Vulval pre-cancer and Cancer-Diagnosis & Management.pptx

Vulval Pre-cancer and Cancer: Diagnosis and Management
Akin-Tunde Ademola ODUKOGBE
Professor / Honorary Consultant
Gynaecologic Oncology Unit
Department of Obstetrics and Gynaecology
College of Medicine, University of Ibadan / University College Hospital, Ibadan, Nigeria
22/09/2023 Akin-Tunde Ademola ODUKOGBE. 2022. 1

Vulval Pre-cancer: Diagnosis & Management
•Introduction
• Definitions
• Abbreviations
• Embryology, Anatomy and Physiology
• Early Development
• Phenotype, blood supply, lymphatic drainage, nerve supply
• Functions
• Epidemiology
• Age distribution
• Geographical spread
• Aetiopathogenesis
• Risk factors
• Aetiological factors
• Clinical Features
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Life style changes, including use of condom
• Vaccination

Introduction
• The vulva is the external female genitalia
• Its size belies its importance in the function of the female, spanning urination,
sexual intercourse in its varied forms and female reproduction
• It is affected by numerous diseases, most of which originate from other systems,
while its diseases also affect many systems

Introduction
• Definitions
- VIN consists of varied neoplastic changes from mild cellular atypia to almost
invasive carcinoma
• Abbreviations
(1). VSCC – vulval squamous cell cancer. (2). VC – vulval cancer.
(3). HPV – human papilloma virus. (4). ISSVD – International Society for the Study
of Vulvovaginal Disease. (5). HPV-d – HPV-dependent vulval cancer, HPV-i – HPV-
independent. (6). VIN – vulval intraepithelial neoplasia. (7). uVIN – usual VIN. (8).
dVIN – differentiated VIN.

• Introduction
• Definitions
• Abbreviations
•Embryology, Anatomy and
Physiology
• Functions
• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Vaccination

Embryology, Anatomy and Physiology
Early Development
• 3rd WOL. Mesenchymal cells from primitive streak form pair of cloacal folds
• Cranially unite to form genital tubercle, caudally split into urethral, anal folds
• Genital swellings form on each side of urethral folds. Later form labia majora
• Genital tubercle forms the clitoris, and urethral folds, the labia minora
• Urogenital groove forms the vestibule

EMBRYOLOGY OF THE VULVA
• A and B: Indifferent stages of the
external genitalia (A is
approximately 4 weeks, B is
approximately 6 weeks)
• C: Scanning electron micrograph
of the external genitalia of a human
embryo at approximately the
seventh week – AF = anal fold,
arrowhead = anal opening; GS =
genital swelling; GT = genital
tubercle; T = tail; UF = urethral fold

Phenotype, blood supply, lymphatic drainage, nerve supply
• Mons pubis (mons veneris): pad of fat, hair bearing, alters in course of life
• Labia majora: lateral boundaries of vulva. External-dark, hairy. Pink inner has SGs.
Subcutaneous layer has Camper’s and Colles’ fascia similar to abdominal wall.
Forms anterior commissure and posterior commissure (posterior limit of vulva)
• Labia minora: cutaneous folds, flank vaginal orifice, splitting anteriorly to form
the hood (prepuce) and frenulum of clitoris. Numerous SGs on medial surface.
• Vestibule: has six openings [a. urethral meatus, b. Skene’s ducts (lesser vestibular
glands, like prostate glands) – 2, c. vaginal orifice, d. Bartholin’s ducts (greater
vestibular glands) – 2]. Shallow vestibular fossa

• Clitoris: erectile structure; has root, body (two corpora cavernosa with dense
fibrous tissue) and glans. Attached to pubic symphysis, ischiopubic rami.
• Bulbs of vestibule: one each side of the vestibule
• Abundant arterial supply: Femoral – superficial external pudendal (labia minora).
Internal pudendal – (most of skin, external genitalia, perineal muscles), labial
artery
• Venous drainage of vulval skin is through external pudendal to long saphenous.
Drainage of clitoris is through deep dorsal to internal pudendal, superficial dorsal
to external pudendal and both to long saphenous

