TUMOR GINEKOLOGIS 

dr Rimonta F Gunanegara, SpOG

Department of Obstetrics & Gynecology
School of Medicine Maranatha Christian University
 Cell Cycle
 The cell cycle consists of an ordered set of events,
resulting in the production of two daughter cells.
 Embryonic cells divide very rapidly mature cells
divide rarely  response to signals such as wounding,
or not at all control mechanisms.
 Transitions out of gap phases (G1, G2) are regulated
by cyclins and cyclin dependent kinases (CDK).
 Cyclins are only present at certain times during the
cell cycle.  MPF (Maturation Promoting Factor)
includes the CDK and cyclins that triggers progression
through the cell cycle.
Growth factors  stimulate cell division  signals to cell cycle.
blocking the cell cycle cell suicide, or apoptosis.
cells have a finite lifespan
 Cell cycle

Cancer cell
Cancer
 Cancers are diseases in which there is a defect in
the regulation of the cell cycle.
 Cancer cells are rapidly dividing cells that no longer
are controlled by the mechanisms  unchecked
growth  tumors

Metastasizing cancer cell

 Three classes of genes
 Proto-oncogenes (unmutated oncogenes) stimulate cell
division in a regulated manner. Proto-oncogenes include
growth factors, growth factor receptors, and cyclins.
 Oncogenes are mutated forms of these genes that result
in unregulated stimulation of cell division.
 Three classes of genes

 Tumor suppressor genes prevent cell division. Mutations

in tumor suppressor genes result in the loss of this
prevention of cell division.
 DNA repair genes promote repair of mutations that occur
during the cell cycle. Loss of DNA repair genes results in
the accumulation of many mutations within a cell.
 OVARIAN TUMORS

Department of Obstetrics & Gynecology

School of Medicine Maranatha Christian University
Immanuel Hospital
 OVARIAN TUMORS

Functional
Follicular
Corpus luteum
Theca lutein
Inflammatory
Tubo-ovarian abscess or complex
Neoplastic
Germ cell
Benign cystic teratoma
Other and mixed
Epithelial
Serous cystadenoma
Mucinous cystadenoma
Brenner tumor, Mixed tumor,
Other
Endometrioma
Ovarian cancer
Prepubertal Age Group
Differential Diagnosis
Fewer than 5% of ovarian malignancies
occur in children and adolescents.
Ovarian tumors account for approximately
1% of all tumors in these age groups.
Germ cell tumors make up one half to two-
thirds of ovarian neoplasms in individuals
younger than 20 years of age.
As many as 35% of all ovarian
neoplasms occurring during childhood
and adolescence are malignant. In girls
younger than 9 years of age,
approximately 80% of the ovarian
neoplasms were found to be malignant.
Epithelial neoplasms are rare.
Diagnosis and Management
Ultrasonography : excellent tool for
predict-ing the presence of a simple
ovarian cyst.
Unilocular cysts are virtually always
benign and will regress in 3-6 months.
Adolescent Age Group
Differential Diagnosis
Ovarian Masses
The likelihood of functional masses increases
after menarche.
The risk of malignant neoplasms : lower
among adolescents than among younger
children.Epithelial neoplasms occur with
increasing frequency with age.
Germ cell tumors : most common tumors of
the first decade of life, occur less frequently
during adolescence.
Mature cystic teratoma is the most
frequent neoplastic tumor of children
and adolescents, accounting for more
than one-half of ovarian neoplasms in
women younger than 20.

Functional ovarian cysts occur

frequently in adolescence.
Uterine Masses
Uterine abnormalities : rare in
adolescence. Uterine leiomyomas not
commonly seen.
Obstructive uterovaginal anomalies
present at the time of menarche or
thereafter, at wide range: imperforate
hymen, transverse vaginal septa, vaginal
agenesis, etc.
Hemaocolpos, hematometra result in a
large mass.
Inflammatory Masses
Adolescents have the highest rates of PID of
any age group, if one considers only
individuals at risk for STDs.
Inflammatory masses may consist of :
 tubo-ovarian complex (a mass consisting
of matted bowel, tube, and ovary)
 tubo-ovarian abscess
 pyosalpinx
 hydrosalpinx
Pregnancy
In adolescents, pregnancy should always
be considered as a cause of a pelvic mass.
Diagnosis
History and pelvic examination are critical in
the diagnosis of a pelvic mass.
Laboratory studies include a pregnancy test.
Tumor markers, including alpha fetoprotein
(AFP) and hCG, maybe elaborated by germ
cell tumors.
The primary diagnostic technique is ultra-
sonography.
Management
Management depends on the suspected
diagnosis as well as the presenting
complaint.
Asymptomatic unilocular cystic masses
are best managed conservatively,
because the likelihood of malignancy is
low.
If surgical management is required based
on symptoms or uncertainty of diagnosis,
attention should be paid to minimizing the
risks of subsequent infertility resulting
from pelvic adhesions.
In addition, every effort should be made
to conserve the ovarian tissue. In the
presence of a malignant unilateral ovarian
mass, management may include unilateral
oophorectomy rather than more radical
surgery.
Reproductive Age Group

