pathology

1. Chapter 22
Female
Reproductive
System
1
52
1

2. TOPICS
• TODAY (Part I)
–Vulva
–Vagina
–Cervix, uterus
–Body, uterus
–Tubes
• NEXT CLASS (Part II)
–Ovaries
–Placenta
2
2

3. Female Reproductive System Outline
• Vulva
• Vagina
• Cervix
• Uterus
• Ovaries
• Fallopian tubes
• Pregnancy diseases
• Breast
3
3

4. VULVA
• Synonymous with EXTERNAL genitalia
• Everything ANTERIOR to the INTROITUS
• Usual classification of Degen., Inflam.,
Neopl.
• Common Diseases:
– BARTHOLIN Cyst
– Vulvar Vestibulitis
– Deg./Inflam. Epithelial: LICHEN diseases
– BENIGN tumors: Condyloma(ta)
– MALIGNANT tumors: VIN, SCC 4
4

5. Result from
Inflammation/Obstruction
of the Bartholin glands
(i.e., greater vestibular
glands)
Often result in abscesses
Surgical removal is
curative when local
procedures are
inadequate or often
recurrent
NEVER become
malignant
5
5

6. VULVAR VESTIBULITIS, assoc. w. vulvodynia
6
6

7. “LICHEN” DISORDERS
LICHEN Sclerosis (atrophic skin)
LICHEN Simplex Chronicus
(hypertrophic skin)
Common features of
FIBROSIS and INFLAMMATION 7
7

8. 8
8

9. Mucosal Atrophy
Fibrosis (sclerosis)
Inflammation
9
9

10. LICHEN SIMPLEX
CHRONICUS 10
10

11. The types of lichen lesions
which show HYPER-plastic
mucosal changes are often
regarded as being potentially
malignant
11
11

12. CONDYLOMA(TA) 12
12

13. VIN, SCC
• Like condylomas, HIGHLY
linked to HPV
• VIN=changes leading to SCC-
in-situ, look like “plaques”
• BEYOND VIN =
INFILTRATION
13
13

14. VIN 14
14

15. 15
15

16. 16
16

17. MALIGNANT
MELANOMA
17
17

18. VAGINA
• CONGENITAL: Parallel Uterus
• INFLAMMATORY
–PRE-menopausal: STD
–POST-menopausal: ATROPHY
• BENIGN: Hidradenoma, Condyloma
• MALIGNANT: VIN, INFILTRATING SCC
18
18

19. CONGENITAL
• Imperforate hymen
(hematocolpos)
• Atresia
• Absence (agenesis)
• Septate
• Double (didelphys) 19
19

20. Atresia,
Double vagina,
Double uterus.
20
20

21. VAGINITIS
• 90%
• Bacterial Vaginitis is the most common cause of vaginitis,
accounting for 50% of vaginitis cases. As previously mentioned, BV is
caused by an overgrowth of organisms such as Gardnerella vaginalis
(gram-variable coccobacillus), Mobiluncus species, Mycoplasma
hominis, and Peptostreptococcus species. Risk factors include
pregnancy, intrauterine device (IUD) use, and frequent douching.
• Candida species (C albicans, C tropicalis, and C glabrata) are
airborne fungi that are natural inhabitants of the vagina in as many as
50% of women, and vaginal candidiasis is the second most common
cause of vaginitis. Risk factors include oral contraceptive use, IUD use,
young age at first intercourse, increased frequency of intercourse,
receptive cunnilingus, diabetes, HIV or other immunocompromised
states, chronic antibiotic use, and pregnancy.
• T. vaginalis infection, the third most common cause of vaginitis, is
caused by trichomonads. These organisms are flagellated protozoans.
Trichomonads primarily infect vaginal epithelium, and they less
commonly infect the endocervix, urethra, and Bartholin and Skene
glands. Trichomonads are transmitted sexually and can be identified in
as many as 80% of male partners of infected women. Risk factors
include tobacco use, unprotected intercourse with multiple sexual
partners, and the use of an IUD.
21
21

