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Society of Gynecologic Oncologists of the Philippines

CLINICAL PRACTICE GUIDELINES November 2010

Gina Carmencita Bacnis. MD

SGOP CPG
Objectives: 1. To equip the obstetrician-gynecologist

with the sufficient knowledge about the screening, diagnosis, and management of cancer of the female genital tract,
2. To provide a quick reference guide which may be used in the daily clinical practice.

CERVICAL CANCER

CERVICAL CANCER I. INCIDENCE


2ND mc cancer among women worldwide,
493,000 new cases, 274,000 deaths in 2002 83% occur in developing countries, Representing 15% of female cancers Philippines: stable 22.5 cases/ 100,000 women Overall 5-year survival rate of 44%, Mortality rate of 1/10,000 women

2/3 diagnosed in an advanced stage, high mortality

CERVICAL CANCER II. RISK FACTORS


1.HPV infection is the necessary cause of

cervical cancer. (Level II, Grade A)


HPV 16, 18, 45, 31, 33, 58, 52, 35, 59, 56, 6, 51,

68, 39, 82, 73, 66, and 70 HPV DNA in cervical neoplasia is the first necessary cause of a human cancer ever identified.

CERVICAL CANCER II. RISK FACTORS


2. Parity of 7 or more increases the risk for

cervical cancer. (Level II-2, Grade A)


4-fold increased risk vd nulliparous HPV(+)women High parity: maintains the transformation zone on

the ectocervix for many years facilitating the direct exposure to HPV, and or other co-factors Hormonal changes: modulate the immune response to HPV and influence risk of persistence or progression

CERVICAL CANCER II. RISK FACTORS


3. Long-term use of OCPs could increase the risk

of cervical Ca by up to 4-fold in women with HPV infection. ( level II-2, Grade A)


Hormone-related mechanisms may influence the

progression from pre-malignant to malignant cervical lesions by promoting integration of HPV DNA into the host genome deregulation of E6 and E7 expression RR of cervical cancer is increased in current users of OCP, and declines after use ceases.

CERVICAL CANCER II. RISK FACTORS


4. The risk of squamous cell carcinoma increases

in current smokers with the number of cigarettes smoked per day and with younger age at starting smoking. (Level II-2, Grade A)
5. women who are co-infected with HPV and

another ST agent, such as Chlamydia trachomatis or HSV-2, are more likely to develop cervical Ca than are women who are not coinfected. (Level II-2, Grade B)

CERVICAL CANCER II. RISK FACTORS


6. Women infected with HIV are more readily infected

with high risk HPV types and are more likely to develop cervical Ca, than HIV-negative women in the same age category. (Level III, Grade C)
7. Early age at first intercourse increases the risk for

cervical Ca ( age < 14 ). (Level II-2, Grade A)


8. the risk of invasive cervical Ca increased with

lifetime number of sexual partners ( 6 or more ). (LevelII-2, Grade B)

CERVICAL CANCER II. RISK FACTORS


9. Early age at 1st full term pregnancy (age < 17 )

increases the risk for invasive cervical cancer. (Level II-2, Grade B)
10. Male circumcision is associated with a

reduced risk of penile HPV infection, and in the case of men with a history of multiple sexual partners, a reduced risk of cervical cancer in their current female partners. (Level II-2, Grade B)

CERVICAL CANCER II. RISK FACTORS


11.The risk of developing invasive cervical cancer

is 3-10x greater in women who have not been screened. (Level II-2, Grade A) Lower socioeconomic status is recognized as a risk factor for many
12. Lower socio-economic status is recognized as

a risk factor for many health problems, including cervical Ca, particularly in low-resource setting. (Level III, Grade C)

CERVICAL CANCER III. PRIMARY PREVENTION


1. Total sexual abstinence prevents HPV infection.

(Level II-2, Grade A)


2. Lifetime mutual monogamy prevents HPV infection.

(Level II-2, Grade A)


3. Consistent and correct use of barrier protection

decreases cervical cancer incidence. (Level II-2, Grade A)


4. Vaccination against HPV 16/ 18 is efficacious

against persistent HPV infection and >CIN 2+. (Level I, Grade A)

CERVICAL CANCER IV. SECONDARY PREVENTION


1. Screening via regular gynecologic

examinations and cytologic test (Pap smear) with treatment of pre-cancerous abnormalities decreases the incidence and mortality of cervical cancer. (Level II-2, Grade A)
2. Liquid based cytology offers the advantage of

doing HPV testing on the same preparation. However, it is not more sensitive or specific than conventional Pap smear. (Level II-2, Grade B)

CERVICAL CANCER IV. SECONDARY PREVENTION


3. In low resource settings, visual inspection with

acetic acid (VIA) is an acceptable alternative to Pap smear. (Level II, Grade A)
4. Screening should begin approximately 3 years

after the onset of vaginal intercourse but not earlier than 21. (Level II-2, grade A)