Differential Diagnosis
Nonovarian or nongynecologic
conditions may be confused with an
ovarian or uterine mass.
Uterine Masses
Uterine leiomyomas (uterine myomas or
fibroids) are the most common benign
uterine tumors.
Ovarian Masses
During reproductive years : most
common ovarian masses are benign.
Two-thirds of ovarian tumors :
encountered during reproductive years.
Most (80-85%) of ovarian tumors :
benign.
The chance that a primary ovarian tumor
is malignant in a patient younger than
45 years of age is less than 1 in 15.
Most tumors produce few or mild,
nonspecific symptoms.
Most common symptoms :
 abdominal distension
 abdominal pain/discomfort
 lower abdominal pressure sensation
 urinary symptoms
 gastrointestinal symptoms
If hormonally active, may be present :
hormonal imbalance
(vaginal bleeding, etc)

Other symptom, possibly :

 acute pain
(due to adnexal torsion, cyst
rupture, bleeding into cyst, etc)
Pelvic findings:
 unilateral
 cystic  benign ?
 mobile
 smooth

 
 bilateral
 solid
 fixed
 irregular  malignant ?
 with ascites
 with cul-de-sac nodules
 with rapid growth
Nonneoplastic ovarian cyst =
functional ovarian cyst
e.g.:
Follicular cyst
Corpus luteum cyst
Theca lutein cyst
Follicular cyst:
 the most common functional cyst
 rarely larger than 8 cm
 usually found incidentally
 usually resolve in 4-8 weeks
Corpus luteum cyst:
 called a cyst when its diameter is
greater than 3 cm
Theca lutein cyst:
 the least common of functional
ovarian cyst
 usually bilateral
 usually occurs with pregnancy
 may be associated with ovulation
induction treatment
Other benign masses :
Endometriosis/endometrioma

Polycystic Ovarian Syndrome (PCOS)

or Disease (PCOD)
Neoplastic Masses: Benign
Benign cystic teratoma (dermoid cyst)
Serous cystadenoma
Mucinous cystadenoma

Benign cystic teratomas:

 80% occur during reproductive years
 Malignant transformation: less than 2%
 mostly in women > 40 years
 More likely to undergo torsion
Serous cystadenomas:
 Second most common after benign cystic
teratoma
 5-10% have borderline malignant potential
 20-25% malignant
Mucinous cystadenomas:
 5-10% malignant
 Other benign ovarian tumors:
Fibroma
Brenner tumor, etc
Diagnosis
A complete pelvic assessment including
rectovaginal examination should be performed
to determine the origin, nature and size of the
pelvic mass.
The most commonly indicated imaging study
is pelvic ultrasonography. An ultrasonic
scoring system has been developed to
predict benign versus malignant adnexal
masses by detecting the nature of the tumor
(solid, cystic), clear or smooth appearance of
the cyst border, nodularity of the tumor, and
presence of ascites.
Management
Treatment for ovarian masses suspected to be
functional tumors: expectant. The use of oral
contraceptives unproven to resolve more
rapidly, but effective in reducing the risk of
subsequent ovarian cysts.
Surgical intervention is warranted in the face
of significant pain or the suspicion of
malignancy.
On ultrasonography, large cysts and those
that have multiloculations, septa, papillae, and
increased blood flow are all suspected signs of
neoplasia.
If a malignant cyst is suspected, at any
age, explorative laparotomy should be
performed promptly.
Aspiration procedures (ultrasonographic or
CT scanning) should not be used in women
in whom there is a suspicion of
malignancy.
Laparoscopic surgery should be reserved
for diagnostic or therapeutic purposes for
patients at very low risk for malignancy.
Postmenopausal Age Group
Differential Diagnosis
Ovarian Masses
During the postmenopausal years, the ovaries
become smaller.
Before menopause, the dimensions are approximately
: 3.5 cm x 2 cm x 1.5 cm.
In early menopause : 2 cm x 1.5 cm x 0.5 cm.
In late menopause : 1.5 cm x 0.75 cm x 0.5 cm.
Postmenopausal palpable ovary
(PMPO) syndrome : any ovary that is
palpable on examination beyond the
menopause is abnormal  deserves
evaluation. However, this has not
been shown to be a reliable predictor
of malignancy.
The incidence of ovarian cancer increases
with age and is predominantly a disease
of postmenopausal women; the average
patient age is 61 years.
When a cyst is asymptomatic, small (<5
cm in diameter), unilocular, and thin-
walled, the risk of malignancy is
extremely low and these masses can be
followed conservatively, without surgery.
The risk of malignancy for women older
than 50 years of age or for
postmenopausal women (approximately
the same groups) at the time of
laparotomy for a pelvic mass is
approximately 50%.
Diagnosis
A personal and family medical history is
helpful in detecting individuals at
increased risk for the development of
ovarian cancer. However, patients with
hereditary forms of epithelial ovarian
cancer account for only a small
percentage of all cases; 95% of cases of
ovarian cancer are sporadic.
Management

