symptom is bone
pain, often in the vertebrae (bones of the spine),
pelvis, or ribs. Spread of cancer into other bones
such as the femur is usually to the part of the bone
nearer to the prostate. Prostate cancer in the spine
can compress the spinal cord, causing tingling, leg
weakness, and urinary and fecal incontinence.
van der Cruijsen-Koeter IW, Vis AN, Roobol MJ, Wildhagen MF, de Koning HJ, van der Kwast TH, Schröder FH (July 2005). "Comparison of
screen detected and clinically diagnosed prostate cancer in the European randomized study of screening for prostate cancer, section rotterdam".
The Journal of Urology. 174 (1): 121–5. doi:10.1097/01.ju.0000162061.40533.0f. PMID 15947595.

28. Diagnosis
The American Cancer Society's position regarding
early detection by PSA testing/ Prostate cancer
screening
o A histopathologic diagnosis mainly includes
assessment of whether a cancer exists, as well as
any subdiagnosis, if possible. Histopathologic
subdiagnosis has implications for the possibility and
methodology of Gleason scoring.
o If cancer is suspected, a biopsy is offered
expediently.

29. o Biochemical diagnosis Alkaline phosphatase is more
elevated in metastatic than non-metastatic cells.
High levels of alkaline phosphatase is associated
with a significant decrease in survival.
o Tumor markers Tissue samples can be stained for
the presence of PSA and other tumor markers to
determine the origin of malignant cells that have
metastasized.
The oncoprotein BCL-2 is associated with the
development of androgen-independent prostate
cancer, due to its high levels of expression in
androgen-independent tumours in advanced stages.

30. o Imaging Ultrasound and magnetic resonance
imaging (MRI) are the two main imaging methods
used for prostate cancer detection.
o Per rectal digital examination
o Rule out metastasis by also doing other systemic
investigations.
Q U E S T I O N S T O D I S C U S S

31. STAGING OF Ca
PROSTATE

32. Clinical T stage (cT) Description
cTX cannot evaluate the primary tumor
cT0 no evidence of tumor
Ct1 tumor present, but not
detectable clinically or with
imaging
cT1a tumor was incidentally found in 5% or less of prostate
tissue resected (for other reasons)
cT1b tumor was incidentally found in greater than 5% of
prostate tissue resected
cT1c
tumor was found in a needle biopsy performed due to
an elevated serum PSA
cT2 the tumor can be
felt on examination,
but has not spread
outside the prostate
cT2a the tumor is in half or less than half of one of the
prostate gland's two lobes
cT2b the tumor is in more than half of one lobe, but not
both
cT2c the tumor is in both lobes but within the prostatic
capsule
cT3 the tumor has
spread through the
prostatic capsule
cT3a the tumor has spread through the capsule on one or
both sides
cT3b the tumor has invaded one or both seminal vesicles
cT4 : the tumor has invaded other nearby structures

33. Pathological T
stage (pT)
DESCRIPTION
pT2organ
confined
pT2a Unilateral, one-half of one side or less
pT2b Unilateral, involving more than one-half of side but not both
sides
pT2c Bilateral disease
pT3Extraprostatic
extension
pT3a Extraprostatic extension or microscopic invasion of bladder
neck
pT3b Seminal vesicle invasion
pT4 Invasion of rectum, levator muscles, and/or pelvic wall

34. Evaluation of the regional lymph nodes
('N')
DESCRIPTION
NX cannot evaluate the regional lymph nodes
N0 there has been no spread to the regional
lymph nodes
N1 there has been spread to the regional
lymph nodes

35. Evaluation of distant metastasis ('M')
MX cannot evaluate distant metastasis
M0 there is no distant metastasis
M1 M1a the cancer has spread to lymph nodes
beyond the regional ones
M1b the cancer has spread to bone
M1c the cancer has spread to other sites
(regardless of bone involvement

36. Gleason grading system GGS
The Gleason grading system is used to help evaluate
the prognosis of men with prostate cancer using
samples from a prostate biopsy.
Together with other parameters, it is incorporated
into a strategy of prostate cancer staging which
predicts prognosis and helps guide therapy. A
Gleason score is given to prostate cancer based
upon its microscopic appearance.