CERVICAL CANCER IV. SECONDARY PREVENTION


5.Annual screening with conventional cervical

cytology smears, or biennial screening using liquid based cytology, is recommended until age 30. At, or after 30, a woman who has had 3 consecutive, technically satisfactory normal/ negative for intra-epithelial lesions, or malignancy cytology results, may undergo screening every 23yrs using either conventional or liquid based cytology. (Level II-3, Grade A)

CERVICAL CANCER IV. SECONDARY PREVENTION


6. women aged 30 years and older

- had 3 consecutive negative cervical cytology screening test results - no history of CIN 2 or CIN 3, - not HIV infected, or not immunocompromised, - not exposed to DES in utero may extend the interval between cervical cytology examinations to every 3 years. (Level I-II-2, Grade A)

CERVICAL CANCER IV. SECONDARY PREVENTION


7. Women treated in the past for CIN 2-3 or

gynecologic cancers remain at risk for persistent or recurrent disease for at least 20 years after treatment, and after initial post treatment surveillance, and should continue to have annual screening for at least 20 years. (Level II-2, Grade B)
8. In women who have had a total hysterectomy

for benign indications and have no prior history of high grade CIN, routine cytology testing should be continued. (Level II-2, Grade B)

CERVICAL CANCER IV. SECONDARY PREVENTION


Discontinue cervical cancer screening between

65-70 years of age in women who have 3 or more negative cytology test results in a row and no abnormal test results in the past 10 years. (Level II-2, Grade B)
10. Co-testing using the combination of cytology

plus HPV DNA testing is an appropriate screening test for women older than 30 years. (Level II-3, Grade A)

CERVICAL CANCER IV. SECONDARY PREVENTION


11. Testing for HPV DNA currently is used in

cervical Ca screening as a triage test to stratify risk to women aged 21 years and older with a cytology diagnosis of ASC-US and postmenopausal women with a cytology diagnosis of LSIL. (Level III-B)
12. Annual gynecologic examination is

recommended regardless of the frequency of screening. (Level III, Grade C)

CERVICAL CANCER IV. SECONDARY PREVENTION


13. Women who have been immunized against

HPV 16 and 18 should be screened by the same regimen as non-immunized women. (Level III, Grade C)
14. A pap test should be obtained 2x in the 1st

year after diagnosis of HIV infection and, if the results are normal, annually thereafter. (Level III, Grade C)

FIGO 2009 CLINICAL STAGING FOR CERVICAL Ca


I IA The carcinoma is strictly confined to the cervix Invasive Ca that can be diagnosed only microscopiclally, with deepest invasion of < 5mm, largest extension of < 7mm Measured stromal invasion of < 3mm and not >5mm in depth, and extension of < 7mm Measured stromal invasion of >3mm and not >5mm in depth, extension of < 7mm Clinically visible lesions limited to the cervix uteri or subclinical cancers greater than stage IA Clinically visible lesions < 4cm Clinically visible lesions > 4cm

IA 1 IA 2 IB IB 1 IB 2

FIGO 2009 CLINICAL STAGING FOR CERVICAL Ca


II Carcinoma extends beyond the uterus but has not extended to the pelvic wall or to the lower third of the vagina Without parametrial invasion Clinically visible lesion < 4cm

IIA IIA 1

IIA 2
II B

Clinically visible lesion > 4cm


With obvious parametrial invasion

FIGO 2009 CLINICAL STAGING FOR CERVICAL Ca


III Carcinoma involves the lower 1/3 of the vagina and/or causes hydronephrosis, or non-functioning kidney

III A
III B IV

Tumor involves the lower 1/3 of the vagina, with no extension to the pelvic wall
Extension to the pelvic wall and/or hydronephrosis or nonfunctioning kidney Carcinoma has extended beyong the true pelvis or has clinically involved the mucosa of the bladder or rectum. A bullous edema, as such, does not permit a case alloted to be stage IV. Spread of growth to the adjacent organs Spread to distant organs

IV A IV B

CERVICAL CANCER
VI. Modified WHO Histological Classification of Cervical
tumors
A.EPITHELIAL TUMORS
1. Squamous cell carcinoma a. Micro-invasive squamous cell Ca b. Invasive squamous cell Ca c. Verrucous Ca d. Warty ( Condylomatous ) Ca e. Papillary squamous cell ( transitional ) Ca f. Lymphoepithelioma-like Ca 2. Adenocarcinoma a. Mucinous adenoCa b. Endometrioid adenoCa c. Clear cell adenoCa d. Minimal deviation AdenoCa e. Serous adenoCa f. Mesonephric Ca g. Well-differentiated villoglandular adenocarcinoma 3. Other epithelial tumors a. Adenosquamous carcinoma b.Glassy cell Ca c. Mucoepidermoid Ca

d. Adenoid basal Ca f. Carcinoid-like tumor g. Small cell Ca h. Undifferentiated Ca

B. MESENCHYMAL TUMORS & MIXED EPITHELIALMESENCHYMAL TUMORS


1. Leiomyoma 2. Endocervical stromal sarcoma 3. Embryonal rhabdomyosarcoma 4. Alveolar soft part sarcoma 5. Malignant mixed mesodermal tumor
1.Primary malignant melanoma 2. Primary choriocarcinoma 3.. Lymphoma 4. Leukemia 5. Primary germ cell tumor

C. MISCELLANEOUS TUMORS

CERVICAL CANCER
VII. General Guidelines in the Diagnosis and Management of Cervical Ca
1. Cervical ca is diagnosed by biopsy. 2. Cervical Ca is staged clinically. 3. If clinically indicated, proctosigmoidoscopy and

cystoscopy should be done to rule out invasion. Metastatic work-ups include renal imaging studies ( IVP ), LFTs, CXR, and skeletal survey. 4.Special diagnostic imaging studies that may be done to guide treatment planning include: UTZ, MRI, CT scan, PET, and bone scintigraphy, but not part of staging.