22. 22
22

23. VAGINAL NEOPLASIA
•VIN
•INFILTRATING SCC
•ADENOSIS (D.E.S.) 
•ADENOCARCINOMA
(Di-Ethyl-Stilbestrol) 23
23

24. VIN
24
24

25. NORMAL VIN 25
25

26. SCC26
26

27. 27
27

28. 28
28

29. CHILDHOOD EMBYRONAL
RHABDOMYOSARCOMA
29
29

30. CERVIX
• NORMAL
• METAPLASIA
• INFLAMMATION
• POLYPS
• DYSPLASIA
• CIN
• INFILTRATING SCC 30
30

31. 31
31

32. Normal cervix, young adult
Transformation zone
32
32

33. Transformation zone 33
33

34. 34
34

35. 35
35

36. 36
36

37. 37
37

38. Development
of
transformation
zone
38
38

39. 39
39

40. 40
40

41. 41
41

42. 42
42

43. 43
43

44. 44
44

45. Cytology of CIN (Pap smear)
normal CIN I CIN II CIN III
45
45

46. Cytology of CIN (Pap smear)
normal CIN I CIN II CIN III
“Low-grade dysplasia”
“High-grade
dysplasia”
46
46

47. DYSPLASIA / CIN / SIL
47
47

48. 48
48

49. Cervical Intraepithelial Neoplasia (CIN)
• Precursor to carcinoma
• Almost all carcinomas arise in CIN; but not all cases
of CIN progress to carcinoma!
• Three grades:
• CIN I: mild dysplasia (half regress, 20% progress)
• CIN II: moderate dysplasia
• CIN III: severe dysplasia (30% regress, 70% progress)
• The higher the grade, the more likely the lesion will
progress to carcinoma
49
49

50. Normal (left) turning into CIN (right) 50
50

51. Cervical Carcinoma
• Once the most common cancer in women –
now not even in top 10.
• Decrease due to Pap test!
• At the same time, precursor lesions are
increasing (early detection)
51
51

52. Invasive Cervical Carcinoma
• Most cases are squamous, arising from CIN
• Small number are adenocarcinomas
• Peak age: 45 (10-15 years after CIN develops!)
• Spreads slowly
• Most cases are diagnosed early
• Mortality is related to stage:
• stage 0 (preinvasive): 100% 5 year survival
• stage 4: 10% 5 year survival
52
52

53. Cervical carcinoma 53
53

54. INFILTRATION
54
54

55. How have we “CURED” Cervical Carcinoma? 55
55

56. Cervical Carcinoma Risk Factors
• Early age at first intercourse
• Multiple sexual partners
• A male partner with multiple previous partners
• Persistent infection with “high-risk” HPV
• Smoking
• Immunodeficiency
56
56

57. Cervical Carcinoma and HPV
• HPV is detectable in almost all CIN and cancer.
• “High-risk” types:
• 16, 18, 45, 31
• Found in carcinomas
• Integrate into genome, inactivate p53, RB
• “Low-risk” types:
• 6,11
• Found in condylomas (benign lesions)
• Do not integrate into genome
57
57

58. 58
58

59. ENDOMETRIUM
• FUNCTIONAL HISTOLOGY
• D.U.B. (Dysfunctional Uterine Bleeding)
• INFLAMMATION
• ADENOMYOSIS/ENDOMETRIOSIS
• POLYPS/HYPERPLASIA
• ADENOCARCINOMA and/or STROMAL
• LEIOMYOMAS, -SARCOMAS
• MITOSES differentiate benign from malignant
59
59

60. 60
60

61. MITOSES (Glandular and Stromal) = PRE-ovulatory
VACUOLES/SECRETION = POST-ovulatory
61
61

62. DYSFUNCTIONAL UTERINE
BLEEDING (DUB)
• Anovulatory Cycle
• Inadequate Luteal Phase
• Oral Contraceptives
• Menopause
• Post-Menopause
62
62

63. ENDOMETRITIS
•PID
•Post-partum Sepsis
•BCP’s
•TB
63
63

64. ADENOMYOSIS
• Defined as normal endometrial glands
deep within the myometrium
64
64

65. 65
65

66. ENDOMETRIOSIS
Defined as normal endometrial glands OUTSIDE
the confines of the myometrium
Reverse menstruation vs. Embryologic “rest”
theories
EXTREMELY common cause of cyclical
abdominal/pelvic pain
Broad Ligament, Ovary (“chocolate cysts”),
Peritoneum, Bowel, Umbilicus
66
66

67. 67
67

68. Endometriosis
• Location of endometrial glands outside uterus
• Usually peritoneum, rarely lymph nodes
• Endometrium undergoes cyclic bleeding
• Causes scarring, pain, sometimes sterility
• How does endometrium get out?
68
68