• Connecting lymph vessels from labial skin, clitoris and perineum form 3 – 4
collecting trunks to drain into superficial inguinal nodes on the cribriform fascia
onwards to deep inguinal nodes medial to femoral vein. The deep inguinal nodes
drain through femoral canal to pelvic nodes. Cloquet’s node is the last deep
inguinal node. From the clitoris, drainage is to deep inguinal nodes or directly to
internal iliac nodes. Rectal plexus drain lower part of labia majora and perineum
• Nerve supply: inferior rectal and perineal nerves (vulva) and dorsal nerve (clitoris)
– from pudendal nerve (S2,3,4). Ilioinguinal [L1, anterior third of labium majus],
posterior labial branches of perineal [S3, posterior two-thirds], perineal branch of
posterior cutaneous nerve of thigh [S2, lateral aspect of labium majus.

Quantitative Distribution of Nerve Endings: Vulva Vs Vagina (Current Diagnosis)
Sites Touch Pressure Pain Other types
Meissner
Corpuscle
(corpuscula
tactus)
Merkel
Tactile Disks
(corpuscula
tactus)
Peritrichous
Endings
Vater-Pacini
Corpuscles
(corpuscula
lameliosa)
Free Nerve
Endings
Ruffini
Corpuscles
(corpuscula
lameliosa)
Dogiel and
Krause
Corpuscles
(corpuscula
bulboidea)
Mons pubis ++++ ++++ ++++ +++ +++ ++++ +
Labia majora +++ ++++ ++++ +++ +++ +++ +
Clitoris + + 0 ++++ +++ +++ +++
Labia minora + + 0 + + + +++
Hymenal ring 0 + 0 0 +++ 0 0
Vagina 0 0 0 0 +
occasionally
0 0

• Introduction
• Definitions
• Abbreviations
• Functions
•Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Vaccination

Epidemiology
• Disease of the elderly (seventh decade)
• Younger women (third to fourth decades) increasingly affected due to HIV / AIDS
Form over 90% of cases
• Compared with CIN (6% of those screened – population based), VIN has a low
incidence

• Introduction
• Definitions
• Abbreviations
• Functions
• Epidemiology
•Aetiopathogenesis
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Vaccination

Aetiopathogenesis
• Two pathways
1. HPV related: 16, 18. Multifocal, in younger women,
2. Prior vulval lesions or non-HPV related: older women
• Part of ‘Field Carcinogenesis Phenomenon’ or ‘Field Effect’. Concomitant lesions
in up to 44%
• Predisposing lesions
Lichen sclerosus – chronic inflammation from vulval irritation / itching / scratching
• Autoimmune diseases

• Introduction
• Definitions
• Abbreviations
• Functions
• Epidemiology
• Risk factors
•Clinical Features
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Vaccination

Clinical Features
SYMPTOMS
• May be asymptomatic
• Vulval itching
• Irritation
• Burning
• Dyspareunia
SIGNS
• General examination – physical and mental state examination
• Markers of ill – health (systematic systemic examination)
• Lesions may be white, red, leukoplakic, velvety, erythematous, ulcerated,
hyperpigmented indistinct macular, well-defined raised plaque (single or
multiple). Most on labia minora, and may involve perianal region in 40%

• Introduction
• Definitions
• Abbreviations
• Functions
• Epidemiology
• Risk factors
• History
• Examination
•Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Vaccination

Investigations
General
FBC, HIV I & II, OGTT, HPV test, E & U, Cr & UA, CXR, Lipid profile, TFT
Specific
• Simple inspection using white light
• Acetic acid painting (3-5% acetic acid), with magnifying glass
• Pap smear
• Colposcopy
• Biopsy – colposcopically directed, using Keyes dermal punch
Histology
• Loss of polarity
• Features of neoplasia
• Exclusion of invasion

Investigations
GRADING
Type Extent Remarks / Progression ISSVD (2015)
VIN 1 Mild. Dysplastic cells in lower
third
VIN 2 Moderate. Lower two – thirds
VIN 3 Severe. Carcinoma – in – situ.
Whole layer
• Warty or condylomatous.
HPV+
Undulating or spiked surface. Koilocytes
seen. Surface keratinocytes
Vulval LSIL, flat condyloma, HPV
effect
• Basaloid or undifferentiated.
HPV+
Flat surface, with immature parabasal cells. Vulval HSIL, VIN usual type
• Differentiated or simplex.
Older women
Basal or parabasal cells, normal
maturationkeratin pearls
Differentiated type VIN