CERVICAL CANCER
VII. General Guidelines in the Diagnosis and Management of Cervical Ca l
5. Concurrent chemotherapy and complete

radiotherapy ( chemoradiation ) is the standard of treatment. 6. For patients who are unable to receive chemotherapy, radiation treatment alone may be given. 7. Adenocarcinomas have shown no significant difference in clinical behavior from squamous cell carcinoma.

OVARIAN CANCER

OVARIAN CANCER I. INCIDENCE


Overall incidence: Epithelial Ovarian Ca 9 to

17/100,000
Rate increase proportionately with age Largest number of age group: 60-64 Est. 21, 550 new cases for 2009, 3% of all new

cases in women in US 9th most common cancer, 5th most lethal Cancer of the ovary is the 10th leading site for both sexes combined (3.1%), and 5th among women (6%) Incidence rises steeply starting age 40.

OVARIAN CANCER II. RISK FACTORS


1. A strong family history of either breast or

ovarian cancer is the most important risk factor for the development of epithelial ovarian cancer. (Level II-2, Grade B)
2. Ages at menarche and menopause are weak

predictors of risk for epithelial ovarian cancer. (Level II-3, Grade C)


3. the use of fertility drugs does not increase the

risk for ovarian cancer. (Level II-2, Grade B)

OVARIAN CANCER II. RISK FACTORS


4. Long term use of unopposed estrogen or

estrogen+progestin is associated with increased ovarian cancer risk. (Level II-2, Grade B)
5. Endometriosis is linked to an increased risk of

epithelial ovarian cancer particularly the endometrioid and clear cell types. (Level II-3, Grade B)
6. PID is positively associated with epithelial

ovarian cancer. (Level II-3, Grade C)

OVARIAN CANCER II. RISK FACTORS


7. the relationship between PCOS and epithelial

ovarian cancer is less extensively evaluated but points to an increased risk. (Level II-3, Grade C)
8. Adult obesity in early adulthood confer an

increased risk of ovarian cancer. (Level II-2, Grade B)


9. Current cigarette smoking increases the risk for

development of mucinous epithelial ovarian cancer but not the other histologic types. ( Level II-2, Grade B)

OVARIAN CANCER II. RISK FACTORS


10. There is no association between moderate

alcohol intake and ovarian cancer risk. (Level II-2, Grade C)


11. A diet characterized by high meat and fat

intake may increase the risk of epithelial ovarian cnacer. (LevelII-2, Grade B)
12. there is no causal relationship between

perineal talc use and ovarian cancer. (Level II-2, Grade B)

OVARIAN CANCER III. PRIMARY PREVENTION


1. Bilateral salpingo-oophorectomy is the

preventive measure of choice for women with a known germline mutation in BRCA1 or BRCA2. (Level II-2, Grade B)
2. Use of OCP confers ling term protection

against ovarian cancer. (Level II-2, Grade B)


3. Analgesics such as aspirin, NSAIDs and

acetaminophen are potential chemopreventive agents for ovarian cancer. (Level III, Grade C)

OVARIAN CANCER III. PRIMARY PREVENTION


4. Increasing parity reduces the risk of epithelial

ovarian cancer. (Level II-2, Grade B)


5. Lactation confers protection against ovarian

cancer risk, most significant with duration of 18 months or more. (Level II-2, Grade B)
6. Tubal ligation confers a reduction in the risk for

ovarian cancer. (Level II-2, Grade B)

OVARIAN CANCER III. PRIMARY PREVENTION


7. Carotenoids significantly protect against

ovarian cancer, either as food or supplement. (Level II-2, Grade B)


8. The consumption of tea may reduce the risk of

epithelial ovarian cancer. (Level II-3, grade C)


9. Recreational physical activity confers at best a

weak to modest protection against epithelial ovarian cancer. (Level II-2, Grade B)

OVARIAN CANCER IV. SECONDARY PREVENTION


1. General population: there is no evidence yet to

support routine screening for ovarian cancer using pelvic examination, CA-125, and TVS. (Level I, Grade A)
2. Although there is lack of evidence for routine

screening among BRCA mutation carriers who have not undergone risk-reducing BSO, carriers are advised semi-annual screening using pelvic examination, TVS, CA-125, or their combination. (Level III, GPP)

