| What is benign nodular hyperplasia? | • Most common benign prostatic disease ˃50 yrs.
• Results from nodular hyperplasia of prostatic stromal
and epithelial cells and often leads to urinary
obstruction.
• DHT, an androgen derived from testosterone, is the
major hormonal stimulus for proliferation.
• Formation of large, fairly discrete nodules in the
periurethral region of the prostate, which may
compress and narrow the urethral canal to cause
partial, or complete, obstruction of the urethra. |
| How is management of BPH? | • Transurethral resection of the prostate (TURP) has been the gold standard in terms of reducing symptoms, improving flow rates, and decreasing postvoiding residual urine. |
| What are prostate tumors? | • Adenocarcinoma (˃95%)
• Poorly differenciated neuroendocrine carcinoma (small cell/large cell): rarely de novo, usually post HT for prostatic adenocarcinoma.
• Other very rare tumors (RMS, stromal tumor…) |
| What are subtypes of prostate tumors? | • Acinar adenocarcinoma
• Ductal adenocarcinoma
• Atrophic adenocarcinoma
• Pseudohyperplastic adenocarcinoma
• Microcystic adenocarcinoma
• Foamy gland adenocarcinoma
• Mucinous adenocarcinoma
• Signet ring variant of adenocarcinoma |
| What is prostate adenocarcinoma? | • Is not the result of a transformation of BPH.
• Usually develops in the peripheral zone (90%),
rarely in the transitional zone.
• Can result in LN metastases (pelvic, then
distant LN)
• Bone metastases (sclerotic) +++
• Rarely liver or lung metastases.
• Usually androgen dependant
• Synthesis of PSA
• 2 phases:
– Initial phase of hormonodependance
– Resistance phase:
• Usually after 2 years of HT
• Adaptation-selection phenomenon
• NE differentiation |
| How is dx of prostate adenocarcinoma? | • Rarely on TURP, or adenomectomy
• Tru-cut biopsies (transrectal)
• US or MRI guided
Prostate Biopsies (PB)
• Systematic approach may involve sextant (6) samples from selected regions of prostate by a spring loaded 18 gauge biopsy (2 cores /site)
• Region of interest (ROI) biopsies at a multiparametric MRI targeted lesion
• Different sites in separate containers + indication of biopsy site
– Base, apex, etc
– +/- Inked
– Number of cores and lengths should be recorded
– Correlation between length of core and PCa detection |
| How is dx of PRCa on biopsies? | • Low PF +++: Architectural criterias ++++
- Microglandular foci
- Loss of lobular architecture +++
- Infiltration |
| What are major and minor criteria of PRCa dx? | . |
| What are other criteria for PRCa? | • Mucinous fibroplasia
• Glomerulation
• Perineural invasion+++
• Extraprostatic extension (rare)
• Lymphovascular invasion (extremly rare) |
| What is Gleason's grading of prostate hx? | • Grading based on the architectural resemblance
to benign glands, low- medium magnification
• 5-tier grades (patterns)
• Remains as the single most important
prognostic parameter
• Used in all risk stratification tools for treatment
decision
Gleason grade 3 (Frequent, Small well differenciated or sharpened Glands, Infiltrative, No fusion no cribriform pattern)
Gleason grade 4 (Fused, Cribriform, Poorly formed glands, Glomeruloid frequent)
Gleason grade 5 (No glandular differenciation, No glandular lumen, Isolated cells, Comedocarcinoma patterns, Solid nests) |
| What are histoprognostic groups/grade groups? | • Group 1 (G 3+3 or under)
• Group 2 (G 3+4)
• Group 3 (G 4+3)
One should indicate % of grade 4 in group 2 and 3
• Group 4 (G 4+4, 3+5, 5+3)
• Group 5 (G 4+5, 5+4, 5+5) |
| What is high grade PIN? | • Precancerous lesion (if extended)
• PZ
• Pre-existing ducts and acini
• Cribriform, tuffed, micropapillary, plane.