69. 69
69

70. “CHOCOLATE”
CYST 70
70

71. Endometrial Hyperplasia
• Proliferation of endometrium due to estrogen excess
• Risk factors: anovulatory cycles, obesity, estrogen-
producing ovarian tumors, exogenous hormone use
• Three categories: simple, complex, and atypical
• The more severe the hyperplasia, the greater the
chance that it will evolve into carcinoma
71
71

72. Normal endometrium 72
72

73. Endometrial hyperplasia
Simple Complex Atypical
73
73

74. 74
74

75. 75
75

76. 76
76

77. Leiomyoma
• “Fibroid”
• Benign tumor of smooth muscle
• Common!
• Stimulated by estrogen
• Menorrhagia, metrorrhagia, or asymptomatic
77
77

78. 78
78

79. 79
79

80. Leiomyosarcoma
• Malignant tumor of smooth muscle
• Necrotic, with atypical cells and lots of mitoses
• Often recur after surgery
• Many metastasize, especially to lungs
• 5 year survival = 40%
80
80

81. Leiomyoma Leiomyosarcoma 81
81

82. Leiomyoma Leiomyosarcoma 82
82

83. Endometrial Carcinoma
• Peak age: 55-65 (not before 40)
• Frequently arises in endometrial hyperplasia
• Risk factors: obesity, nulliparity, estrogen replacement
• Symptoms: leukorrhea, irregular bleeding
• Metastasizes late
83
83

84. Adenocarcinoma of the Endometrium
=
Carcinoma of the Uterus 84
84

85. 85
85

86. 86
86

87. ADENOCARCINOMA
of the ENDOMETRIUM
• Papillary, Polypoid
• Clear Cell
• Adeno-Squamous
• Mucinous
• Serous
• Preceded by hyperplasia (EIN), dysplasia
• Estrogenic, DES effects
• Ass. w.: obesity, diabetes, hypertension, infertility
• Stromal “sarcomatous” conditions can co-exist,
i.e., “adenosarcoma”
87
87

88. GRADING and STAGING
• GRADING
– 1, 2, 3
– Well, Moderate, Poor
• STAGING
– (I) Corpus
– (II) Corpus + Cervix
– (III) Beyond uterus,
but inside true pelvis
– (IV) Outside true
pelvis or involving
bladder or rectal
mucosa
88
88

89. Fallopian Tubes
•Inflammation
•Cysts
•Neoplasms
89
89

90. SALPINGITIS/PID
GC and
CHLAMYDIA
PYOSALPINX
PERITONITIS
TUBO-OVARIAN
ADHESIONS
STERILITY
INFERTILITY
90
90

91. Peritubal CYSTS
• Endometriosis
• Hydatid Cysts of Morgagni
(Mullerian rests) Para-, Peri-
tubal)
91
91

92. TUBAL NEOPLASMS
Adenocarcinomas
Leiomyomas
92
92

93. Female Reproductive System Outline
• Ovaries
• Nonneoplastic
diseases
• Tumors
93
93

94. CHAPTER 22
DISEASES of
OVARIES
PREGNANCY
PLACENTA 94
94

95. GENITAL RIDGE
6 WEEKS
95
95

96. 96
96

97. 97
97

98. Everything
you can see
or feel is
lined by
serosa (i.e.,
mesothelial
cells,
visceral and
parietal 98
98

99. 99
99

100. 100
100

101. TERMS
• “Germinal” Epithelium (Mesothelium)
• Ovum (Oocyte)
• Tunica Albuginea
• Primordial Follicle
• Primary Follicle
• Mature “Graffian” follicle (antral or secondary)
• Granulosa cells ( Estrogen)
• Thecal cells ( Estrogen)
• Corpus luteum ( Progesterone)
• “Atretic” follicle
• Corpus Albicans
• “Stroma”
101
101

102. 102
102

103. 103
103

104. 104
104

105. 105
105

106. B=GRANULOSA D=THECA INTERNA E=THECA EXTERNA
106
106

107. 107
107

108. 108
108

109. ESTROGEN
• Controlled by FSH and LH
• Develop, Lactate Breast Lobules
• Proliferate Endometrial Glands
• “Cardioprotective”
• “Bone Mass” protective
109
109