• Introduction
• Definitions
• Abbreviations
• Functions
• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
•Treatment
• Ablative
• Medical
• Surgery
• Prognosis
• Prevention
• Vaccination

Treatment
• VIN II and VIN III should be treated, and all women with HSIL, uVIN
• Options
- Topical agents (Interferon gel, retinyl acetate gel, 5-fluoro-uracil, imiquimod). No
specimen for histology
- CO2 laser. Ideal for women less than 40 years, with no invasive lesions. Depth 3 –
4mm. Little scarring. No specimen for histology
- Wide local excision. Curative in 75% of cases if only VIN. Treatment of choice in
older women
- Simple vulvectomy (complete or partial)
- Skinning vulvectomy with split-thickness skin graft. Less distortion of anatomy

Treatment
• Rules when excising
- Gross margins to be 0.5 – 1.0cm
- Avoid injury to clitoris, urethra, anus
COMPLICATIONS
• Altered psychosexual function from defects, scarring, injury to clitoris and glands
• Missing invasive lesions (18.8% - Chua et al 1996)
• Hair bearing areas have deeper involvement which can be easily missed

• Introduction
• Definitions
• Abbreviations
• Functions
• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
•Prognosis
• Prevention
• Vaccination
Treatment

Prognosis
• Lesion may regress spontaneously, recur after local excision (significant, 10% if
edges are free or 50% if involved) or progress to VSCC (10%)
• Markers of progression – increasing age, immunosuppression, smoking, raised
lesions with irregular surface
• Long term follow-up is crucial
- yearly, using VIA (3 – 5% acetic acid) and magnifying glass / colposcope

• Introduction
• Definitions
• Abbreviations
• Functions
• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Treatment
• Ablative
• Medical
• Surgery
• Prognosis
•Prevention
• Vaccination
Treatment

Prevention
• Vulval self examination
• Education
• Lifestyle adjustment. Smoking cessation
• Protected sex – especially female condom which covers the vulva
• Vaccination. 2 types (16, 18), 4 types (6, 11, 16, 18), 9 types (6, 11, 16, 18, 31, 33,
45, 52, 58)
• Screening of high risk groups – hrHPV, smokers, immunocompromised, previous
VIN, CIN, VAIN or perianal IN

Vulval Cancer: Diagnosis & Management
•Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Adjuvant therapy
• Neoadjuvant
• Prognosis
• Prevention
• Life style changes
• Vaccination
• Conclusion

Epidemiology
• GLOBOCAN 2018 worldwide estimates – 44,235 new cases, 15,222 deaths. Age
adjusted incidence 0-4.6/100,000. Less than 5% of female genital tract cancers
(Forman D et al 2014, De Martel C 2012, Odukogbe et al 2004).
• 20th most common cancer among women in the UK, 3.7/100,000
• Incidence of VIN is increasing worldwide.
• Age distribution:
• Geographical distribution:
HICs have higher rates (65%) than Africa and Asia (35%)

11st
12nd
13rd
14th 5th

• Epidemiology
•Aetiopathogenesis
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Neoadjuvant
• Prognosis
• Prevention
• Vaccination
• Conclusion

Aetiopathogenesis
• Risk Factors
-Young women: smoking, high number of sexual partners, and compromised
immune status (Del Pino M – 2013, Van der Avoort IA – 2006, McCluggage WG – 2013).
Associated with HPV-d.
-Older women, p53 mutation, history of lichen sclerosus or chronic dermatosis
with autoimmune diseases (Del Pino M – 2013, Van der Avoort IA – 2006, McCluggage WG – 2013).
-HIV infection increases women’s risk for genital warts and VIN. High CD4 can lead
to spontaneous regression or enhances response to treatment of warts.
-Low CD4 (<500/mm3) increases incidence of VIN 2 and 3 (Massad LS – 2011).
-The burden of hr-HPV infection is high among heterosexual men in sub-Saharan
Africa and most pronounced among the HIV-infected individuals (Tobian et al 2013).
-Vulval carcinoma can arise from normal skin.