• Cytonuclear atypias as in cancer
• But some basal cells remain (IHC) |
| What is ASAP? | • If doubt IHC/levels
• If not conclusive for cancer : atypical small acinar proliferation insufficent for diagnosis of cancer : new biospies are mandatory |
| What are benign mimickers of PRCa? | Most common (atrophy, adenosis, basal cell hyperplasia, benign crowded glands) |
| How is prostatic ductal adenocarcinoma? | • Cribriform, papillary, solid patterns
• Tall columnar cells
• Arises in primary periurethral ducts or in peripheral prostatic ducts
• Frequently is mixed with an acinar component
• Most ductal adenocarcinoma is considered to be Gleason pattern 4 |
| How is reporting prostate biopsies Gleason's? | • According to the WHO 2016 recommendations
• Each positive site GS (modified GS WHO2016)
• Composed of
– Most extensive AND
– Most agressive (highest grade)
• Irrespectively of its extent (no 5% rule)
Reporting minor high grade patterns, same rules PB and RP?
• Only validation for PB
• If only 2 patterns, record the HP even if focal
• GG3 + 5% GG4= 3+4
Reporting minor high grade patterns
• If 3 patterns and the HP is the least common
pattern yet still >5% then report the HP as the
secondary grade
• 50% GG3+ 30% GG4+20% GG 3+5=8 |
| How is prostate biopsies? | • Proportion (%) or length (mm) for each biopsy
• Discuss with your pathologist how he/she measures!! |
| How is active surveillence for low-grade prostate cancer? | • Active surveillance (AS)
• Reduce risk of overtreatment of clinically insignificant PCa
• But retaining option of definitive therapy for patients
– Reclassified over the time as high risk
• Overdiagnosis
– Many PCa will not progress or cause harm
– Diagnosed cases exceed number of lethal cases |
| What are advantages of new systems? | • Easier for patient, G1 is lowest grade
• Better reflects biology
• GG1 excellent prognosis, no metastasis, avoids
GGS<6
• GG2 rare metastasis
• GG3<GG2, better distinction between 2 SG7
groups
• GG4 better prognosis GG5
• GG5, no need to distinguish 9 and 10 |
| What is use of radical prostatecetomy? | • Histologic type
• Topography
• GS, GG
• pT
• Surgical Margins
– R0. No residual tumor.
– R1. Microscopic residual tumor.
– R2. Macroscopic residual tumor.
• Bilateral pelvic LN dissection / curage iliobturateur |
| How is GS in pathology report RP? | • GS
– Most and second most dominant GG
– ≤ 5% GG not incoporated
– Tertiary mentionned if > 5%
– No consensus about reporting
• Extraprostatic extensionpT3a
• PCa volume
– Not perfectly established
– Measure most important focus
• MRI+++
• Index tumor
– No consensus
• Biggest tumor
• Highest GS
Measure focus
• X x Y x number of blocs |
| How is T in stagning of prostate cancer? | • pT2: confined to prostate
– a, b, c non recommended any more
• pT3a: extraprostatic extension or microscopic
invasion of bladder neck ( EPE is defined as presence of PCa beyondconfines of prostate gland or PCa glands
admixed with periprostatic adipose tissue)
• pT3b: seminal vesicle muscle invasion
• pT4: fixed tumor or invasion of structures such
as external sphincter, rectum, bladder, levator
muscles or pelvic wall |
| What is T3a staging? | Extraprostatic Extension (T3a)
•Prostate has no true capsule
•“Capsule” is a condensed fibromuscular layer of prostate
stroma
•Best recognized in posterior and posterolateral aspects
At apex, anterior and base, “capsule” not readily
recognized and contour is irregular
When EPE is identified, location and extent should
be documented
Focal (< one 40x field AND < 2 sections); nonfocal |
| How is N in staging of prostate cancer? | Regional lymph nodes (pN)
• pNX: cannot be assessed
• pN0: no regional lymph node metastasis
• pN1: regional lymph node metastasis
(including periprostatic, pelvic, hypogastric,
obturator, internal iliac, external iliac, sacral)
Lymph node metastasis
• % tumor, +/- extracapsular growth |
| How is M in staging of prostate cancer? | Distant metastasis (pM)
• pM1a: metastasis in nonregional lymph node
• pM1b: metastasis in bone
• pM1c: metastasis in other distant site
Nonregional lymph nodes include:
aortic, common iliac, deep / superficial
inguinal, retroperitoneal
Surgical margins: negative, doubt, positive |