110. PROGESTERONE
• Controlled by FSH and LH
• SECRETE Endometrial Glands
• IMPLANTATION of the blastocyst
• Lactation
110
110

111. DISEASES of
OVARIES
•CYSTS:
–Follicular
–Luteal
111
111

112. FOLLICULAR CYST
MOST COMMON
112
112

113. CORPUS LUTEUM
CYST
113
113

114. POLY-Cystic Ovarian Disease
(Stein-Leventhal syndrome)
5% Prevalence
Anovulation
Oligomenorrhea
Obesity
Hirsutism
114
114

115. Polycystic Ovaries
115
115

116. B=GRANULOSA D=THECA INTERNA E=THECA EXTERNA
116
116

117. DISEASES of
OVARIES
• DEGENERATIVE?
• INFLAMMATORY?
• CYSTS
• TUMORS
– Müllerian (“Germinal”)
– Germ Cell
– Sex Cord/Stromal
– Metastatic
117
117

118. Surface epithelial tumors
• Cystadenoma
• Cystadenocarcinoma
Germ cell tumors
• Teratoma
• Dysgerminoma
• Yolk sac tumor
• Choriocarcinoma
• Granulosa-theca cell tumor
• Sertoli-Leydig cell tumor
Sex cord-stromal tumors
Origin of Ovarian Tumors
118
118

119. Cystadenoma
• Benign tumor derived from surface epithelium
• Repeated ovulation, scarring, infolding of
epithelium leads to cysts, which can undergo
neoplastic transformation
• Typically large, occasionally bilateral
119
119

120. Patient with ovarian cystadenoma
120
120

121. Patient with ovarian cystadenoma
121
121

122. Ovarian cystadenoma
122
122

123. Ovarian cystadenoma
123
123

124. Ovarian cystadenoma
124
124

125. Teratoma
• Benign tumor with differentiation along all three
germ cell layers (ectoderm, endoderm, mesoderm)
• Usually cystic, with skin inside (“dermoid cyst”)
• Sebaceous material, matted hair, teeth, bone…
• Malignant variant has immature tissues
125
125

126. Teratoma
126
126

127. Teratoma
127
127

128. Ovarian Cancer
• 23,000 new cases / 15,000 deaths in 2007
• 5th commonest, 5th most deadly cancer in women
• Danger: no definitive signs until advanced
• Peak age: 50
• Most are cystadenocarcinomas
128
128

129. Papillary cystadenocarcinoma
129
129

130. Papillary cystadenocarcinoma
130
130

131. Ovarian Cancer
Symptoms
• feeling of fullness or bloating
• pelvic pain
• back pain
• abnormal menses
Risk factors
• nulliparity
• family history (BRCA gene mutation)
• NOT using oral contraceptives!
131
131

132. Ovarian Cancer
• Treatment: surgery, radiation, chemotherapy
• Prognosis depends on stage
• cancer confined to the ovary: 5y survival 70%
• cancer through ovarian capsule: 5y survival 13%
132
132

133. OVARIAN TUMORS
• MÜLLERIAN (MAJORITY)
– Serous (Benign, Borderline, Malignant)
– Mucinous (Benign, Borderline, Malignant)
– Endometroid (Benign, Borderline, Malignant)
– Adenosarcoma (Carcinoma AND Sarcoma)
– Mesodermal Mixed (MULTIPHASIC Sarcoma)
– Clear Cell
– Brenner (almost always benign)
– Transitional (almost always look like Brenner)
• Germ Cell
• SEX-CORD/STROMAL
• METASTATIC 133
133

134. OVARIAN TUMORS
• Solid vs. Cystic
• Functional vs. NON-functional
• Benign vs. Malignant
• First clinical presentation may be ascites
• Malignant ascites in a woman is ovarian
cancer until proven otherwise
• CA-125 is THE important tumor marker in
ovarian cancer, especially as a follow up.
134
134

135. SEROUS, BENIGN
135
135

136. MUCINOUS, BENIGN
136
136

137. 137
137

138. 138
138

139. 139
139

140. PSAMMOMA bodies are dried up papillae of papillary adenocarcinomas, usually in
the thyroid, but in ANY papillary adenocarcinoma 140
140

