the pathology of common renal tumors victor e. reuter, … the patholo… · 1976: papillary renal...

THE PATHOLOGY OF

COMMON RENAL TUMORS

Victor E. Reuter, M.D

Memorial Sloan Kettering Cancer Center

Disclosures: none

A Practical Approach to Genitourinary Pathology

Firenze, Italy

May, 2016

RENAL NEOPLASIA

Landmarks in the pathological classification

over the past 4+ decades

1970 WHO classification:

Clear cell, Papillary, Granular, Sarcomatoid

1976: Oncocytoma (Klein and Valensi)

Cancer 1976;38:906

1976: Papillary Renal cell carcinoma (Mancilla-Jimenez et al)

Cancer 1976: 38:2469

1985: Chromophobe RCC (Thoenes and Storkel)

Virchow’s Arch 1985;48:207 and J Pathol 1988;155:277

1986: Classification of RCC (Thoenes and Storkel)

Pathol Res Pract 1986;181:125

1997: The Heidelberg classification

2004: WHO classification

2013: ISUP-Vancouver classification

Am J Surg Pathol 2013;37:1469

2016 WHO classification

2011-2014: IGC, TCGA et al ;

genomic classification of RCC

CLASSIFICATION OF RENAL EPITHELIAL TUMORS*

Clear cell carcinoma

Papillary carcinoma

Chromophobe carcinoma

Oncocytoma

Multilocular cystic renal cell neoplasm

Renal cell carcinoma with fibromuscular stroma

Collecting duct carcinoma

Medullary carcinoma

Mucinous Tubular and Spindle Cell carcinoma

MiTF-family translocation associated carcinoma

BHD-associated renal tumor

Tubulocystic carcinoma

Clear cell papillary

Hereditary leiomyomatosis renal cell carcinoma

SDH related carcinoma

TSC related carcinoma

Circa 1985:

Clear cell

Papillary

Granular cell

Sarcomatoid

Heidelberg, 1995

Comprehensive molecular characterization of clear cell renal cell

carcinoma: The Cancer Genome Atlas Network

Nature. 2013 Jul 4;499:43-9

Oostewijk et al Eur Urol, 2011;60:620

CLEAR CELL RENAL CELL CARCINONA

• 60% - 65% of renal epithelial neoplasms

• mean age at presentation: 6th to 7th decade

- younger in hereditary cases

• M:F 1.7- 2.0:1

• Most are asymptomatic at presentation

- triad (hematuria/ pain/ mass) in < 10%

• 10% multifocal, 3% bilateral

•VHL is a tumor suppressor gene at 3p25.3

•Well established role in CCRCC tumorigenesis

• Silencing via multiple mechanisms

• PBRM1 mutations (41%) SWI/SNF

• Inactivation of histone modifying genes

VHL


Microscopic features:

• variable growth pattern, loosely related to grade

- solid/acinar, delicate fibrovascular septa

- sheet-like, pseudopapillary, rhabdoid, sarcomatoid

• fibrosis and hyalinization are common

• geographic necrosis and hemorrhage are common

• cell shape is variable, loosely related to grade

• cytoplasm is variable, loosely related to grade

The many cytomorphologies of clear cell RCC

Feature Score

T stage:

pT1 0

pT2 1

pT3 2

pT4 2

N stage:

pNx or pN0 0

pN1 or pN2 2

M stage:

pM0 0

pM1 4

Tumor size (cm):

<5 0

≥5 2

Nuclear grade:

1 0

2 0

3 1

4 3

Necrosis:

Absent 0

Present 2

The SSIGN scoring algorithm

The scores from each category in this table are added together

and the total is used to determine survival

Frank et al. J. Urol. 2005;.173: 48–51)