Aetiopathogenesis
• Aetiological Factors
-HPV DNA prevalence in vulval cancer is 20 – 40% (Bruni L et al – 2014, De Sanjosé S – 2013): HPV –
dependant and HPV – independent (HPV 16 forms 75% of HPV-D)
-DNA damage from pelvic irradiation

Aetiopathogenesis
HPV – dependent HPV - independent
HPV 16 75% of the cases
Precursor uVIN dVIN
Risk to VSCC 10% of uVIN, and 3% if uVIN treated Higher
Social status
Age
Smoking
Number of sexual partners
Immune status
p53
Younger
+
High
Compromised
-
Older women
Nil
Autoimmune diseases
+
Benign lesions - More
Prognosis Fair Worse
Comorbidity

• Epidemiology
• Risk factors
•Clinical Features
• History
• Examination
• Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Neoadjuvant
• Prognosis
• Prevention
• Vaccination
• Conclusion

Clinical Features
There may be no specific symptoms, leading to delay in treatment!
Itching
Dyspareunia
Soreness
Burning sensations
Bleeding
Lump
Ulcer

• Epidemiology
• Risk factors
• History
• Examination
•Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Neoadjuvant
• Prognosis
• Prevention
• Vaccination
• Conclusion

Investigations
• General
FBC, Clotting profile, Grouping and crossmatching blood
HIV I & II
OGTT
E & U, Cr & UA
Liver function tests
Lipid profile
Urinalysis, Urine MCS
ECG / Echocardiography

Investigations
• Specifics
1. Visual inspection after staining
2. Vulvoscopy
3. Colposcopy: Preceded by Pap smear because of ‘Field Effect’
4. Anoscopy
5. Cystoscopy
6. Rectoscopy
7. Radiology – Chest and bone Xray, IVU, CT Scan, MRI, PETScan
8. Lymphography Blue dye and radioactive colloids injected peri-lesionally
9. Lymphscintigraphy
10. Near-infrared fluorescence optimal imaging
• Histological distribution
VSCC - >90%. Keratinizing, basaloid, warty, and verrucous
• Distribution of sites – labia (80%), clitoris (10%), lower commissure (10%)

Investigations
• Staging
Vulval cancer can spread from the original site through
- Local invasion of adjacent tissues
- Embolization to regional lymph nodes (superficial, deep inguinal to pelvic nodes)
- Haematological to lungs, liver and bones

Simpler Version For The Patient

Investigations
TNM [Union for International Cancer Control, UICC (Sobin et al 2009)]
Comparison of both staging methods
T NM FIGO TNM
T1 Tumour confined to vulva and/or perineum N1a One or two nodules < 5mm 1A T1 N0 M0
T1a < 2cm with stromal invasion < 1.0mm N1b One nodule > 5mm 1B T1b N0 M0
T1b > 2cm with stromal invasion > 1.0mm N2b Two or more nodules > 5mm II T2 N0 M0
T2 Tumour with invasion of the lower part of
urethra/vagina/anus
N2c Extracapsular invasion IIIA T1, T2 N1a, N1b M0
T3 Invasion of the upper part of urethra/vagina,
bladder, rectal mucosa, bone, fixation in
pelvis
N3 Fixed, ulcerated IIIB T1, T2 N2a, N2b, M0
M0 Absence of distant
metastases
IIIC T1, T2 N3, M0
M1 Distant metastases IVA T1, T2 N3 M0, T3 any N M0

• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Staging
•Treatment
• Surgery
• Neoadjuvant
• Prognosis
• Prevention
• Vaccination
• Conclusion

Treatment
• Surgery
Major form of therapy
Principles:
o Work up to reduce post operative infection (cleansing, enema, antibiotics)
o Aim is 1-2cm macroscopic margin, or less than 0.8cm histologic tumour-free
margin (Chan JK 2007). 50% recurrence rate if margins are less than 1cm
o Stage, size, site of tumour, previous excision, cell type (local recurrence, depth of
invasion)
o Distal 1/3 of urethra can be excised without loss of continence
o Lymph node dissection crucial. Sentinel node in early disease (mapping and
biopsy first described by Cabanas in 1976)
o Evolution – radical vulvectomy with en bloc bilateral inguinofemoral
lymphadenectomy (to triple incision technic: advanced cases) and radical local
excision + inguinofemoral lymphadenectomy: early disease