The use of improved imaging techniques

may allow the nonoperative management
of ovarian masses that are probably
benign.
When surgery is indicated, selection of the
appropriate surgical procedure is critical
for effective therapy.
 Ovarian cancer

brenner, mucinous, cervik ca

 TUMOUR
OF
UTERINE CERVIX

Department of Obstetric and Gynaecology

School Medicine of Maranatha Christian University
Immanuel Hospital Bandung
 BENIGN TUMOUR Of UTERINE CERVIX

• CONDYLOMA ACUMINATA
• CERVICAL POLYP
• NABOTHIAN CYST
CONDYLOMA
ACCUMINATA
• LOW RISK, HPV TYPE 11
• RARE ( VULVA : THE COMMON SITE )
• TH/ : ELECTRO SURGERY/ CAUTERIZATION
 CERVICAL POLYP

• EXCESSIVE GROWTH OF ENDOCERVIX

• PEDUNCULATED
• USSUALY ASYMPTOMATIC
CONTACT BLEEDING, VAGINAL DISCHARGE
• Th/ : EXTIRPATION,
ECC (ENDOCERVICAL CURETTAGE )
 NABOTHIAN CYST/ OVULE

• ENDOCERVIX REPLACED BY SQUAMOUS EPITHEL

( = SQUAMOUS METAPLASIA )
UNDER LYING CERVICAL GLAND CYST
• SMALL
• Th/ - NONE, UNNECESSARY
- LARGE SIZE : INCISION, CAUTERIZATION
MALIGNANT TOMOUR OF UTERINE
CERVIX ( CERVICAL CANCER )

COMMON  INDONESIA NUMBER 1’s!

 EARLY FINDING IS POSSIBLE
 EARLY STAGE  CURABLE
 DEVELOPING COUNTRY  LATE STAGE
ETIOLOGI : HPV (STD)
RISK FACTORS :
- MULTIPLE SEXUAL PARTNER :
 3-5:8x
 > 6 : 14 x
- TEENAGE MARRIED (15-20 YEARS) : 2,5 x
- SMOKING : 3 x
- CANCER HISTORY IN FAMILY
- NUTRIENT DEFICIENCY : Vit. A, Folic acid
SYMPTOM : PREINVASIVE STAGE NONE

INVASIVE STAGE

• MALODOROUS VAGINAL DISCHARGE

• CONTACT / SPONTANEOUS VAGINAL BLEEDING

• SYMPTOM & SIGN OF METASTASIS

 HISTORY OF DISEASE
CIN I Performing :

PAP Smear
CIN II
1-10 year
Colposcopy
CIN III

Biopsy

Invasive cancer
Spread to : parametrium, pelvic lymph node,
bladder, rectum, bone, lung
DIAGNOSIS :
1. PAP
 Easy
 Cheap
The best tool
 No pain for screening
 Sensitive
 Low false negative
Pathologist : rare Mass screening (?)
Fail to reduced invasive cancer
in Indonesia
2. Colposcopy
Three dimensions, Magnified
Examine surface condition of the
cervix and the underneath vessels
 No pain
 Colposcopic finding :
 Normal
 Suspicious area  biopsy
 Invasion
3. VIA = IVA ( Visual Inspection with
Acetic Acid Application )
 Apply acetic acid 3 - 5 %
 Observe : acetowhite epithelium
 Biopsy if necessary
4. Schiller Test
 Apply : KI (Potassium Iodine)
Normal epithelium  brown
Dysplasia, infection  pale
PREVENTION
 Avoid risk factors
 Early detection
Treatment
Precancer/ preinvasive
Pap Smear, VIA, Schiller test
Treatment at pre invasive stage :
Electro surgery
Cryosurgery
Laser vaporization
Conization
Hysterectomy