SSIGN score % Estimated cancer specific survival

1-year 3-year 5-year 7-year 10-year

0–1 100 99.7 99.4 98.7 97.1

2 99.1 95.9 94.8 90.3 85.3

3 97.4 90.3 87.8 81.8 77.9

4 95.4 87.1 79.1 70.8 66.2

5 91.1 71.3 65.4 57.1 50.0

6 87.0 69.8 54.0 46.4 38.8

7 80.3 52.4 41.0 34.0 28.1

8 65.1 38.9 23.6 12.7 12.7

9 60.5 26.8 19.6 18.1 14.8

≥10 36.2 11.9 7.4 4.6 4.6

International Journal of Urology 2010;18:20

http://onlinelibrary.wiley.com/doi/10.1111/j.1442-2042.2010.02642.x/full

Kapur P et al, Lancet Oncol. 2013;14:159

Hakimi AA et al Eur Urol. 2012

Renal-call carcinoma: a step closer to a new classification

Choueri et al, Lancet Oncol.2013;14:105

49% 29% 8% 8% 6%

WILL THE FURHMAN NUCLEAR GRADING SYSTEM SURVIVE?

• Virtually nobody applies strict size criteria

• Follow-up data does not support 4 risk groups

• Four tiered grading schemes suffer from

reproducibility issues

Furhman Nuclear Diameter Nuclear Shape Nucleoli

G1 10 μm Round, uniform Absent

G2 15 μm Subtle irregularities Visible at 400X

G3 20 μm Obvious irregularities Visible at 100X

G4 20 μm, bizarre, spindle

WILL THE FURHMAN NUCLEAR GRADING SYSTEM SURVIVE?

Delahunt et al, AJSP, 2011;35:1134

• Nucleolar grade is superior to nuclear grade in clear cell RCC

• Difference between nucleolar grade 2 & 3 is magnification-dependent

Delahunt et al, AJSP, 2013;37:311

• Novel grading system for clear cell carcinoma incorporating necrosis

• Nucleolar (ISUP) grade

• Coagulative necrosis

• Sarcomatoid or rhabdoid morphology

NUCLEOLAR GRADE

100X magnification

Grade 1 Grade 2 Grade 3

Grade 4:

Rhabdoid,

Sarcomatoid

THE IMPORTANCE OF THE RENAL

SINUS AND ITS VESSELS IN

PREDICTING TUMOR PROGRESSION

Bonsib SM et al Am J Surg Pathol, 2000;24:451

Leibovich BC et al, J Urol, 2005;73:716

Bonsib SM, Am J Surg Pathol, 2004;28:1594

Thompson RH et al Am J Surg Pathol, 2007;31:1089

Bonsib SM, Mod Pathol, 2007;20:44

The end result is modification of the AJCC/UICC staging classification

(2010, 7th ed) where Renal Vein Invasion below the diaphragm

and Invasion of Muscular Branches of the Renal Vein are both pT3a

ANATOMY OF THE KIDNEY

CLEAR CELL CARCINOMA

Feifer A, et al. J Urol. 2011;185:35-42


Differential diagnosis:

• Papillary RCC

• Chromophobe RCC

• Epithelioid AML

• RCC with fibromuscular stroma

• Translocation-associated

RCC

• Adrenal cortical

carcinoma

• Metastatic disease

TUMORS COMPOSED PREDOMINANTLY OF “CLEAR” CELLS

Tumor type CA IX CK7 CD 117 Cathepsin-K HMB45

Clear cell RCC Positive, diffuse membranous

Negative Negative Negative Negative

Clear cell papillary RCC

Positive, cup-like

Positive Negative Negative Negative

Chromophobe RCC, classic

Negative Positive, cytoplasmic

Positive, membranous

Negative Negative

Epithelioid AML

Negative Negative Negative Positive, cytoplasmic

Positive, cytoplasmic

MiTF-TFE tumors

Xp11 family Variable but focal

Negative Negative Positive (50%), cytoplasmic

Negative *

t (6;11) Variable but focal

Negative Negative Positive, cytoplasmic

Positive (always focal)

