Prostate cancer

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Prostate carcinoma
Diagnosis in short

Prostate carcinoma. H&E stain.

LM major criteria: abnormal architecture (increased gland density, usu. small circular glands, "infiltrative growth" pattern), basal cells lost, cytological abnormalities (nuclear enlargement, nucleoli); minor criteria: nuclear hyperchromasia, wispy blue mucin, pink amorphous secretions, intraluminal crystalloid, amphophilic cytoplasm, adjacent HGPIN, mitoses
LM DDx high-grade prostatic intraepithelial neoplasia, atypical small acinar proliferation (biopsy only), prostatic atrophy, seminal vesicle, basal cell hyperplasia, others
IHC PSA +ve, PSAP +ve, AMACR +ve, p63 -ve, CK34betaE12 -ve
Molecular +/-BRCA1 mutation (genetic predisposition), +/-BRCA2 mutation (genetic predisposition)
Gross usu. posterior aspect of the prostate - often not apparent at gross
Grossing notes prostate biopsy, prostate chips, radical prostatectomy
Staging prostate cancer staging
Site prostate gland

Signs firm, nodular prostate on digital rectal exam
Symptoms often asymptomatic
Prevalence very common
Blood work PSA elevated (common)
Radiology hypoechoic areas, no apparent abnormality
Prognosis good-to-poor (depends on grade (Gleason score) and stage)
Clin. DDx prostatitis, nodular hyperplasia of the prostate
Treatment observation (common for low-grade, low tumour burden), radiation or radical prostatectomy

This article deals with prostate cancer.

The vast majority of prostate cancers are carcinomas and could be labelled prostatic carcinoma. Most prostatic carcinomas are gland forming; thus, they can be labelled prostatic adenocarcinoma or adenocarcinoma of the prostate.

Benign pathology of the prostate gland, and prostate histology and anatomy are dealt with in the prostate gland article.

Conventional prostate cancer

General

  • Very common.
  • Increasing incidence with age - the age in years is an approximation of the percentage of men with prostate cancer.[1][citation needed]
  • Usually an indolent course - most old men die with prostate cancer not from prostate cancer.
  • Risk increased with a BRCA1 or BRCA2 mutation[2] - families have a mix of breast cancer and prostate cancer.
    • BRCA2 mutation risk >8x for men over 65 years old.[3]
    • A BRCA2 founder mutation is described in French Canadians.[4]

Management

Dirty first approximation

  • The management changes between Gleason score 6, 7 (3+4), 7 (4+3) and 8.

Typically, the implications are:

  • Gleason 6: observation or radioactive seeds; surgery if patient wants.
  • Gleason 7 with a bit of Gleason pattern 4 and a low tumour volume: it is reasonable to watch or do something. ‡
  • Gleason 7 with a lot of Gleason pattern 4 or a high tumour volume: do something -- surgery or radiation therapy.
  • Gleason 8+: bad cancer -- do something quickly!

Note:

  • ‡ It has been said that Gleason score 7 with a bit of Gleason pattern 4 is the new Gleason score 6.

Bottom line:

  • You want to be sure when you call something Gleason pattern 4.

Observational strategies

  • Delay of definitive treatment (surgery or radiation).
  • Common in the management of prostate cancer.

Classification:[5]

  • Active surveillance (AS).
    • Low risk of progression.
    • May get definitive treatment later.
  • Watchful waiting (WW).
    • Higher risk of progression.

Note:

  • There is no agreed upon set of criteria for active surveillance, and the large number of criteria out there vary significantly.[6]
Active surveillance

The Klotz criteria for active surveillance - pathologic factors only:[6][7]

  • Gleason score 6 or less.
  • All biopsies cores < 50% involvement.
  • One or two cores involved.[8][9][10]

Clinical criteria:

  • PSA <= 10 ng/mL.[6]

Gross

  • Prostate cancer is uncommonly apparent on gross.
  • Classic location: posterior aspect of the prostate.