Invasive Speculum Exam., Biopsy

TREATMENT INVASIVE CANCER
Stage IA – IIA : Surgery
Stage IIB-III B : Radiation +
Chemotherapy
Stage IV : Chemotherapy
 cancer

normal
 Fibroids
 Myomas
Pedunculated
subserosal Myoma
subserosal

intramural

Pedunculated
submucosal

submucosal

intra ligamenter
Cevical Myoma
Pedunculated
Submucosal
Symptom sign

 Asymptomatic discovered incidentally

 Irregular enlarged uterus
 Menorrhagia
 Chronic pelvic pain - dysmenorrhea,
dyspareunia, pelvic pressure
(Acute: torsion, infark red degeneration)
 Urinary symptoms :
 frequency
 partial ureteral obstruction
 completely ureteral obstruction
 Infertility < 3% of infertile woman
 Management

 Principally : Hysterectomy
 Exception :
 Myomectomy :
Reproductive function preservation
 Sub serous without tubal involvement
 Laparotomy / Hysteroscopy
 GnRH :
Small, fertility
 Pre myomectomy
 Small, premenopause
 Medical contraindication to surgery
Leiomyoma and pregnancy

 Reduces fertility
 Pregnant hypertrophy rapid
uterine enlargement
 Abortion, preterm, IUGR
 Subserosal obstructed labour
 Cervical
Adenomyosis

= internal endometriosis
: endometrial glands within the myometrium

 Reproductive age everage age > 40

years

Symptom sign
 Often asymptomatic
 Menorrhagia
 Dysmenorrhea, before - during menses
 Diffusely enlarged uterus,
usually < 14 cm length, mobile.
Management

 Depend on patient age - desire for

fertility
 Conservative treatment :
 Young woman, preserve fertility
 premenopause
- NSAID
- Contraseptive agent
 Hysterectomy
Endometrial Hyperplasia

Spectrum of morphologic and biologic alteration of

endometrial gland and stroma (physiologic - Ca insitu)

Type of Hyperplasia Progresssion to

Cancer ( % )

Simplex ( Cystic (-) atypia 1

Complex ( Adenomatous (-) Atypia 3
Atypical :
Simplex ( cystic (+) atypia 8
Complex ( adenomatous (+) atypia 29
 Influenced by :
 age
 underlying ovarian disease
 Endocrinopathy
 obesity
 exogenous hormones exposure

 Sign : metrorrhagia
Management

 Young age progestin

 Old women D & C PA :
 atypia (-) progeteron th/ +
curretage 3-6 month
 atypia (+) HT
Progesteron + curretage
Ca endometrium

 Mostly in 5th - 6th decades of life

 Risk factors :
nullipara
 infertility & history of irregular menses
 late menopausal age
 overweight
 estrogen replacement th (-) Progesteron
 tamoxifen administration
 DM
Symptom sign

 50% asymptomatic
 Vaginal bleeding / discharge, perimenopause
 Pelvic pressure / discomfort,
 Cervical stenosis hemato / pyometra
 Uterine enlargement, adnexal involvement
Diagnosis

 Endometrial sampling : aspiration biopsy

 D & C
 Hysterectomy
 USG
 Tumor marker : Ca 125
Treatment

 Depend on grade, type & stage of tumors

 Surgical : - extended hysterectomy
- lymphadenectomy
 Hormonal
 Radiation
Uterine Sarcoma

Rare, Premenopausal age

Uterine enlargement, vaginal bleeding
3 most common :
 endometrial stromal sarcoma (EES)
 Leiomyosarcoma (LMS)
 Malignant Mix Mullerian Tumors (MMS)
Prognosis : poor
Adenosarcoma of the uterus
Therapy

Surgery
Radiotherapy Pelvic recurrence of
ESS & MMS
Chemotherapy for LMS : Doxorubicin
 Tumor vulva