37. Histological patterns in GGS
Pattern 1 - The cancerous prostate
closely resembles normal
prostate tissue. The glands are
small, well-formed, and closely
packed. This corresponds to a
well differentiated carcinoma.
Pattern 2 - The tissue still has well-
formed glands, but they are
larger and have more tissue
between them, implying that the
stroma has increased. This also
corresponds to a moderately
differentiated carcinoma.
Pattern 3 - The tissue still has
recognizable glands, but the cells
are darker. At high magnification,
some of these cells have left the
glands and are beginning to
invade the surrounding tissue or
having an infiltrative pattern.
This corresponds to a
moderately differentiated
carcinoma.
Pattern 4 - The tissue has few
recognizable glands. Many cells
are invading the surrounding
tissue in neoplastic clumps. This
corresponds to a poorly
differentiated carcinoma.

38. Pattern 5 - The tissue does not have any or
only a few recognizable glands. There are
often just sheets of cells throughout the
surrounding tissue. This corresponds to an
anaplastic carcinoma.
In the present form of the Gleason system,
prostate cancer of Gleason patterns 1 and
2 are rarely seen. Gleason pattern 3 is by
far the most common.

39. Primary, secondary and tertiary
grades in GGS
After analyzing the tissue
samples, the pathologist
then assigns a grade to the
observed patterns of the
tumor specimen.
Primary grade - assigned to the
dominant pattern of the
tumor (has to be greater
than 50% of the total pattern
seen).
Secondary grade - assigned to
the next-most frequent
pattern (has to be less than
50%, but at least 5%, of the
pattern of the total cancer
observed).
Tertiary grade - increasingly,
pathologists provide details
of the "tertiary" component.
This is where there is a small
component of a third
(generally more aggressive)
pattern.

40. Scores and prognoses in GGS
The pathologist then sums the pattern-number of the primary and secondary grades
to obtain the final Gleason score. If only two patterns are seen, the first number of the
score is that of the tumor's primary grade while the second number is that of the
secondary grade, as described in the previous section.
If three patterns are seen, the first number of the score would be the primary grade
and the second number the pattern with the highest grade.
For example, if the primary tumor grade was 2 and the secondary tumor grade was 3
but some cells were found to be grade 4, the Gleason score would be 2+4=6.
This is a slight change from the pre-2005 Gleason system where the second number
was the secondary grade (i.e., the grade of the second-most common cell line pattern).
Gleason scores range from 2 to 10, with 2 representing the most well-differentiated
tumors and 10 the least-differentiated tumors. Gleason scores have often been
categorized into groups that show similar biologic behavior: low-grade (well-
differentiated), intermediate-grade, moderate to poorly differentiated or high-grade.

42. Score descriptions
Gleason 1
Gleason pattern 1 is the most well-
differentiated tumor pattern. It
is a well-defined nodule of
single/separate, closely/densely
packed, back-to-back gland
pattern that does not invade
into adjacent healthy prostatic
tissue. The glands are round to
oval shaped and proportionally
large, compared to Gleason
pattern 3 tumors, and are
approximately equal in size and
shape to one another
Gleason 2
Gleason 2 is fairly well-circumscribed
nodules of single, separate glands.
However, the glands are looser in
arrangement and not as uniform as in
pattern 1.
Minimal invasion by neoplastic glands
into the surrounding healthy prostate
tissue may be seen. Similar to Gleason
1, the glands are usually larger than
those of Gleason 3 patterns, and are
round to oval in shape. Thus the main
difference between Gleason 1 and 2 is
the density of packing of the glands
seen; invasion is possible in Gleason 2,
but by definition not in Gleason 1.