Radiology

  • Hypoechoic areas = suspicious for cancer.
    • It seems that size of the area matters.
      • Small hypoechoic areas (<0.2 cm3) have cancer less than 4% of the time.[11]
      • One study suggests hypoechoic lesions tend to have a worse outcome;[12] however, this is not supported by an older study.[13]

Prostatectomy grossing

Cytoprostatectomy grossing

  • Limited sampling of the prostate may lead to undersampling error.[14]

Microscopic

Criteria as a list

Major criteria (the ABCs of prostate pathology):[15]

  1. Architecture.
    • Increased gland density.
    • Small circular glands.
      • In rare subtypes - large branching glands.
    • "Infiltrative growth" pattern - malignant glands between benign ones.
  2. Basal cells lacking.
  3. Cytological abnormalities:
    • Nuclear enlargement (subtle).
    • Nucleoli (prominent).

Minor criteria:[15]

  1. Nuclear hyperchromasia.
  2. Wispy blue mucin.
  3. Pink amorphous secretions.
  4. Intraluminal crystalloid.
  5. Amphophilic cytoplasm.
  6. Adjacent HGPIN.
  7. Mitoses - quite rare.

Extent/quantity criteria:

  • There is no agreed upon minimum number of glands; however, one paper suggests that agreement among experts is low with 5 or less glands.[18]
    • Thus, it has been suggested that six or more glands should be present to diagnose cancer.[18]

Features considered pathognomonic for prostate carcinoma by some authorities:[19][20]

  1. Perineural invasion.
  2. Glomeruloid bodies.
  3. Collagenous micronodules also known as mucinous fibroplasia.

Divided into high and low power

Low power features

  • Architecture is the key to diagnosing low grade cancer.
    • Back-to-back glands or crowding of glands -- think low grade cancer (Gleason pattern 3).
    • Sharp transition between gland border and lumen.
      • Loss of epithelial folding at the epithelium-gland lumen interface - "punched-out" appearance.
    • Eosinophilic debris within the gland lumen (pink amorphous secretions, intraluminal crystalloid).
    • Blue-tinged acellular material within the gland lumen (mucin) -- uncommon.
    • "Infiltrative": small round/oval (malignant) glands (approx. 5 cells across) interspersed with larger (benign) glands that are 2-3 times larger.

High power features

  • Nuclear changes.
    • Hyperchromatic nuclei (like in HGPIN).
    • Nuclear enlargement, mild (10%?).
      • Difficult to appreciate (if cancer isn't side-by-side with normal prostate).
      • Difficult/impossible to see at low power.
  • "Large" nucleoli.
    • Visible on intermediate and high power (100x / 200x magnification).
      • May be difficult to see - especially if light intensity is low or the staining is of poor quality.
      • One should not use 400x to look for nucleoli (it is a waste of time + you risk over-calling something benign).
    • "Large" is rarely precisely quantified; 3 micrometres has been suggested as "large" based on one study.[21]
      • Three micrometres is a little more than 1/3 of RBC diameter.
  • Loss of basal cells - diagnostic feature.
    • Like in breast pathology (where one looks for loss of myoepithelial cells) - this may be difficult to see.

Notes:

  • Mitoses are not a common feature.
    • If you find them the lesion is probably high-grade.
    • Generally, it isn't worth looking for them.

Mimics

Mimics of prostate adenocarcinoma:[22]

Entity Key feature Detailed microscopic Other Image
Adenosis (AKA atypical adenomatous hyperplasia) gradual transition between normal & small gland (NOT two populations) many small glands, lack nuclear size variation, basal layer present nucleoli may be present; may need to do p63 or 34betaE12 to find basal layer
Adenosis of prostate. (WC)
Sclerosing adenosis gradual transition between normal & small gland (NOT two populations), fibrosis many small glands, lack nuclear size variation, basal layer present analogous to sclerosing adenosis of the breast[citation needed] Sclerosing adenosis (webpathology.com)
Atrophy sharp angulation of gland nuclear hyperchromasia, scant cytoplasm may appear right beside non-atrophic tissue
Prostatic atrophy. (WC)
Basal cell hyperplasia two distinct cell populations (in epithelial component) abundant epithelial cells; nucleoli in pale ('blue') nuclei of basal cells, glandular cell nuclei darker ('purple') vaguely similar to epithelial hyperplasia of usual type (EHUT) in breast
Prostatic BCH. (WC)
Bulbourethral gland no nuclear atypia clear cytoplasm apex of prostate
Bulbourethral gland. (WC)
Seminal vesicles / ejaculatory ducts lipofuscin (yellow granular material in cytoplasm), smudge cells (smeared appearance + hyperchromatic) fern-like arrangement of epithelium (low power), nucleoli, surrounded by muscle, +/- nuclear inclusions involvement by cancer changes staging, lipofuscin may be present in prostate, often has marked nuc. size var.; location: usu. base of prostate
Seminal vesicles. (WC)
Radiation effect marked nuclear size variation increased stroma (fibrosis), lack nucleoli ??? history of Rx; uniform nuc. size with Hx of Rx should raise susp. of postradiation cancer
Radiation change. (WC)
Prostatitis inflammatory cells (lymphocytes, plasma cells, PMNs) no nuclear atypia, normal gland arch. clinical mimic of cancer (elevated PSA); usu. not a problem for the pathologist
Prostatic inflammation. (WC)
Vasitis nodosa sperm within ducts, clinical history (usu. post-vasectomy) small tubules, nucleoli common, mild atypia, may "invade" vessels, track along nerves mimics metastatic prostate carcinoma, IHC stains: PSA-, PSAP-
VN. (WC)