FIGO SURGICAL STAGING FOR OVARIAN CANCER I IA IB IC II II A II B II C III III A Growth limited to the ovaries 1 ovary; no ascites; capsule intact; no tumor on ext. surface 1 ovary; no ascites; capsule intact; no tumor on ext. surface 1 or both ovaries with ruptured capsule, surface tumor, (+)ascites, or (+) peritoneal washing Pelvic extension Involvement of uterus or fallopian tubes Involvement of other pelvic tissues Stage IIA or IIB with ruptured capsule, surface tumor, (+) ascites, or (+) peritoneal washings Peritoneal implants outside the pelvis, or (+) retroperitoneal or inguinal lymph nodes Grossly limited to the true pelvis with microscopic seeding of abdominal peritoneum

III B
III C IV

Implants on abdominal peritoneum < 2cm in diameter


Implants on abdominal peritoneum > 2cm in dia, or (+) retroperitoneal or inguinal lymph nodes Distant metastasis; parenchymal liver metastasses

OVARIAN CANCER
IV. WHO HISTOLOGICAL CLASSIFICATION OF OVARIAN TUMORS
A. SURFACE EPITHELIAL-STROMAL TUMORS

B. SEX CORD STROMAL TUMORS


C. GERM CELL TUMORS D. GERM CELL S TUMORSEX CORD

STROMAL TUMORS E. TUMORS OF THE RETE OVARII F. MISCELLANEOUS TUMORS G. LYMPHOID AND HEMATOPOIETIC

OVARIAN CANCER
IV. WHO HISTOLOGICAL CLASSIFICATION OF OVARIAN TUMORS
A. SURFACE EPITHELIAL-STROMAL TUMORS
1. Serous tumors A. borderline malignancy ( of LMP ) i.cystic tumor and papillary tumor ii. Surface papillary tumor

B. SEX CORD STROMAL TUMORS C. GERM CELL TUMORS D. GERM CELL S TUMORSEX CORD STROMAL

TUMORS E. TUMORS OF THE RETE OVARII F. MISCELLANEOUS TUMORS G. LYMPHOID AND HEMATOPOIETIC

OVARIAN CANCER IV. GENERAL GUIDELINES


1. Symptoms of ovarian cancer are fairly non-specific

and often occur after the disease has spread throughout the abdominal cavity.
2.The presence of a pelvic mass at PE is the most

important sign.
3. Gray-scale TVS remains the standard for the

evaluation. Color doppler makes it even more useful in predicting the diagnosis of adnexal masses.
4. The accuracy of CA-125 in the diagnosis of ovarian

tumors is high and is very important in the preoperative evaluation of adnexal masses.

OVARIAN CANCER IV. GENERAL GUIDELINES


5. The addition of biomarker HE4 to CA-125 has

improved the sensitivity and specificity over CA125 alone, for the risk assessment of a malignancy in patients with a Specificity ( % ) pelvic mass. Sensitivity ( % )
HE4 CA-125 + HE4 64.2 98 more accurate predictor of malignancy

6. Cancer of the ovary is staged surgically. The

basis of staging is the 2009 FIGO Ovarian Cancer Staging ( same as the 1998 classification )

OVARIAN CANCER IV. GENERAL GUIDELINES


7. The guidelines for complete surgical staging of

ovarian cancer include:


A. Systematic abdominal exploration via a midline

incision. B. Sampling of washings of 4 areas of the peritoneal cavity, diaphragm, right and left hemiabdomen, pelvis. C. Careful inspection and palpation of all peritoneal surfaces. D. Biopsy and resection of any suspicious lesions, masses, and adhesions. E. TAHBSO

OVARIAN CANCER IV. GENERAL GUIDELINES


7. The guidelines for complete surgical staging of

ovarian cancer include:


F. USO with frozen section is permitted in young

patients with stage IA disease wanting to retain their fertility. G. Infracolic omentectomy. For gross omental involvement, total omentectomy or ifragastric omentectomy should be performed. H. Random biopsies of normal peritoneal surfaces. 2 samples from each of the following:

-undersurface of the R hemidiaphragm, bladder reflaction, cul-de-sac, R and L paracolic recesses, and pelvic sidewalls.

OVARIAN CANCER IV. GENERAL GUIDELINES


7. The guidelines for complete surgical staging of

ovarian cancer include:


I. Pelvic and para-aortic lymph node sampling.

Systematic lymphadenectomy is recommended for early stage and optimally debulked advanced ovarian cancer. J. For mucinous tumors, or other types of ovarian tumors with the appendix grossly involved with tumor, appendectomy must be performed.

OVARIAN CANCER IV. GENERAL GUIDELINES


8. Optimal debulking in ovarian cancer is

complete resection with zero residual. The hazard reduction with complete resection versus any residual tumor is 66% for progression-free survival, and 68% for over-all survival.
9. The standard frontline adjuvant chemotherapy

for epithelial ovarian cancer is the combination of paclitaxel and carboplatin.


The addition of targeted therapy bevazicumab with

a maintenance phase shows promise with longer progression-free survival.