43. Gleason 3
Gleason 3 is a clearly infiltrative
neoplasm, with extension into
adjacent healthy prostate
tissue. The glands alternate in
size and shape, and are often
long/angular. They are usually
small/micro-glandular in
comparison to Gleason 1 or 2
grades. However, some may be
medium to large in size. The
small glands of Gleason 3, in
comparison to the small and
poorly defined glands of
pattern 4, are distinct glandular
units. Mentally you could draw
a circle around each of the
glandular units in Gleason 3.
Gleason 4
Gleason pattern 4 glands are no longer
single/separated glands like those
seen in patterns 1-3.
They look fused together, difficult to
distinguish, with rare lumen
formation vs Gleason 1-3 which
usually all have open lumens (spaces)
within the glands, or can be
cribriform-(resembling the cribriform
plate/similar to a sieve: an item with
many perforations). Fused glands are
chains, nests, or groups of glands that
are no longer entirely separated by
stroma-(connective tissue that
normally separates individual glands
in this case).
Fused glands contain occasional stroma
giving the appearance of "partial"
separation of the glands. Due to this
partial separation, fused glands
sometimes have a scalloped (think
looking at a slice of bread with bite
taken out of it) appearance at their
edges.

44. Gleason 5
Neoplasms have no glandular
differentiation (thus not
resembling normal prostate
tissue at all). It is composed of
sheets (groups of cells almost
planar in appearance (like the
top of a box), solid cords (group
of cells in a rope like fashion
running through other
tissue/cell patterns seen), or
individual cells. You should not
see round glands with lumenal
spaces that can be seen in the
other types that resemble more
the normal prostate gland
appearance.
Prognosis
Gleason scores 2-4 are typically
found in smaller tumors located
in the transitional zone (around
the urethra). These are typically
found incidentally on surgery
for benign prostatic hyperplasia
(Note: not a precursor lesion for
prostatic carcinoma).
The majority of treatable/treated
cancers are of Gleason scores 5-
7 and are detected due to
biopsy after abnormal digital
rectal exam or prostate specific
antigen evaluation. The cancer
is typically located in the
peripheral zone usually the
posterior portion, explaining
the rationale of performing the
digital rectal exam.

45. Tumors with Gleason scores 8-10
tend to be advanced neoplasms
that are unlikely to be cured.
Although some evidence
suggests that prostate cancers
will become more aggressive
over time, Gleason scores
typically remain stable for
several years.
The Gleason scores then become
part of the TNM or Whitmore-
Jewett prostate cancer staging
system to provide prognosis.
Whitmore-Jewett staging
Although it is no longer
commonly used in practice,
the Whitmore-Jewett
system (also known as ABCD
rating) is similar to the TNM
system and has
approximately equivalent
stages
Roman numerals are
sometimes used instead of
Latin letters for the overall
stages (for example, Stage I
for Stage A, Stage II for
Stage B, and so on).

46. MANAGEMENT OF Ca PROSTATE
Treatment for prostate cancer may involve:-
1. active surveillance,
2. surgery,
3. radiation therapy – including brachytherapy (prostate
brachytherapy) and external-beam radiation therapy,
4. proton therapy,
5. high-intensity focused ultrasound (HIFU), cryosurgery,
6. hormonal therapy,
7. chemotherapy,
or some combination.

47. 1. Active surveillance
Active surveillance is observation and regular monitoring
without invasive treatment.
In the context of prostate disease this usually comprises
regular PSA blood tests and prostate biopsies.
Active surveillance is often used when an early stage,
slow-growing prostate cancer is suspected.
However, watchful waiting may also be suggested when
the risks of surgery, radiation therapy, or hormonal
therapy outweigh the possible benefits.
Study results in 2011 suggest active surveillance is the best choice for
older 'low-risk' patients.
"Active Surveillance May Be Preferred Option in Some Men with Prostate Cancer". Archived from the original on 3
May 2011.