Memory device: AAABBRS = atrophy, adenosis, adenosis (sclerosing), basal cell hyperplasia, bulbourethral gland, radiation, seminal vesicles.

Prostatic adenocarcinoma variants that mimic benign

Prostate cancer grading

It covers the Gleason grading system and the (new) prognostic grade groupings.

Staging parameters, margins and more

Surgical margins

  • Positive is tumour touching ink.† [23]
    • "Close" margins (<0.1 mm) have an increased recurrence risk.[23]

Notes:

  • Surgical margin - where the surgeon cut.
    • It is possible to have EPE without a positive margin.
    • It is possible to have a positive margin without EPE.
  • † Epstein says not touching may be enough, as tumour close to the margin is damaged from the surgery.[24]
Rates and implication

Positivity rate varies substantially (13-44%):

  • Norway: 26% -- strong dependence on surgeon volume (18% high case load vs. 44% low case load).[25]
  • France: 13-17% -- PSA and prostate size predictors of positivity.[26]

Note:

  • Stage and grade (Gleason score) seem to have less impact than surgeons volume on margin positivity rate.[25]

The impact of positive margins:

  • Significant modest negative affect on long-term outcome in node negative cancers (pT2-4 pN0).[27]
  • Weaker impact than stage and Gleason score.[28]
  • Bladder neck margin positivity may change the T-stage - see below.
Bladder neck margin
AKA invasion of the bladder neck.[29]
  • Bladder neck margin positivity typically is pT3a.[30]
  • Seen in approximately 1% of prostatectomies.[29]
Image

Extraprostatic extension

Abbreviated EPE.

Seminal vesicle invasion

Abbreviated SVI.

Perineural invasion

  • Not a staging parameter.
  • Seen in approximately 20% of core biopsies.[32]
  • Complete wrapping of a nerve by epithelium is considered pathognomonic for cancer.[20][32]

Note:

  • Occasionally, benign glands are found perineural.[32]
    • These should not completely wrap around the nerve and should be cytologically benign.

IHC

General recommendations

ISUP consensus statement:[33]

  • Should not be used if cancer is obvious.
  • Should not be used if it isn't going change the clinical management.

Prostate markers

  • PSA (prostate specific antigen) +ve.
  • PSAP (prostatic specific acid phosphatase) +ve. †
  • P501S +ve. ‡
  • NKX3.1 +ve. ‡

Notes:

  • † PSAP may be positive in hindgut neuroendocrine tumours.[34]
  • ‡ P501S and NKX3.1 are considered second line markers.[33]
  • Prostate carcinoma is typically CK7 -ve and CK20 -ve; however, in high Gleason score cancers focal positivity of these markers can be seen.[35]
    • CK7: >25-50% staining seen in ~5% of cases.
      • >50% staining with CK7 is not report.
    • CK20: >25-50% staining seen in ~10% of cases.
      • >50% staining with CK20 is not reported.

Benign prostate versus neoplastic prostate

  • AMACR +ve.
  • p63 -ve.
  • HMWCK (34betaE12) -ve.

Combination immunostains:

  • PIN-4 -- consists of: CK5 + CK14 + p63 + P504S (AMACR).[36][37][38]
    • AKA PIN.
    • AKA CAP.
      • Why CAP?
        • A. CAncer of the Prostate.