ENDOMETRIAL CANCER I. INCIDENCE


3RD most common genital tract malignancy in the

Phils., next to cervical and ovarian Ranks 15th among malignancies affecting both sexes, 9th among females Median diagnosis is 61 yrs, women between ages 50 60, 90% occur in women over 50, 20% diagnosed before menopause, 5% develop before the age of 40 Worldwide stat: mc type of endometrial cancer generally present at an early age of the disease.
70%- stage I 12%- stage II 13%- stage III 3%- stage IV 23%- stage III 11%- stage IV

However, at PGH
47%- stage I 19%- stage II

ENDOMETRIAL CANCER II. RISK FACTORS


1.Unopposed estrogen therapy substantially

increases risk of endometrial cancer 2-10-fold, and this increased risk persists for several years after discontinuation of estrogen use. (Level I, Grade A)
2. Women treated with Tamoxifen for >2yrs have

statistically significant increased risk of endometrial cancer. (Level 2, Grade B)


3. Obesity predisposes to 2-4-fold RR of

endometrial cancer. (Level II-2, Grade B)

ENDOMETRIAL CANCER II. RISK FACTORS


4. Nulliparity confers an approximately 2-fold risk

of developing endometrial cancer compared with parity of one or more. (Level II-2, Grade B)
5. Diabetes is an independent risk factor for

endometrial cancer and confers about a 2-fold RR after adjusting for obesity. (Level II-2, Grade B)
6. Infertility may elevate risk of endometrial

cancer. (Level II-2, Grade B)

ENDOMETRIAL CANCER II. RISK FACTORS


7. Late menopause ( age > 55yrs ) increases risk of

endometrial cancer 2-fold. (Level II-2, Grade B)


8. There is an inverse association between age at

menarche and endometrial cancer incidence. (level II2, Grade B)


9. PCOS may be a risk factor for endometrial cancer

in younger women. (Level II-2, Grade B)


10. Women with hereditary non-polyposis colorectal

cancer have a 22-50% lifetime risk of developing endometrial cancer and the disease tends to occur at a younger age. (Level II-2, Grade B)

ENDOMETRIAL CANCER III. PRIMARY PREVENTION


1. OCP use reduced the risk of endometrial

cancer. (Level I, Grade A)


2.Raloxifene reduced the risk of developing

endometrial cancer. (Level I, Grade A)

ENDOMETRIAL CANCER IV. SECONDARY PREVENTION


1. For low-risk patients, there is no routine screening

warranted. (Level II-2, Grade B)


2. For moderate-risk patients, there is also no routine

screening warranted. (Level II-2, Grade B)


3. For high risk patients, annual screening for

endometrial cancer with endometrial biopsy should be offered by age 35 for women with, or at risk for HNPCC. (Level III, Grade C)
4. There is no role for routine screening with

endometrial biopsy or TVS in asymptomatic women on Tamoxifen. (Level I, Grade B)

FIGO 2009 Surgical Staging for ENDOMETRIAL CANCER I* IA IB II* III* IIIA IIIB IIIC Tumor confined to the corpus uteri No less than half myometrial invasion Invasion > half of the myometrium Tumor invades cervical stroma, does not extend beyond the uterus ** Local and/or regional spread of the tumor *** Tumor invades the serosa of the corpus uteri and/or adnexae Vaginal and/or parametrial involvemnet Mets to pelvic and/or para-aortic lymph nodes C1 (+) pelvic nodes C2 (+) para-aortic LN with or without (+) pelvic LN

Tumor invades bladder and/or bowel mucosa, and /or distant mets * Either G1, G2, G3 Architectural grading of endometrial carcinoma
IVA Tumor invadesof tumor is of and/or bowel mucosa G2 6-50% bladder solid masses
G3 more than 50% of tumor is solid masses G1 No more than 50% of tumor is of solid masses

IV *

IVB Distant mets, including intra-abdominal mets, and/or inguinal **Endocervical glandular involvement only should be considered as stage I, and no longer as LN stage II

***Positive cytology is no longer included in the surgical staging but it still has to be reported separately without changing the stage

ENDOMETRIAL CANCER V. WHO CLASSIFICATION


A. Adenocarcinoma
1. Endometrioid

o A. Variant with squamous differentiation o B. Villoglandular variant o C. Secretory variant o D. Ciliated cell variant 2. Mucinous 3. Serous 4. Clear cell

B. Mixed Cell Carcinoma C. Squamous Cell Carcinoma D. Transitional Carcinoma E. Small Cell Carcinoma F. Undifferentiated carcinoma G. Carcinocarcinoma

ENDOMETRIAL CANCER VI. GENERAL GUIDELINES IN THE DIAGNOSIS AND MANAGEMENT


1. 90% with endometrial Ca presents with

abnormal vaginal bleeding, or abnormal discharge.


2. Endometrial biopsy is the gold standard to

obtain endometrial tissue for histologic evaluation.