Immunohistochemistry for classification

General comments (isuporg.org)

• Over a dozen entities to deal with

• Dozens of antibodies have been evaluated in at least one publication

• Nothing better than level II or Level III evidence (no validation studies)

• Inter-laboratory variability

• clone, methodology

• Most studies do not focus on “hard to classify” tumors but rather classic cases

• Best applied as Ab panels, taking into consideration a differential diagnosis

• tumors with clear cell cytology

• tumors with a predominant papillary pattern of growth

• high grade tumors with pleomorphic features

Clear cell RCC

Vimentin

CA IX EMA

PAPILLARY RENAL CELL CARCINOMA

• 13% to 18% of renal epithelial neoplasms

• M:F 2.1-3.9:1

• mean age at presentation in the 6th-7th decade

- earlier in hereditary cases

•most cases are asymptomatic

Met receptor

HGF

Activating mutation

Therapeutic approach to selected “type 1” papillary RCC

Tyrosine kinase inhibition



• broad morphologic spectrum

- papillary, papillary/tubular, papillary/solid

• classic features

-discrete papillary fronds with central fibrovascular core

- cuboidal, columnar or polygonal cells

- cytoplasmic basophilia, amphophilia or eosinophilia

- psammoma bodies, foamy macrophages

- geographic necrosis


GROWTH PATTERN

Pure papillary 27 (32.5%)

> 50% papillary* 36 (43.4%)

< 50% papillary* 20 (24.1%)

* also tubular, solid, spindled,

glomeruloid

CYTOPLASMIC FEATURES

Eosinophilic 10 (12.0%)

Amphophilic 13 (15.7%)

Basophilic 4 ( 4.8%)

Mixed 56 (67.5%)

Amin et al. Am J Surg

Pathol. 21:621,1997.

Type 1 PRCC Type 2 PRCC

Delahunt et al. Hum Pathol. 32:590,2001

Delahunt et al. AJSP 37:311;2013

- ISUP nucleolar grade but not necrosis

Sukov et al. J Urol 187:54;2012

- Furhman grade superior to tumor type


HISTOLOGIC SUBCLASSIFICATION

Type Cell size Cytoplasm Grade Molecular

classification

1 small pale 1-2 1

1 and 2A small and

large

pale and

eosinophilic

1-2 1

2A large eosinophilic 1-2 1

2B large eosinophilic 3-4 2

Yang, X. J. et al. Cancer Res 2005;65:5628-5637

Type “1” Type “2a’ Type “2b”

Current state of papillary renal neoplasia

• It’s a mess

• Type 2 papillary RCC is not an entity

• How many morphologic, clinical and molecular entities are included is yet to be defined

• Type 1 papillary RCC is better defined but needs fine tuning

• Some papillary RCC have morphologic features of both type 1 and type 2 tumors

• Morphologic

continuum?

• Grade related?

Papillary Renal Cell Carcinoma

MSKCC study on Type 1 Papillary RCC

•We investigated the clinicopathological features, including cancer specific (CSS) and progression free survival (PFS), of PRCC with any type 1 component, based on the premise that the presence of even focal typical type 1 morphology would define the tumor classification

•199 cases of PRCC with the WHO-defined type 1 features, diagnosed at our institution from 1995 to 2008.

•Tumors with type 2 features were included if any identifiable type 1 areas were present. The type 2 areas were quantified in tumors with mixed histology. Various pathological features were evaluated.

•Clinical features and follow up information were obtained from an IRB-approved annotated clinical database.

Murugan P et al, USCAP 2015

0%

2%

4%

6%

8%

10

%12

%

Pro

bability o

f R

ecurr

ence

0 3 6 9 12 15

Years since Nephrectomy

199 169 130 67 24 5 Number at risk

Figure 1: Probability of a recurrence

0%

2%

4%

6%

8%

10

%12

%

Pro

bability o

f C

ancer-

Spe

cific

Mort

ality

0 3 6 9 12 15

Years since Nephrectomy

199 175 133 68 24 5 Number at risk

Figure 2: Probability of cancer-specific mortality

• There were 10 patients who died of disease and 12

who recurred.