Other IHC stains:

  • AR +ve -- in prostate confined cancer.
    • Usually -ve in lymph node +ve disease.[39]

Note:

  • Bcl-2 marks basal cells in prostate cancer.[40]

Prostate carcinoma versus urothelial carcinoma

The ISUP panel recommends:[33]

  • PSA +ve (-ve in UCC).
  • GATA3 -ve (+ve in UCC).

Another panel - if GATA3 isn't available:

  • Prostate: PSA +ve, p63 -ve, HWMCK -ve.
  • Urothelial: p63 +ve, HWMCK +ve, PSA -ve.

Notes:

  • AMACR not useful; it is positive in ~50% of UCC.[41]
  • CK7 and CK20 are typically negative in prostate carcinoma, and classically positive in urothelial carcinoma.
  • CK34betaE12 may be positive in prostate cancer; 43% of cases in one small series of cases with lymph node metastases.[42]

Rate of utilization

  • Dependent on practise setting.
    • One tertiary academic institution uses it on ~ 40% of cases.[43]

Molecular changes in prostate cancer

A fusion gene between TMPRSS2 and ERG is described.[44][45]

  • Both genes are on chromosome 21.
  • Currently not used diagnostically.
  • Fusion gene seen in approximately 50% of prostate cancer.[45]
  • A subset of TMPRSS2-ERG known as 2+Edel (seen in ~7% of all prostate cancer cases) predicts poor survival.[46]

Sign out

Prostatectomy specimens

A. LYMPH NODES, RIGHT PELVIC, EXCISION:
- ONE LYMPH NODE NEGATIVE FOR MALIGNANCY ( 0 POSITIVE / 1 ).

B. LYMPH NODES, LEFT PELVIC, EXCISION:
- ONE LYMPH NODE NEGATIVE FOR MALIGNANCY ( 0 POSITIVE / 1 ).

C. PROSTATE GLAND AND SEMINAL VESICLES, RADICAL PROSTATECTOMY:
- ADENOCARCINOMA, GLEASON SCORE 7/10 (3+4), pT2c pN0.
-- SURGICAL MARGINS NEGATIVE.
-- PLEASE SEE TUMOUR SUMMARY.

Transurethral resection of prostate

PROSTATE TISSUE, TRANSURETHRAL RESECTION OF PROSTATE (TURP):
- ADENOCARCINOMA, GLEASON SCORE 7/10 (3+4);
- APPROXIMATELY 5% OF TISSUE INVOLVED;
- PLEASE SEE TUMOUR SUMMARY.


TUMOUR SUMMARY - TRANSURETHRAL RESECTION OF PROSTATE (TURP).

PROCEDURE: TRANSURETHRAL PROSTATIC RESECTION.
SPECIMEN SIZE: WEIGHT: 10 GRAMS.
HISTOLOGIC TYPE:  ADENOCARCINOMA (ACINAR, NOT OTHERWISE SPECIFIED).

HISTOLOGIC GRADING:
PRIMARY PATTERN: 3.
SECONDARY PATTERN: 4 (40% OF TUMOUR).
TOTAL GLEASON SCORE: 7 (3+4).

TUMOUR QUANTITATION - PERCENTAGE OF PROSTATIC TISSUE INVOLVED BY TUMOUR: 80 %.

PERIPROSTATIC FAT INVASION: NOT IDENTIFIED.
SEMINAL VESICLE INVASION: NOT IDENTIFIED.
LYMPH-VASCULAR INVASION: NOT IDENTIFIED.
PERINEURAL INVASION: NOT IDENTIFIED.

ADDITIONAL PATHOLOGIC FINDINGS:
HIGH-GRADE PROSTATIC INTRAEPITHELIAL NEOPLASIA (HGPIN).
NODULAR PROSTATIC HYPERPLASIA.
CHRONIC INFLAMMATION.
 PROSTATE TISSUE, TRANSURETHRAL RESECTION OF THE PROSTATE (TURP):
- ADENOCARCINOMA, GLEASON SCORE 6/10 (3+3);
- APPROXIMATELY 5% OF TISSUE INVOLVED;
- PLEASE SEE TUMOUR SUMMARY.
Prostate Tissue, Transurethral Resection of Prostate (TURP):
- Adenocarcinoma, Gleason score 7 (3+4)
- Approximately 3% of sampled tissue involved
- Please see tumour summary

Tumour summary:
Procedure: Transurethral resection of prostate
Specimen weight: 11.7 g
Histologic type: Adenocarcinoma, acinar type