3. Further evaluation is warranted in the ffg

circumstances:
Failure to obtain an adequate specimen Inconsistencies between biopsy and imaging,

ENDOMETRIAL CANCER VI. GENERAL GUIDELINES IN THE DIAGNOSIS AND MANAGEMENT


4. Using a 4mm cut-off point for endometrial

thickness, TVS has 100% sensitivity, and 60% specificity as a predictor of endometrial ca in women reporting post-menopausal bleeding.
5.Saline infusion sonography/ Sonohysterography

is often used as a second step in the evaluation of abnormal bleeding, when UTZ suggests a focal lesion, when endometrial biopsy is nondiagnostic, or when abnormal bleeding persists despite normal initial workup

ENDOMETRIAL CANCER VI. GENERAL GUIDELINES IN THE DIAGNOSIS AND MANAGEMENT


6. Hysteroscopy is highly accurate in diagnosing

endometrial cancer in women with abnormal bleeding.


7.Once the diagnosis of endometrial cancer is

made, the patient should be referred to a gynecologic oncologist.


8. Endometrial cancer follows a surgico-

pathologic staging in the form of PFC, Extrafascial Hysterectomy with BSO, and

ENDOMETRIAL CANCER VI. GENERAL GUIDELINES IN THE DIAGNOSIS AND MANAGEMENT


9. In selected cases, where there is histopath evidence

of tumor extension into the cervical stroma, primary PFC, radical hysterectomy, BSO, pelvic and para-aortic lymphadenectomy may be performed by a gynecologic oncologist.
10. Adjuvant treatment in the form of RT alone, or

chemotherapy followed by RT is given depending on the disease stage, histologic type, tumor grade, and presence of lymphovascular invasion.
11. The treatment of endometrial cancer requires a

multi-disciplinary approach involving a gynecologic oncologist, and a radiation oncologist.

VULVAR CANCER

VULVAR CANCER I. INCIDENCE


Vulvar cancer makes up 3-5% of all gyecologic

cancers National Cancer Institute: 1 of the 12 cancers rising in incidence PGH: 7 new vulvar cases in 2009, mc histology: SCCA The increasing incidence in US correlates with increasing incidence of HPV infection. The increase of in-situ vulvar carcinoma has occurred predominantly in women younger than 65, with a peak incidence observed in the 40-49 y/o age group and steadily decreases thereafter

VULVAR CANCER I. INCIDENCE


SEER database: Increase of in-situ vulvar

carcinoma may be secondary to an increased incidence of screening, detection, and reporting, both by the patient and the physician.
There is relatively little change in the incidence of

invasive vulvar cancer, particularly in women younger the 50, there is a steady increase in incidence of invasive vulvar cancer with age. The different age distributions between invasive vulvar and cervical cancers ( in combination with in-situ disease ) suggest that other risk factors, aside from HPV, are related to the development of invasive vulvar cancer.

VULVAR CANCER II. RISK FACTORS


1. HPV infection increases the risk of developing

vulvar cancer. (Level II-2, Grade B)


2. HSV 2 infection increases the risk of

developing vulvar cancer. (Level II-2, Grade B)


3. Smoking increases the risk of developing

vulvar cancer. (Level II-2, Grade B)

VULVAR CANCER III. PRIMARY PREVENTION


1. Total sexual abstinence and practice of lifetime

mutual monogamy. (Level II-2, Grade B)


2. Prophylactic HPV vaccination can protect women

from developing vulvar intraepithelial neoplasia (VIN). (Level I, Grade A)


3. There should be prompt and appropriate diagnosis

and treatment of VIN. (Level III, GPP)


4. Prompt diagnosis and treatment of lichenoid

pattern dermatotes may decrease the likelihood of type II vulvar cancer development. (Level III, GPP)

VULVAR CANCER IV. SECONDARY PREVENTION


1. There is no routine screening recommended

for vulvar cancer. (Level III, GPP)

FIGO 2009 Surgical Staging for VULVAR CANCER I IA IB II Tumor confined to the vulva or perineum, no nodal mets Lesions < 2cm in size with stromal invasion < 1mm Lesions >2cm in size with stromal invasion >1mm Tumor of any size with extension to adjacent lower perineal structures ( 1/3 lower urethra, 1/3 lower vagina, anus ) with (-) nodes Tumor of any size with or without extension to adjacent perineal structures ( 1/3 lower urethra, 1/3 lower vagina, anus ) with (+) inguinofem nodes

III

IIIA
IIIB IIIC IV IVA

With 1 LN mets ( > 5mm) or 1-2 LN mets (< 5mm)


With > 2 LN mets ( > 5mm) or > 3 LN mets (< 5mm) With (+) nodes with extracapsular spread Tumor invades other regional ( 2/3 upper urethra, 2/3 upper vagina ) or distant structures Tumor invades any of the following: upper urethral and/or vaginal mucosa, bladder mucosa, rectal mucosa or fixed to pelvic bone or fixed or ulcerated inguino-femoral nodes Any distant mets, including pelvic LN

IVB

VULVAR CANCER VI. WHO CLASSIFICATION


A. Epithelial neoplasms F. Other malignant

of skin and mucosa B. Bartholin gland carcinomas C. Carcinoma and sarcoma of ectopic Breast tissue D. Carcinoma of Sweat gland origin E. Soft tissue sarcoma

tumors G. Secondary and metastatic tumors H. Unclassified tumors

VULVAR CANCER VII. GENERAL GUIDELINES


1. Any suspicious vulvar discoloration, ulceration, and

lesion should be biopsied.