48. 2. Surgery Prostatectomy
o Radical prostatectomy
Radical prostatectomy is effective for tumors that have
not spread beyond the prostate
However, it may cause nerve damage that may
significantly alter the quality of life of the prostate
cancer survivor. Radical prostatectomy has been
associated with a greater decrease in sexual function
and increased urinary incontinence (mainly stress
incontinence) than external beam radiotherapy, an
alternative treatment.
1 2 Chen C, Chen Z, Wang K, Hu L, Xu R, He X (November 2017). "Comparisons of health-related quality of life
among surgery and radiotherapy for localized prostate cancer: a systematic review and meta-analysis".
Oncotarget. 8 (58): 99057–65. doi:10.18632/oncotarget.21519. PMC 5716791. PMID 29228751.

49. Hint on Prostatectomy
There are two main types of prostatectomies. A
simple prostatectomy (also known as a subtotal
prostatectomy) involves the removal of only part of
the prostate. Surgeons typically carry out simple
prostatectomies only for benign conditions. A
radical prostatectomy, the removal of the entire
prostate gland, the seminal vesicles and the vas
deferens, is performed for malignant cancer
McAninch, Jack W. (2008). Smith and Tanagho's General Urology. New York: McGraw Hill Medical. p. 368.
ISBN 978-0-07-162497-8.

50. o Laparoscopic approach
Laparoscopic radical prostatectomy (LRP) is a new way
to approach the prostate surgically with intent to
cure. Contrasted with the open surgical form of
prostate cancer surgery, laparoscopic radical
prostatectomy requires a smaller incision. Relying
on modern technology, such as miniaturization,
fiber optics, laparoscopic radical prostatectomy is a
minimally invasive prostate cancer treatment but is
technically demanding and seldom performed in
the United States.

51. o Transurethral resection
Transurethral resection of the prostate, commonly called
a "TURP," is a surgical procedure performed when the
tube from the bladder to the penis (urethra) is blocked
by prostate enlargement. In general, TURP is done for
benign prostatic hyperplasia and is not meant as
definitive treatment for prostate cancer. During a TURP,
a small instrument (cystoscope) is placed into the penis
and the blocking prostate is cut away by cautery.

52. o Cryosurgery
Cryosurgery is a minimally invasive method of treating prostate
cancer in which the prostate gland is exposed to freezing
temperatures.
Under ultrasound guidance metal rods are inserted through the
skin of the perineum into the prostate. Highly purified argon
gas is used to cool the rods, freezing the surrounding tissue at
−186 °C (−302 °F). As the water within the prostate cells
freezes, the cells die. The urethra is protected from freezing
by a catheter filled with warm liquid.
General anesthesia is less commonly used for cryosurgery
meaning it can often be performed in an outpatient clinic
setting.
Jung JH, Risk MC, Goldfarb R, Reddy B, Coles B, Dahm P, et al. (Cochrane Urology Group) (May 2018). "Primary cryotherapy for
localised or locally advanced prostate cancer". The Cochrane Database of Systematic Reviews. 2018 (5): CD005010.
doi:10.1002/14651858.CD005010.pub3. PMC 6494517. PMID 29845595.

53. o Surgical removal of the testicles
In metastatic disease, where cancer has spread beyond
the prostate, removal of the testicles (called
orchiectomy) may be done to decrease testosterone
levels and control cancer growth. (See hormonal
therapy, below).
oRobotic assistance
Some believe that in the hands of an experienced
surgeon, robotic-assisted laparoscopic prostatectomy
(RALP) may reduce positive surgical margins when
compared to radical retropubic prostatectomy (RRP)
among patients with prostate cancer according to a
retrospective study.
Smith JA, Chan RC, Chang SS, Herrell SD, Clark PE, Baumgartner R, Cookson MS (December 2007). "A comparison of the
incidence and location of positive surgical margins in robotic assisted laparoscopic radical prostatectomy and open retropubic radical
prostatectomy". The Journal of Urology. 178 (6): 2385–9, discussion 2389–90. doi:10.1016/j.juro.2007.08.008. PMID 17936849.