Histologic grade:
Primary pattern: 3
Secondary pattern: 4 (<15% of tumor)
Total Gleason score: 7/10 (3+4)

Tumor volume: 3% of tissue

Periprostate fat invasion: Periprostatic fat not identified
Seminal vesicle invasion: Seminal vesicle not identified
Lymphovascular inasion: Not identified
Perineural invasion: Not identified

Additional findings:
Glandular and stromal hyperplasia
Mild chronic inflammation

Biopsy specimens

Important elements - a list:[15]

  1. Type of cancer, e.g. "prostatic adenocarcinoma, acinar type".
  2. Gleason score including primary and secondary pattern, e.g. "Gleason score 3+4=7".
  3. Number of cores and number involved, e.g. "2/3 cores involved by cancer".
  4. Percent area involved, i.e. how much of the core is cancer, e.g. "75% of specimen is tumour". ‡
  5. Percent area involved that is Gleason pattern 4 or 5, e.g. "25% of the tumour is Gleason pattern 4 or 5".
  6. Presence of perineural invasion.
  7. Presence of extension into fat (extraprostatic extension).

Notes:

  • ‡ "Percent area involved" may seem like an odd thing to request 'cause it is sampling dependent, i.e. if the radiologist sticks the biopsy needle deeper into the lesion more of the core is positive, but urologists think it is important -- more important than perineural invasion.[47]
    • There is disagreement on how one should measure patchy cancer (cancer when there is interspersed normal). Epstein believes one should include the interspersed benign if the cancer is patchy, as the groupings of tumour likely join out of the plane of section.[48]
    • A review by Epstein on the topic of tumour volume suggests it does not have predictive value in multivariante analyses.[48]
    • The biopsy tumour volume is a predictor of Gleason score upgrading on prostatectomy.[49]

Completely negative

A. PROSTATE, RIGHT LATERAL SUPERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

B. PROSTATE, RIGHT MEDIAL SUPERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

C. PROSTATE, RIGHT LATERAL MIDZONE, BIOPSY:
- BENIGN PROSTATE TISSUE.

D. PROSTATE, RIGHT MEDIAL MIDZONE, BIOPSY:
- BENIGN PROSTATE TISSUE.

E. PROSTATE, RIGHT LATERAL INTERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

F. PROSTATE, RIGHT MEDIAL INFERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

G. PROSTATE, LEFT LATERAL SUPERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

H. PROSTATE, LEFT MEDIAL SUPERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

I. PROSTATE, LEFT LATERAL MIDZONE, BIOPSY:
- BENIGN PROSTATE TISSUE.

J. PROSTATE, LEFT MEDIAL MIDZONE, BIOPSY:
- BENIGN PROSTATE TISSUE.

K. PROSTATE, LEFT LATERAL INTERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

L. PROSTATE, LEFT MEDIAL INFERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE.

Negative biopsy in surveillance

COMMENT:
The previous results are noted. The absence of cancer in this biopsy may
be due to sampling.

No glands

F. PROSTATE, RIGHT MEDIAL MIDZONE, BIOPSY:
- BENIGN FIBROMUSCULAR TISSUE;
- NO PROSTATIC GLANDULAR TISSUE PRESENT.

Inflammation

G. PROSTATE, LEFT LATERAL SUPERIOR, BIOPSY:
- BENIGN PROSTATE TISSUE;
- FOCAL CHRONIC INFLAMMATION. 
F. PROSTATE, RIGHT MEDIAL MIDZONE, BIOPSY:
- BENIGN PROSTATE TISSUE;
- CHRONIC INFLAMMATION. 
F. PROSTATE, RIGHT MEDIAL MIDZONE, BIOPSY:
- BENIGN PROSTATE TISSUE;
- ACUTE AND CHRONIC INFLAMMATION. 