2.Expert opinion recommends that any lesion

increasing in size or with an unusual warty appearance should be biopsied. The clinician must be diligent in observing any vulvar lesion and use biopsy aggressively on any lesion of concern to the clinician or patient.
3. The biopsy should include surrounding skin with

underlying dermis and connective tissue so that the pathologist can evaluate the depth of stromal

VULVAR CANCER VII. GENERAL GUIDELINES


4. Vulvar cancer is clinically staged.
5. If clinically indicated, proctosigmoidoscopy and

cystoscopy should be done to rule out bladder and bowel involvement.


6. Imaging studies like CT scan and MRI of the pelvis

and groins is often helpful in detecting enlarged LN in the groins and pelvis.
7. Sentinel LN biopsy provides an accurate and safe

alternative to conventional groin node dissection with

VAGINAL CANCER

VAGINAL CANCER I. INCIDENCE


Vaginal cancer is rare accounting for about 0.3% of all invasive

cancers among women, and 1-2% of all gynecologic malignancies in US.


In 2009: 4 new cases of vaginal cancecer in PGH

VAGINAL CANCER II. RISK FACTORS


1. HPV infection increases the risk of vaginal cancer.

(Level II-2, Grade B)


2. A 5 or more lifetime sexual partner increases the

risk of developing vaginal cancer. (Level II-2, Grade B )


3. A history of cervical cancer increases the risk of

developing vaginal cancer. (Level II-2, Grade B)


4. In-utero DES exposure increases the risk of

developing Vaginal cancer. (Level II-3, Grade C)

VAGINAL CANCER III. PRIMARY PREVENTION


1. Total sexual abstinence and practice of lifetime

mutual monogamy. (Level II-2, Grade C)


2. Use of barrier methods decrease the risk of

HPV infection, thus decreasing the risk of developing vaginal cancer. (Level II-2, Grade B)
3. HPV vaccination can protect women from

developing VAIN. (Level I, Grade A)

VAGINAL CANCER III. SECONDARY PREVENTION


1. There is no routine screening recommended for

vaginal cancer. (Level II-2, Grade B)


2. For patients who underwent TAH for benign

gynecologic disease, vaginal smear is not recommended. (Level II-2, Grade A)


3. Patients who underwent TAH for cervical dysplasia

or cancer and those who had history of previous genital dysplasia or cancer should undergo routine annual vaginal smear (for the next 20 years). (Level

FIGO 2009 Surgical Staging for VAGINAL CANCER I II The carcinoma is limited to the wall The carcinoma has involved the subvaginal tissue but has not extended to the pelvic wall.

III
IV

The carcinoma has extended to the pelvic wall.


The carcinoma has extended beyond the true pelvis or has involved the mucosa of the bladder or rectum, bullous edema as such does not permit a case to be alloted to stage IV Spread of the growth to the adjacent organs and/or direct extension beyond the true pelvis Spread to distant organs.

IV A IV B

VAGINAL CANCER VI. WHO HISTOLOGICAL CLASSIFICATION OF VAGINAL TUMORS

I. Epithelial Tumors

A. Squamous cell carcinoma B. Adenocarcinoma C. Other invasive tumors A. Leiomyosarcoma B. Sarcoma botryoides C. Endometrioid stromal sarcoma

II. Mesenchymal tumors


III. Mixed Epithelial and mesenchymal tumors


A. Mixed tumor B. Adenocarcinoma C. Malignant mesodermal mixed tumor D. tumor resembling synovial sarcoma

IV. Other

A. Malignant melanoma B. Yolk sac tumor C. Lymphoma/ Leukemia

V. Metastatic tumor

VAGINAL CANCER VII. GENERAL GUIDELINES


1. A thorough PE with detailed speculum

inspection, digital palpation, colposcopic and cytologic evaluation, and biopsy should be done in order to diagnose and clinically stage vaginal cancer.
2. Biopsy of the cervix, if present, is

recommended to rule out a primary cervical tumor.

VAGINAL CANCER VII. GENERAL GUIDELINES


3. Complete systematic evaluation for patients

with malignant melanoma and advanced stage vaginal cancer should be performed.
4. Radiation therapy is the treatment of choice for

most patients with vaginal cancer, and comprises of integration of teletherapy and intracavitary/ interstitial therapy.

BREAST CANCER

BREAST CANCER I. INCIDENCE


Breast cancer is the 2nd leading site for both

sexes combined Ranks 1st among women 2005: Est. 14,043 new cases, and 6,357 deaths were expected Philippines: median survival among females is 60 months Survival rate at 5th year 50.10% 10th year 32.38% Incidence starts rising steeply at age 30.