• The median follow-up time among those who did not

die of disease was 7.8 years (IQR: 5.7, 10.0).

The Kaplan Meier estimated probability of recurrence at 15 years of follow-up

was 7% (95% CI 4%, 11%) and for cancer-specific death was 6% (95% CI 3%, 10%).

Type 1 Papillary RCC Study


MSKCC phase 1 study on Type 1 Papillary RCC

• 95 tumors (48%) contained some type 2 component; the median

amount of type 2 morphology was 25% (IQR: 10%, 70%).

• PFS and CSS showed no significant association with the

presence of type 2 morphology in the tumor (p=0.2 and 0.2,

respectively) or its percentage (p=0.052 and 0.13, respectively).

• Associations with cancer specific survival (CSS) rates:

Tumor size (p=0.003)

Mitotic rate (<0.0001)

Circumscription (0.0002)

Lymphovascular invasion (LVI) (<0.0001) (6/6 pts DOD)

Sarcomatoid and solid architectures (<0.0001, and 0.014)


MSKCC phase 1 study on Type 1 Papillary RCC

conclusions

• PRCC with any component of type 1 morphology, regardless of

presence or amount of type 2 features, have excellent long-term

outcome.

• Both predominant Fuhrman and ISUP nucleolar grades are

significantly associated with clinical outcome, but focal high

grade nuclear or nucleolar features are not.

• Tumor size, mitotic rate, tumor circumscription, lymphovascular

invasion, sarcomatoid and solid architectures are significantly

associated with outcome in type 1 papillary RCC.




• Clear cell RCC with pseudopapillary areas

• Clear cell papillary RCC

• Metanephric adenoma

• Translocation-associated RCC

• Metastatic carcinoma

• ACDK-associated RCC

• Hereditary leiomyomatosis PRCC syndrome

TUMORS WITH A SIGNIFICANT PAPILLARY COMPONENT

CAIX CK7 AMACR Cathepsin-K 4A4 TFE3/TFEB

Clear cell RCC with papillary growth


Negative Negative Negative Negative Negative

Papillary RCC “type I”

Negative Positive Positive Negative Negative Negative

Papillary RCC “type II”

Negative +/- positive Positive Negative Negative Negative

Clear cell papillary RCC

Positive, cup-like

Positive, diffuse

Negative Negative Negative Negative

MiTF-TFE trans-assoc

Variable but focal

Negative Positive Positive (50%)

Negative Positive*

Collecting duct Ca

Negative Positive +/- positive

Negative Positive Negative

Papillary RCC

CK7

AMACR Vimentin CAIX

WT-1 +

CD57 +

BRAF +

CK7 +

AMACR + WT-1 +

Metanephris adenoma Type 1 PRCC (solid) Wilms tumor

Papillary adenoma

Definition (WHO 2016)

Size: 15 mm or less

Papillary, tubulo-papillary or

solid

Fuhrman grade 1-2

Nucleolar grade 1-2

No peritumoral pseudocapsule

CHROMOPHOBE RENAL CELL

CARCINOMA

• 6% to 11% of renal epithelial neoplasms

• M:F 1.5-2.0:1

• mean age at presentation in the 6th-7th decade

• 10% multifocal, 3% bilateral

• asymptomatic in 58%

• hematuria in 19%, palpable mass in 30%

MICROSATELLITE ANALYSIS IN

CHROMOPHOBE CELL RENAL CARCINOMA

CASE: 1 2 3 6 10 13 17 21

17

18

19

20

21

22

= LOH = No LOH NI= Not informative

Bugert et al. Lab Invest 76:203-208,1997.