Positive

F. PROSTATE, RIGHT MEDIAL INFERIOR, BIOPSY:
- ADENOCARCINOMA, GLEASON SCORE 6/10 (3+3);
- 1/1 CORE INVOLVED; APPROXIMATELY 5% OF TISSUE INVOLVED.
F. PROSTATE, RIGHT MEDIAL INFERIOR, BIOPSY:
- ADENOCARCINOMA, GLEASON SCORE 6/10 (3+3);
- 1/1 CORE INVOLVED; APPROXIMATELY 25% OF TISSUE INVOLVED;
- PERINEURAL INVASION PRESENT.
G. PROSTATE, LEFT LATERAL SUPERIOR, BIOPSY:
- ADENOCARCINOMA, GLEASON SCORE 7/10 (4+3);
- 1/1 CORE INVOLVED; APPROXIMATELY 5% OF TISSUE INVOLVED;
- PERINEURAL INVASION PRESENT.
H. PROSTATE, LEFT MEDIAL SUPERIOR, BIOPSY:
- ADENOCARCINOMA, GLEASON SCORE 8/10 (4+4);
- 1/1 CORE INVOLVED; APPROXIMATELY 15% OF TISSUE INVOLVED.
H. PROSTATE, LEFT MEDIAL SUPERIOR, BIOPSY:
- ADENOCARCINOMA, GLEASON SCORE 8/10 (4+4);
- 1/1 CORE INVOLVED; APPROXIMATELY 15% OF TISSUE INVOLVED;
- PERINEURAL INVASION PRESENT.
Tumour summaries
  • These are not completely without controversy.
  • It should be noted that treatment is driven by the highest Gleason score.[citation needed]
TUMOUR SUMMARY - PROSTATE CORE BIOPSIES:
- HISTOLOGIC TYPE: ADENOCARCINOMA (ACINAR, NOT OTHERWISE SPECIFIED).
- TOTAL GLEASON SCORE: 7.
- PRIMARY PATTERN: 4.
- SECONDARY PATTERN: 3.
- PERCENT OF TUMOUR WITH PATTERN HIGHER THAN GRADE 3: 75%.

- NUMBER OF CORES POSITIVE: 10.
- TOTAL NUMBER OF CORES: 12.
- TOTAL LINEAR MILLIMETERS OF NEEDLE CORE TISSUE: 152 MM.
- PERCENT OF NEEDLE CORE TISSUE THAT IS TUMOUR: 44%.

- PERIPROSTATIC FAT INVASION: NOT IDENTIFIED.
- SEMINAL VESICLE INVASION: SEMINAL VESICLE NOT IDENTIFIED.
- LYMPHOVASCULAR INVASION: NOT IDENTIFIED.
- PERINEURAL INVASION: PRESENT.

- ADDITIONAL FINDINGS: HIGH-GRADE PROSTATIC INTRAEPITHELIAL NEOPLASIA, CHRONIC INFLAMMATION (FOCAL).
TUMOUR SUMMARY - PROSTATE CORE BIOPSIES:
- HISTOLOGIC TYPE: ADENOCARCINOMA (ACINAR, NOT OTHERWISE SPECIFIED).
- HIGHEST GLEASON SCORE: 8 (4+4).
- SUMMARY GLEASON SCORE: 7 (4+3).
- PERCENT OF TUMOUR WITH PATTERN 4: 55%.
- PERCENT OF TUMOUR WITH PATTERN 5: 0%.

- NUMBER OF CORES POSITIVE: 12.
- TOTAL NUMBER OF CORES: 12.
- TOTAL LINEAR MILLIMETERS OF NEEDLE CORE TISSUE: 178 MM.
- PERCENT OF NEEDLE CORE TISSUE THAT IS TUMOUR: 80%.

- PERINEURAL INVASION: PRESENT.
- PERIPROSTATIC FAT INVASION: PRESENT.
- LYMPHOVASCULAR INVASION: NOT IDENTIFIED.
- SEMINAL VESICLE INVASION: NOT IDENTIFIED.

Seminal vesicle/ejaculatory duct invasion on biopsy

COMMENT:
The seminal vesicles and ejaculatory ducts have the same histology; thus, it is not
usually possible to confidently differentiate them in a needle biopsy.

SV/ED invasion was demonstrated with CK7, CK34betaE12/AMACR, PSA and p63 immunostaining.
The tumour is PSA and AMACR positive.

Intraductal spread of prostate cancer

Intraductal carcinoma of the prostate

Unusual forms of prostate cancer

Prostatic ductal adenocarcinoma

  • AKA ductal adenocarcinoma of the prostate.
  • AKA prostatic adenocarcinoma, large duct type.

PIN-like prostatic ductal adenocarcinoma

General

Microscopic

Features:[50]

  • Stratified malignant epithelium.

Note:

  • Vaguely similar to a tubular adenoma of the colon.