Department of Obstetric and Gynaecology

School Medicine of Maranatha Christian University
Immanuel Hospital Bandung
TUMOR GANAS VULVA
 jarang terjadi
 frekuensinya + 3-4% dari seluruh tumor ganas
primer genitalia wanita.
 Karsinoma epidermoid merupakan 90-92% dari
seluruh kasus, sisanya terdiri atas melanoma,
adenokarsinoma, karsinoma sel basal, dan
sarkoma.
 Blm ditemukan faktor penyebab Ca.vulva yang
spesifik
 hubungan antara Ca.invasif dg distrofi vulva &
neoplasi intra-epitel vulva (NIV) belum jelas.
TUMOR GANAS VULVA (Lanjutan)
 Pruritus vulva merupakan gejala penting yang
mendahului kejadian kanker vulva invasif.
 Infeksi “human papilloma virus” (HPV) ditemukan
pada 20-60% pasien kanker vulva invasif.
 Kanker vulva biasanya dihubungkan dengan sifilis
dan limfo-granuloma venereum serta granuloma
inguinale.
 Sekitar 90-92% kanker vulva invasif berjenis
karsinoma epidermoid (karsinoma sel skuamosa).
Karsinoma Sel Skuamosa
 Karsinoma vulva mikroinvasif : ukuran < 2 cm
dan invasi stroma < 1 mm.
 >>> pada masa pascamenopause
 Rata-rata usia + 65 tahun.
 Umumnya datang dg benjolan / massa di vulva
 Kadang-kadang keluhan awal dapat berupa
massa anak sebar di lipat paha.
 >>> pd labia mayora, dapat juga di labia
minora, klitoris, dan perineum.
In situ

cancer
Diagnosis
Ditegakkan dg pemeriksaan histopatologi dari
biopsi tumor.

Cara penyebaran
1.Ekstensi langsung ke organ di sekitarnya
2.Embolisasi limfatik ke kelenjar getah bening
regional
3.Hematogen ke tempat-tempat yang jauh,
seperti paru, hati, dan tulang.
Pengobatan

 Terapi primer : operasi.

 Dulu vulvektomi radikal dan diseksi lipat

paha (“groin dissection”) en bloc dengan
atau tanpa limfadenektomi pelvis
Selama 15 th terakhir ada perubahan pd
manajemen Ca vulva.

Perubahan tersebut :
1.Pengobatan sangat individual.
2.Konservasi vulva pd pasien tumor unifokal
3.Mengurangi tindakan groin dissection pada
penderita T1 tumor & invasi stroma < 1 mm
4.Eliminasi dari limpadenektomi pelvic rutin.
5.Tindakan separate groin insision untuk groin
diseksi untuk mempercepat penyembuhan luka.
Perubahan tersebut (Lanjutan):

6.Mengurangi tindakan kontralateral groin diseksi

pada lesi T1 lateral & negatif node ipsilateral
7.Radiasi prabedah untuk menghindari
eksenterasi pada kasus lanjut.
8.Radiasi pascabedah untuk mengurangi kejadian
kekambuhan di daerah lipat paha pada pasien
dengan kelenjar lipat paha yang multipel positif.
 Rekurensi Ca.vulva erat kaitannya dg jumlah
kelenjar getah bening inguinal yang positif.
 Jumlah KGB yang positif < 3 buah, terutama
jika mikroskopik sifatnya, kemungkinan kecil
mengalami kekambuhan
 > 3 kelenjar positif sering mengalami rekurensi
lokal, regional, dan sistemik.
Stadium kanker vulva (revisi FIGO tahun 1988)
Stadium FIGO TNM Gambaran klinik/patologi
Stadium 0 Tis Karsinoma in situ, karsinoma intraepitel
Std I T1N0M0 Tumor terbatas di vulva atau perineum,
ukuran terbesar < 2 cm, kelenjar negatif
Ia Invasi stroma kurang dari 1 mm
Ib Invasi stroma 1 mm atau lebih
Stadium II T2N0Mo Tumor terbatas di vulva dan/atau perineum,
ukuran terbesar > 2 cm, kelenjar negatif
Stadium III T3N0M0 Tumor dari segala ukuran, dengan :
T3N1M0 1. Penyebaran ke uretra bagian bawah / anus
T1N1M0 2. Metastasis ke kgb regional unilateral
T2N1M0
Stadium IVA T1N2M0 Tumor menginvasi uretra bagian atas, mukosa
kandung kemih, mukosa rektum, tlg panggul,
atau metastasis ke kgb regional bilateral
T3N2M0
T4,segala N,M0
Stadium IVB segala T&N, M1 Metastasis jauh, termasuk ke kgb pelvis