CHROMOPHOBE

RENAL CELL CARCINOMA


• dominated by large round-to-polygonal cells with well defined cell borders and amphophilic to basophilic reticulated cytoplasm

• smaller number of polygonal cells with eosinophilic cytoplasm

• larger cells with abundant foamy cytoplasm

• hyperchromatic nuclei with irregular membranes

• binucleate cells are common

• bizarre nuclei (degenerative atypia) in up to 50%

CHROMOPHOBE RENAL CELL CARCINOMA


May be confused with clear cell RCC.

Alternatively some clear cell RCC may

have chromophobe-like areas

Kidney TCGA

Unsupervised

clustering of DNA

copy number

profiles

KICH TCGA

early data

Clear cell RCC - TCGA

Case Outliers*

Pathology review**

Category Number

Clear cell/likely clear cell 18

Clear cell papillary 4

Chromophobe/likely chromophobe 15

Oncocytoma/likely oncocytoma 2

Not clear cell or chromophobe 6

Not reviewed 16

Total 61

*Outliers:

Chomo-like genotype

wtVHL

No 3p loss

** Pathologists

Satish Tickoo (MSKCC)

Pheroze Tamboli (MDACC)

Maria Merino (NCI)

Sabina Signoretti (DFCC)

Victor Reuter (MSKCC)

CHROMOPHOBE CARCINOMA

Predictors of Aggressive Behavior

on multivariate analysis

Predictor Relative Hazard

ratio (p)

95% CI

Sarcomatoid change 4.7 (0.013) 1.4, 16.0

Microscopic necrosis 3.5 (0.020) 1.2, 10.0

pT stage (3,4 vs 1,2) 3.4 (0.025) 1.1, 9.7

Tumor size (>7.5cm) 1.0 (0.75) 0.9, 2.2

Amin et al. Am J Surg Pathol. 2008

Table 2. Cox regression to evaluate predictors of disease-free survival following

nephrectomy for chromophobe renal cell carcinoma, adjusted for age at surgery

Characteristic Hazard Ratio 95% CI P Value adjusted for age

Gender (Female vs Male) 2.00 1.10, 3.67 0.02

Tumor size (cm) 1.08 1.01, 1.15 0.03

T stage, 2010 AJCC classification

T2a/b vs T1a/b 1.32 0.63, 2.76

T3a/b, T4 vs T1a/b 1.42 0.69, 2.93 0.6

Nodal status at presentation

NX vs N0 1.30 0.70, 2.40

N1 vs N0 7.75 1.72, 34.90 0.03

Microscopic necrosis (yes vs no) 2.69 1.37, 5.27 0.004

Gross necrosis (yes vs no) 0.72 0.28, 1.84 0.5

Sarcomatoid differentiation (yes vs no) 6.80 2.04, 22.60 0.002

Mitotic count (> 1/10 HPF vs ≤ 1/10 HPF) * * *

Vascular invasion (yes vs no) 1.95 0.92, 4.13 0.08

Capsular invasion (yes vs no) 1.38 0.66, 2.89 0.4

Renal sinus invasion

Yes vs No 1.05 0.35, 3.13

Not interpretable vs No 0.84 0.45, 1.58 0.8

Renal sinus vessel invasion

Yes vs No 1.35 0.31, 5.78

Not interpretable vs No 0.94 0.51, 1.75 0.9

Przybycin Am J Surg Pathol 2011;35:962

203 cases

Median f/u: 6.1 yr

Mets at presentation: 5

Progression after surgery: 8

CHROMOPHOBE

RENAL CELL CARCINOMA


• Clear cell RCC

• Oncocytoma

• Epithelioid (pleomorphic) AML

•“Hybrid” oncocytic tumors (HOCT)

•Oncocytosis/Birt-Hogg-Dubé

•Tuberous sclerosis complex (TSC)-associated

• Succinate Dehydrogenase (SDH)-associated

RENAL ONCOCYTOMA

• Peak incidence in 6th to 7th decade

• 5%-10% or renal epithelial tumors

• M : F = 2:1

• Most are asymptomatic

• No consistent genetic abnormalities

- loss of chromosomes 1and Y

- rare translocations (chr 11)