DDx:

Image:

Foamy gland carcinoma

  • AKA foamy gland adenocarcinoma.[52]

Atrophic prostate carcinoma

  • AKA atrophic carcinoma.

Mucinous prostate carcinoma

General

  • Rare.
  • Most often Gleason 3+4 ~ 80% in one series of 47 cases.[53]

Gleason pattern:

  • In the past, it has been suggested that the mucinous component be assigned Gleason pattern 4.[54]
  • The prognosis is similar or may be better than the conventional type of prostate cancer in a large series;[53] thus, it seems reasonable to grade based on the pattern (as advocated by some experts[55]).

Microscopic

Features:

  • Cytologically malignant cells floating in mucin.
  • > 25% of tumour mucinous.[54]

Notes:

DDx:

Pseudohyperplastic prostatic adenocarcinoma

  • AKA pseudohyperplastic adenocarcinoma.

Prostatic signet ring cell carcinoma

General

  • Very rare - 9 cases in a series of 29,783 prostate cancer cases.[58]
  • Criteria vary - percentage of SRCs required for Dx varies from 20% to 50%.[58]

Microscopic

Features:

  • Signet ring cells - see basics article.

DDx:

  • Acinar adenocarcinoma - Gleason pattern 4 with very small glands.

Images

Stains

Sarcomatoid carcinoma of the prostate

Small cell carcinoma of the prostate gland

Adenoid cystic/basal cell carcinoma of the prostate

  • Abbreviated ACBCC.

Postradiation prostate cancer

Metastatic disease and other cancers of the prostate

Urothelial carcinoma

Prostatic urothelial carcinoma redirects here.

General

Treatment:[60]

  • Cystoprostatectomy - stromal invasion or extensive intraductal involvement.
  • Endoscopic resection and BCG - limited extent without stromal invasion.

Microscopic

Features:

  • Divided into tumours with:
    1. Stromal invasion.
    2. Without stromal invasion.

Notes:

  • Stromal involvement common ~ 75% of cases.[61]

DDx:

Images

Sign out

PROSTATE TISSUE, TRANSURETHRAL RESECTION:
- HIGH-GRADE UROTHELIAL CARCINOMA WITH FOCAL STROMAL INVASION, AND EXTENSIVE
  INTRADUCTAL SPREAD IN FRAGMENTS WITH BENIGN PROSTATIC GLANDS.

See also

References

  1. Sakr WA, Haas GP, Cassin BF, Pontes JE, Crissman JD (August 1993). "The frequency of carcinoma and intraepithelial neoplasia of the prostate in young male patients". J. Urol. 150 (2 Pt 1): 379–85. PMID 8326560.
  2. Li, D.; Kumaraswamy, E.; Harlan-Williams, LM.; Jensen, RA. (2013). "The role of BRCA1 and BRCA2 in prostate cancer.". Front Biosci (Landmark Ed) 18: 1445-59. PMID 23747895.
  3. Castro, E.; Eeles, R. (May 2012). "The role of BRCA1 and BRCA2 in prostate cancer.". Asian J Androl 14 (3): 409-14. doi:10.1038/aja.2011.150. PMID 22522501.
  4. Taherian, N.; Hamel, N.; Bégin, LR.; Bismar, TA.; Goldgar, DE.; Feng, BJ.; Foulkes, WD. (Feb 2013). "Familial prostate cancer: the damage done and lessons learnt.". Nat Rev Urol 10 (2): 116-22. doi:10.1038/nrurol.2012.257. PMID 23318356.
  5. Ip, S.; Dahabreh, IJ.; Chung, M.; Yu, WW.; Balk, EM.; Iovin, RC.; Mathew, P.; Luongo, T. et al. (Dec 2011). "An evidence review of active surveillance in men with localized prostate cancer.". Evid Rep Technol Assess (Full Rep) (204): 1-341. PMID 23126653. http://www.ncbi.nlm.nih.gov/books/NBK83054/.
  6. 6.0 6.1 6.2 Palisaar, JR.; Noldus, J.; Löppenberg, B.; von Bodman, C.; Sommerer, F.; Eggert, T. (Sep 2012). "Comprehensive report on prostate cancer misclassification by 16 currently used low-risk and active surveillance criteria.". BJU Int 110 (6 Pt B): E172-81. doi:10.1111/j.1464-410X.2012.10935.x. PMID 22314081.
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