141. 141
141

142. OTHER MÜLLERIAN
• ENDOMETRIOD, malignant
– (looks like endometrium)
• CLEAR CELL, malignant
– (clear cells, reminiscent of renal clear cell ca.)
• CYSTADENOFIBROMA, benign
– (BENIGN “FIBROUS” COMPONENT)
• BRENNER TUMOR, benign
– (transitional cell nests)
• CARCINOMA with SARCOMA
– (adenosarcoma, mixed Müllerian) 142
142

143. “GERM CELL” Tumors
• Teratomas (usually benign in ovary), i.e.,
“mature” cystic teratoma or dermoid cyst
• “Immature” teratomas are regarded as
malignant
• Dysgerminoma (look exactly like the
testicular seminoma), malignant
• Endodermal Sinus (Yolk Sac),
malignant, Just like testicular
• Choriocarcinoma, malignant, just like
testicular 143
143

144. 144
144

145. 145
145

146. 146
146

147. 147
147

148. Dysgerminoma:Female::Seminoma:Male
148
148

149. ENDODERMAL SINUS
TUMOR, aka
YOLK SAC TUMOR 149
149

150. CHORIOCARCINOMA,
Just like testis or placenta
150
150

151. SEX-CORD/STROMAL
TUMORS
• Chiefly benign and NON-cystic,
i.e., “solid”, often functional
(hyper-estrogen-ism)
• Granulosa-Theca
• Fibroma-Theca
• Sertoli-Leydig (Androblastoma)
151
151

152. CALL-EXNER
BODIES 152
152

153. 153
153

154. DISEASES of
PREGNANCY
•EARLY Pregnancy
•LATE Pregnancy
154
154

155. DISEASES of
PLACENTA
• “BENIGN” tumors (MOLES)
• Border line (invasive mole)
• MALIGNANT tumors
(CHORIOCARCINOMA)
155
155

156. EARLY PREGNANCY
• SPONTANEOUS ABORTION
• ECTOPIC PREGNANCY
156
156

157. Spontaneous Abortion
• 15% - 35%
• Fetal Causes
–Usually Genetic
• Maternal Causes (placental,
uterus infections or trauma)
–Toxo, Mycoplasma, Listeria
–Trauma
157
157

158. Ectopic Pregnancy
• Chiefly TUBAL, but ovarian or
abdominal rare
•1% OF NORMAL WOMEN
•35%-50% OF WOMEN with
previous SALPINGITIS/PID
• + HCG, Abdominal pain, 1st
trimester, ultrasound 158
158

159. 159
159

160. LATE PREGNANCY
• PLACENTAL ANOMALIES
• TWIN PLACENTAS
• PLACENTAL INFLAMMATIONS
• TOXEMIA (ECLAMPSIA/PRE-
ECLAMPSIA)
• INTRAUTERINE GROWTH
RETARDATION 160
160

161. PLACENTAL ANOMALIES
• Accessory Lobes
• Bipartite Placenta
• Circumvallate Placenta
• Placenta Accreta, chorion going
DIRECTLY to the myometrium
161
161

162. 162
162

163. 163
163

164. 164
164

165. CIRCUMVALLATE 165
165

166. PLACENTA ACCRETA
NO DECIDUA BETWEEN VILLI AND MYOMETRIUM
166
166

167. MRI of Placenta PREVIA, or LOW-LYING placenta, usually
anatomically normal, but just lies LOWER than it should.
167
167

168. MONOCHORIONIC = MONOZYGOTIC
168
168

169. TOXEMIA of PREGNANCY
(PRE-eclampsia)
• Hypertension
• Proteinuria
• Edema
• Related to Placental Ischemia
• Risk for DIC, convulsions (eclampsia)
169
169

170. Intrauterine Growth Retardation
• Fetal causes: Genetic, malformations
• Maternal Causes, vascular diseases,
toxemia, infections, placental
diseases
• Placenta size (350-700g) ~ Fetal size
(7.5lb)
170
170

171. Placental Infections
• Villitis vs. chorionamnionitis vs. funisitis
• ASCENDING vs. hematogenous
• ASCENDING are usually bacterial, and
chorionamnionitis
• Hematogenous are often TORCH, and
villitis
171
171

172. Placental Neoplasms,
i.e. gestational trophoblastic disease
• Benign: MOLES (Hydatidiform moles)
• Malignant: CHORIOCARCINOMA
• BOTH are associated with increased or
persistent levels of the placental
hormone HCG
172
172