- mitochondrial DNA defects

• Well circumscribed, mahogany brown

• Central scar in 30%

• No necrosis

• Hemorrhage (20%)

RENAL ONCOCYTOMA


• compact nests, acini, tubules or microcysts

• hyalinized hypocellular stroma

• round to polygonal epithelial cells densely

eosinophilic cytoplasm

• round, regular nuclei with dispersed

chromatin and central nucleoli

RENAL ONCOCYTOMA

Acceptable findings:

• degenerative cytologic atypia

• peri-renal or sinus fat invasion

• vascular invasion

Non-acceptable findings:

• more than an isolated mitotic figure

• tumor necrosis

• overt papillary architecture

• true cytologic atypia

Our contemporary study on renal oncocytoma Renal oncocytoma: a clinicopathologic study of 70 cases.

Perez-Ordonez B, Am J Surg Pathol 1997;21:871-883

• Benign

• Considerable controversy regarding the definition of renal

oncocytoma

•RCC unclassified (oncocytic, at worst low grade malignant)

•Renal oncocytic neoplasm

•Hybrid oncocytic tumor

•Renal cell carcinoma with oncocytic features

• In general, because we aim to keep this a benign entity the

morphologic criteria applied by most pathologists are extremely

rigorous

• However, even within our own institution, thresholds vary….

• VER and SKT agree it is oncocytoma

• VER and SKT agree it is NOT oncocytoma

• VER and SKT disagree whether it is oncocytoma or not

Agree yes

Agree no Agree no

Disagree

Our contemporary study on renal oncocytoma

• 183 patients with oncocytic neoplasms resected at our institution from 2000-

2010

• All non-oncocytoma (like) tumors were excluded from the study

• Cases put into one of three groups

1. definite oncocytoma [102 (53%)]

2. disagreement between pathologists whether oncocytoma or not [56 (29%)]

3. definite not oncocytoma [35 (18%)]

• Morphologic features described within each group

• Clinical follow-up information was interrogated

• Median f/u of 60 months (5 d-166 mo)

• No metastases of tumor-related deaths in any of the 3 groups

Conclusions:

1. Renal oncocytoma or oncocytoma-like tumors all have excellent long-term

prognosis

2. “Atypical” morphologic features are likely unduly overemphasized in

excluding the diagnosis of renal oncocytoma

ONCOCYTOMA


• Eosinophilic variant of Chromophobe RCC

• Epithelioid (oncocytic) AML

• “Hybrid” oncocytic tumor (HOCT)

•Oncocytosis/Birt-Hogg-Dubé

•Tuberous sclerosis complex (TSC)-associated

• Succinate Dehydrogenase (SDH)-associated

TUMORS WITH ONCOCYTIC FEATURES

CD117 CK7 Ksp-cadherin HMB-45 Parvalbumin

Oncocytoma Positive, membranous

Negative Positive Negative Positive

Chromophobe RCC, eosinophilic


Positive but variable

+/- positive Negative Positive

Oncocytic papillary RCC

Negative Positive but focal

Not known Negative Unknown

Oncocytic AML

Negative Negative Negative Positive, focal

Negative

Other Abs said to differentially expressed on oncocytomas and chromophobe RCC

Positive in Oncocytoma, negative in Chromophobe EABA, S100A1

Negative in Oncocytoma, positive in Chromophobe MOC31, EpCam, Caveolin-1, CD82

Renal Cortical Tumors

MSKCC

Median Tumor Size

Incidental detection

Lee et al. Urol Oncol 2002;7:135–40

MSKCCMSKCC

0.00

1.00

2.00

3.00

4.00

5.00

6.00

7.00

8.00

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

Nephrectomy Year

Tu

mo

r S

ize (

cm

)