BREAST CANCER II. RISK FACTORS


1. Increased exposure to estrogen increases the

risk of postmenopausal breast cancer. (Level II-2, Grade B)

BREAST CANCER II. RISK FACTORS


2. Increased alcohol consumption increases the

risk of breast cancer. (Level II-2, Grade B)


3. Higher red meat intake in adolescence may

increase the risk of premenopausal breast cancer. (Level II-2, Grade B)


4. High fat diets, phytoestrogen consumption,

high intake of dairy products, high concentrations of polychlorinated biphenyls, and green tea consumption show inconclusive evidence

BREAST CANCER II. RISK FACTORS


5. The use of combined conjugated equine

estrogen (CEE) and MPA as hormone replacement therapy for women age 63.2 (+ 7.1) increases the risk of breast cancer. (Level I, Grade A)
6. The use of CEE replacement therapy in women

age 63.6 (+ 7.3) does not increase the risk of breast cancer. (Level I, Grade A)
7. The use of OCP does not increase the risk of

breast cancer. (Level II-2, Grade B)

BREAST CANCER II. RISK FACTORS


8. Mutations in the BRCA1 or BRCA 2 genes

(Hereditary Breast ovarian Cancer Syndrome) increase the risk for breast cancer. (Level II-2, Grade B)
9. Benign breast lesion which show atypical

proliferation increase breast cancer risk. (Level II2, Grade B)


10.The radiation of mammography does not

increase the risk of breast cancer. (Level ii-2,

BREAST CANCER III. PRIMARY PREVENTION


1. Weight loss after menopause reduces risk of

postmenopausal breast cancer. (Level II-2, Grade B)


2. Folic acid supplementation does not reduce

risk of breast cancer. (Level II-2, Grade B)


3. NSAIDs use reduce the risk for breast cancer.

(Level I, Grade A)

BREAST CANCER III. PRIMARY PREVENTION


4. The use of selective estrogen receptor

modulators (SERMs) decreases the risk of breast cancer development. (Level I, Grade A)
5. Prophylactic oophorectomy for BRCA mutation

carriers decreases the risk of breast cancer. (Level II-2, Grade B)


6. In women who have had cancer in 1 breast

(and thus are at higher risk of developing a primary cancer in the other), prophylactic mastectomy may reduce the incidence of cancer

BREAST CANCER IV. SECONDARY PREVENTION


1. There is insufficient evidence to recommend for

or against routine Clinical Breast Examination (CBE) to screen for breast cancer in women 40 years and older. (Level I, Grade A)
2. Teaching SBE is not recommended to screen

for breast cancer. (Level I, Grade A)


3. Screening mammography is recommended for

average-risk women aged 50-74 years. (Level I, Grade B)

BREAST CANCER IV. SECONDARY PREVENTION


4. Recommended interval for screening

mammography is biennial. (Level I, Grade B)


5. The decision to start regular, biennial

screening mammography before the age of 50 years should be an individual one and take patient context into account, including the patients values regarding specific benefits and harms. (Level II-2, Grade C)
6. For women less than 50years, digital

mammography is superior to film mammography.

BREAST CANCER IV. SECONDARY PREVENTION


7. Screening mammography should be stopped

at age 74. (Level II-2, Grade C)


8. Screening for breast cancer using breast MRI

is not recommended in the general population of asymptomatic, average-risk women. (Level III, Grade C)

BREAST CANCER IV. SECONDARY PREVENTION


9. High risk women should start annual screening

mammography beginning age 30. (Level II-2, Grade B)


10. Women at high risk for developing breast

cancer should receive annual MRI as an adjunct to mammography. (Level III, Grade C)

BREAST CANCER IV. SECONDARY PREVENTION


11-12. Recommendations for women with a

history of chest radiation between ages 10-30 years include the following:
11- For women previously treated with irradiation of

at least 20 Gy to the mantle, minimantle, mediastina, chest or axillary fields, early CBE from the age of puberty until age 25 years, and then every 6months, is recommended. (Level III, Grade C)
12- For the same group of women, an annual

BREAST CANCER IV. SECONDARY PREVENTION


13. For women with personal history of breast

cancer, annual mammography is recommended after the date of diagnosis but annual MRI can also be considered. (Level III, Grade C)
14. MRI should routinely be used for the

contralateral breast at the time of diagnosis of breast cancer in all women. (Level III, Grade C)
15. Sonomammography can be considered as a

complementary tool to mammography. (Level II-2,

BREAST CANCER IV. SECONDARY PREVENTION


15. Sonomammography can be considered as a

complementary tool to mammography. (Level II-2, Grade B)


16. Scintimammography (SMM) can be

considered as a complementary tool in the evaluation of patients with breast lesions.(Level II-2, Grade C)

LEVELS OF EVIDENCE & GRADES OF RECOMMENDATION


LEVEL I DEFINITION Evidence obtained from at least 1 properly RCT

II-1
II-2

Evidence obtained from well-designed CT without randomization


Evidence obtained from well-designed cohort or casecontrol analytic studies, preferably from more than 1 center or research group Evidence obtained from multiple time series with or without the intervention DEFINITION Opinions of respected authorities based on clinical experience

II-3 GRADE III A B C D E GPP

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