173. 173
173

174. Hydatidiform Mole
• 1/1000 in USA
• 1% in Indonesia
• Also called NON-invasive mole in
its most common benign variant,
but can also be “invasive”
• Complete (2% chorioCA incidence)
or partial (0% incidence)
• Grapelike clusters, i.e., swollen villi
174
174

175. 175
175

176. The MAIN thing
differentiating benign
from malignant from
worrisome trophoblastic
neoplasms is
INVASIVENESS
of the trophoblast 176
176

177. 177
177

178. 178
178

179. Breast
• Many breast diseases present as lumps
• Most lumps represent benign things…
• …but a lump always needs to be evaluated
• Ultrasound, mammography, fine needle
aspiration, and biopsy are the usual methods
179
179

180. Most breast lumps are benign
180
180

181. Fibrocystic Change
• Two kinds: nonproliferative and proliferative change
• Cause: exaggeration of normal breast cycles
• Rarely associated with increased cancer risk
• Very common (present in most women at autopsy)
• Called fibrocystic change, not fibrocystic disease
181
181

182. Fibrocystic Change
• Nonproliferative fibrocystic change
• increased stroma
• dilation of ducts, formation of cysts
• Proliferative fibrocystic change
• hyperplasia of breast epithelium
• If epithelium shows atypia, 5x ↑ risk of cancer
182
182

183. Fibrocystic change
183
183

184. Normal breast
184
184

185. Nonproliferative fibrocystic change
185
185

186. Proliferative fibrocystic change
186
186

187. Fibroadenoma
• Most common benign breast tumor
• Stimulated by estrogen
• Peak incidence 20s
• Solitary, discrete, moveable mass
• Fibrous tissue with compressed ducts and lobules
187
187

188. Fibroadenoma
188
188

189. Fibroadenoma
189
189

190. Breast Carcinoma
• 180,00 new cases / 40,000 deaths in 2007
• Most common, 2nd deadliest cancer in women
• Lifetime risk: 1 in 8
• 75% of patients are >50
• Rate was increasing but now stable
190
190

191. Breast Carcinoma Risk Factors
• Age
• Family history
• Increased estrogen exposure
• Obesity
• Alcohol consumption
• High-fat diet
191
191

192. Breast Carcinoma Family History
• 5-10% of all cases are hereditary
• Worry if first degree relative with breast cancer
• Most have BRCA-1 or BRCA-2 mutations
• Tumor suppressor genes; help repair DNA
• Genetic testing difficult
• Most carriers get cancer by age 70
192
192

193. Breast Carcinoma Clinical Findings
If discovered by palpation
• Solitary, painless, moveable mass
• 2-3 cm in diameter
• Axillary nodes positive in 50% of patients
If discovered by mammography
• 1 cm in size
• Axillary nodes positive in only 15% of patients
As disease progresses
• Fixation to chest wall
• Adherence to overlying skin
• Peau d’orange
193
193

194. 194
194

195. Advanced breast carcinoma: fixation to skin
195
195

196. Peau d’orange
196
196

197. Inflammatory breast carcinoma
197
197

198. Inflammatory breast carcinoma
198
198

199. Breast Carcinoma Histologic Types
Non-invasive
• Ductal carcinoma in situ (DCIS)
• Lobular carcinoma in situ (LCIS)
Invasive
• Ductal
• Lobular
• Inflammatory
• Others
199
199

200. Normal breast
200
200

201. Lobular carcinoma in situ
201
201

202. Invasive breast carcinoma
202
202

203. Invasive ductal breast carcinoma low grade
203
203

204. Invasive ductal breast carcinoma high grade
204
204

205. Inflammatory breast carcinoma
205
205

206. Breast Carcinoma Prognostic Factors
• Size of tumor
• Lymph node involvement
• Distant metastases
• Grade of tumor
• Histologic type of tumor
206
206

207. Sentinel node biopsy
207
207

208. Overall stage
Stage 0
Stage I
Stage II
Stage III
Stage IV
TNM staging system for breast cancer
T
DCIS
<2 cm
<5 cm
>5 cm
<5 cm
>5 cm
Any T
Any T
Any T
N
0
0
<3
0
4+
1+
10+
Any N
Any N
M
M0
M0
M0
M0
M0
M0
M0
skin or
chest wall
M1
5y survival
92%
87%
75%
46%
13%
208
208