0.0%

10.0%

20.0%

30.0%

40.0%

50.0%

60.0%

70.0%

80.0%

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

Case Year

HISTOLOGICAL SUBTYPE IN 2,675 PATIENTS

TREATED SURGICALLY FOR A RENAL MASS

Tumors Number of tumors (%)

Benign 311 (11.6)

Oncocytoma 232 (74.5)

Angiomyolipoma 35 (11.2)

Metanephric adenoma 8 ( 2.6)

Other 36 (11.6)

Malignant 2,675 (88.4)

Clear cell 1,679 (71.0)

Papillary 341 (14.4)

Chromophobe 239 (10.1)

Collecting duct 7 ( 0.3)

RCC unclassified 98 (4.1)

Thompson RH, et al J Urol 2009;181:2033-2036 MSKCCMSKCC

BENIGN TUMORS vs RCC ACCORDING TO SIZE IN PATIENTS

TREATED SURGICALLY FOR A RENAL MASS

Size (cm) No. Benign (%) No. RCC (%)

Less than 1 6 (37.5) 10 (62.5)

1 to less than 2 56 (19.2) 236 (80.8)

2 to less than 3 77 (16.5) 391 (83.5)

3 to less than 4 58 (13.0) 390 (87.0)

4 to less than 5 30 (8.7) 315 (91.3)

5 to less than 6 23 (10.0) 206 (90.0)

6 to less than 7 13 (6.6) 183 (93.4)

7 or greater 48 (7.1) 633 (92.9)

Thompson RH, et al J Urol 2009;181:2033-2036

16.1

%

20.2

%

MSKCCMSKCC


4 cm or less

Cases: 74

Follow-up (mos): 73.5 (median)

Outcome:

NED: 73

AWD: 1 (1.4%)

DOD: 0

Przybycin Am J Surg Pathol 2011;35:962 MSKCCMSKCC

TREATMENT OF “SMALL RENAL MASSES”

• Treating blindly

- Surgery

- Ablation

• Active surveillance

- Life expectancy

- Co-morbidities

- Tumor biology

• Cost

Cases (N) Adequate

material (%)

Correct Diagnosis

on H&E alone

Correct Diagnosis

with IHC

Clear Cell (84) 75 (89) 64 (85) 68 (91)

Papillary (18) 18 (100) 17 (94) 18 (100)

Chromophobe (14) 13 (93) 8 (62) 12 (92)

Oncocytoma (11) 6 (55) 4 (67) 6 (100)

Total (127) 112 (88) 93 (83) 104 (93)

Al-Ahmadie et al, Am J Surg Pathol 2011;35:949

Tumor type Total Ablation Nephrectomy Chemotherapy Active

Surveillance

Clear cell RCC 80 12 24 31 13 (16%)

Papillary RCC 7 3 0 2 2 (29%)

LG

oncocytic

neoplasm

Chromophobe 9 2 2 1 4 (44%)

oncocytoma 9 1 2 0 6 (67%)

NOS 9 0 0 0 9 (100%)

Clear cell papillary RCC 4 1 0 0 3 (75%)

Angiomyolipoma 5 0 0 0 5 (100%)

Misc* 5 0 2 3 0 (0%)

Total 128 19 30 37 42 (33%)

Gel

lert

et

al,

US

CA

P 2

01

2

63%

SUMMARY

• Renal tumors are not a single histologic, clinical or

molecular entity

• Proper molecular and morphological classification

of tumors is of clinical importance for risk

stratification

• Further molecular and morphologic dissection of

renal neoplasms will lead to more appropriate

therapies of both primary and metastatic disease

• In vivo classification of tumors is desirable and

possible in the majority of cases

• Judicious use of antibody panels can be useful to

arrive at a proper diagnosis MSKCCMSKCC

the pathology of common renal tumors victor e. reuter, … the patholo… · 1976: papillary renal...

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