54. 3. Radiation therapy
Radiation therapy, also known as radiotherapy,
is often used to treat all stages of prostate
cancer. It is also often used after surgery if the
surgery was not successful at curing the
cancer. Radiotherapy uses ionizing radiation to
kill prostate cancer cells.

55. 4. High intensity focused ultrasound
High intensity focused ultrasound (HIFU) was first used in
the 1940s and 1950s in efforts to destroy tumors in the
central nervous system. Since then, HIFU has been
shown to be effective at destroying malignant tissue in
the brain, prostate, spleen, liver, kidney, breast
HIFU for prostate cancer utilizes ultrasound to
ablate/destroy the tissue of the prostate. During the
HIFU procedure, sound waves are used to heat the
prostate tissue, thus destroying the cancerous cells.,
and bone
Gardner TA, Koch MO (December 2005). "Prostate cancer therapy with high-intensity focused ultrasound". Clinical Genitourinary
Cancer. 4 (3): 187–92. doi:10.3816/CGC.2005.n.031. PMID 16425987. S2CID 22955796.

56. 5. Hormonal therapy
o Androgen deprivation therapy
Blocking DHT often causes prostate cancer to stop growing and
even shrink. However, hormonal therapy rarely cures prostate
cancer because cancers that initially respond to hormonal
therapy typically become resistant after one to two years.
Hormonal therapy is, therefore, usually used when cancer has
spread from the prostate. It may also be given to certain men
undergoing radiation therapy or surgery to help prevent
return of their cancer.
Robson M, Dawson N (June 1996). "How is androgen-dependent metastatic prostate cancer best treated?". Hematology/Oncology
Clinics of North America. 10 (3): 727–47. doi:10.1016/S0889-8588(05)70364-6. PMID 8773508. Review.

57. Antiandrogens are medications such as flutamide,
nilutamide, bicalutamide, enzalutamide, apalutamide,
and cyproterone acetate that directly block the actions
of testosterone and DHT within prostate cancer cells.
Medications that block the production of adrenal
androgens such as DHEA include ketoconazole and
aminoglutethimide.
GnRH antagonists such as abarelix and degarelix
suppress the production of LH directly by acting on the
anterior pituitary. GnRH agonists such as leuprorelin
and goserelin suppress LH through the process of
downregulation after an initial stimulation effect which
can cause initial tumor flare.

58. o Estrogen therapy
High-dose estrogen therapy is used in the treatment of
prostate cancer. Estrogens that have been used include
diethylstilbestrol, fosfestrol, ethinylestradiol,
ethinylestradiol sulfonate, polyestradiol phosphate, and
estradiol undecylate, as well as the dual estrogenic and
cytostatic agent estramustine phosphate. Newer
estrogens with improved tolerability and safety like
GTx-758 have also been studied.
Estrogens are effective in prostate cancer because they
are functional antiandrogens.
Oettel M, Schillinger E (2012). Estrogens and Antiestrogens II: Pharmacology and Clinical Application of Estrogens and Antiestrogen. Handbook
of Experimental Pharmacology. Vol. 135 / 2. Springer Science & Business Media. pp. 540–42. doi:10.1007/978-3-642-60107-1. ISBN 978-3-642-
60107-1. S2CID 35733673

59. Recurrent disease
After surgery or radiation therapy, PSA may start to rise again At
10 years of follow-up after surgery, there is an overall risk of
biochemical recurrence of 30–50%,
SRT is often administered in combination with androgen
deprivation therapy for up to two years.
A retrospective study of patients treated with SRT salvage
radiation therapy between 1987 and 2013 found that 56% of
2460 patients were free from biochemical failure after 5 years
follow-up. Among those with a PSA less than 0.2 before SRT,
this was 71%.
Tendulkar RD, Agrawal S, Gao T, Efstathiou JA, Pisansky TM, Michalski JM, et al. (October 2016). "Contemporary Update of a Multi-Institutional
Predictive Nomogram for Salvage Radiotherapy After Radical Prostatectomy". Journal of Clinical Oncology. 34 (30): 3648–3654.
doi:10.1200/JCO.2016.67.9647. PMID 27528718.

60. Prevention of Ca Prostate
o Diet and lifestyle
Fish may lower prostate-cancer deaths, but does not
appear to affect occurrence.
Some evidence supports lower rates of prostate cancer
with a vegetarian diet/, lycopene, selenium cruciferous
vegetables, soy, beans and/or other legumes.
"American Cancer Society Guidelines on Nutrition and Physical Activity for Cancer Prevention" (PDF). American Cancer Society.
Archived (PDF) from the original on 2012-06-25.
Regular exercise may slightly lower risk, especially vigorous
activity.

61. o Medications
In those who are regularly screened, 5-alpha-
reductase inhibitors (finasteride and dutasteride)
reduce the overall risk of prostate cancer. Data are
insufficient to determine if they affect fatality risk
and they may increase the chance of more serious
cases.
Wilt TJ, MacDonald R, Hagerty K, Schellhammer P, Kramer BS (April 2008). Wilt TJ (ed.). "Five-alpha-reductase
Inhibitors for prostate cancer prevention". The Cochrane Database of Systematic Reviews (, 2): CD007091.
doi:10.1002/14651858.CD007091. PMID 18425978.

62. o Patient education
With the advent of PSA screening, men require
education about prostate cancer and how it is
diagnosed, staged, and treated.
Such education allows patients to make
informed decisions about screening and
treatment options.
Up-to-date information is available through the National Cancer Institute and the American
Cancer Society, as well as Prostate Videos.com.
See Rx protocol at http://emedicine.medscape.com/article/2007095-overview

63. Prostate cancer screening
Prostate cancer screening searches for cancers
in those without symptoms. Options include
the digital rectal exam and the PSA blood test.
Alberts AR, Schoots IG, Roobol MJ (June 2015). "Prostate-specific antigen-based prostate cancer screening: Past
and future". International Journal of Urology. 22 (6): 524–32. doi:10.1111/iju.12750. PMID 25847604.

64. Screening for prostate cancer
The American Cancer Society (ACS) recommends that men
decide whether to be screened for prostate cancer
based on informed consent including limitations.
The recommended age for starting screening is as follows:
1. 50 yrs for men at average risk who have at least a 10-
year life expectancy
2. 40 or 45 yrs for African Americans and men who have
had a first-degree relative diagnosed with prostate
cancer before age 65 yrs
3. 40 yrs for men with several first-degree relatives who
had prostate cancer at an early age

66. Prognosis of prostate cancer
Depending on the PSA value, pathologic stage, and histologic grade of
the tumor, approximately 30% of patients with clinically localized
prostate cancer are estimated to progress despite initial treatment
with intent to cure.
The Cancer of the Prostate Risk Assessment (CAPRA) score for predicting
prognosis is calculated on:
1. PSA level
2. Gleason score
3. Percentage of biopsy cores positive for cancer
4. Clinical tumor stage
5. Age at diagnosis

67. Morbidity and mortality
1. Current prostate cancer treatments, including radical
prostatectomy and radiation therapy, result in erectile
dysfunction and urinary incontinence.
2. African-American patients are more prone to erectile
dysfunction and urinary continence compared with non–
African Americans.
3. Radiation therapy for prostate cancer is associated with
increased risk of secondary malignancy like rectal cancer
bladder cancer.
4. In men with distant disease, however, survival is only 28%.

68. Am a master seed planted by GOD.
Thank You father YAHWE in heaven for the man am
becoming...
I will be a common person but my happiness settle
me up ......... A M E N