SURGICAL STAGING SHEET FOR OPERATIONS FOR GYNAECOLOGICAL
CANCERS – GO 3. Appendix 3
Patient’s name:
Date: Hospital number: Age (years):
Abdominal
incision type:
Low transverse Midline Paramedian
Cytology: Fresh frozen histology:
GROSS FINDINGS
Uterus:
Fallopian tube (right): Fallopian tube (left):
Ovary (right): Ovary (left):
Stomach:
Omentum:
Intestines:
Colon / Rectum:
Liver:
Gall bladder:
Spleen:
Pancreas:
Diaphragm:
Kidney (right): Kidney (left):
Ureter (right): Ureter (left):
Bladder:
Lymph nodes:
1. External iliac – 2. Internal iliac –

3. Obturator – 4. Common iliac –
5. Para – aortic –
Ascites:
Pouch of Douglas:
Peritoneal surfaces:
Peritoneal washings:
Description of operation performed:
FOR VULVAL CANCERS
Lead
Surgeon/s:
Consultant/s- Senior registrar/s-
Assistant surgeons: Senior registrar /s- Registrar/s -
Name and signature of recorder: Date:
Designation:

Treatment
• Complications
- Anaesthetic
- Haemorrhage
- Necrosis of skin flaps. Wound breakdown
- Infection
- DVT, pulmonary embolism
- Pressure sores
- Lymphocyst
- Chronic lymphoedema of the lower limbs (30 – 70%), significant in 10%
- Hernia, genital prolapse, urine/fecal incontinence
- Vaginal stenosis and dyspareunia
- Psychosexual problems

The GROINSS-V (Groningen International Study on Sentinel nodes
in Vulvar cancer)
I – Sentinel nodes in vulvar cancer. Long term follow up (Te Grootenhuis NC et al 2016)
II – Radiotherapy vs Inguinofemoral Lymphadenectomy (Oonk MHM et al 2021)
III – A Prospective Phase II Treatment Trial (Chemoradiation) (Slomovitz B. from 2021)

Treatment
• Radiation
- Adjuvant, after surgery
• Complications
- Radiation dermatitis, fibrosis and ulceration
- Vaginal stenosis

Treatment
• Neoadjuvant therapy
Usually chemoradiation:
- To shrink tumour
- To avoid injury to urethra, anus

• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Neoadjuvant
•Prognosis
• Prevention
• Vaccination
• Conclusion

Prognosis
• Risk of transformation from VIN to VSCC is 10%, or 3% if VIN is treated.
• dVIN is a precursor and has a higher progression towards VSCC. Prognosis worse
in HPV-d compared to HPV-i (Del Pino M – 2013, Van der Avoort IA – 2006, McCluggage WG – 2013).
• Lymph node involvement is the most important prognostic factor
FIGO Stage 5 year survival (%) Remarks
I 79 Stages of presentation of
most cases in HICs
II 59
III 43 Stages of presentation of
most cases in LMICs
IV 13

• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Neoadjuvant
• Prognosis
•Prevention
• Vaccination
• Conclusion

Prevention
• Incidence of vulval cancer can be reduced by half using HPV vaccines 16 and 18
(Hampl M et al 2006), and others
• Early biopsy of vulval lesions

• Epidemiology
• Risk factors
• History
• Examination
• Investigations
• General
• Specifics
• Staging
• Treatment
• Surgery
• Neoadjuvant
• Prognosis
• Prevention
• Vaccination
•Conclusion

Conclusion
• Increasing incidence of VIN / VC
- Increasing life expectancy
- Increasing HPV, HIV diseases
• Better and still evolving diagnostic tools
• Better and still evolving treatment options
• Increasing preventive options – HPV vaccinations

References
• Odukogbe AA, Adebamowo CA, Ola B, Olayemi O, Oladokun A, Adewole IF, Omigbodun OA, Aimakhu, Okunlola MA, Fakulujo O and Oluyemi FA
(2004). Ovarian cancer in Ibadan: characteristics and management. Journal of Obstetrics and Gynaecology, 24:3,294-297.
• Jean-Philippe Spano, Laurence Moureau-Zabotto, Mathieu Minsat and Quéro (2015). Cancer of the penis, anus, and vulva. In: Eds. Jean-Pierre
Droz, Bernard Carme, Pierre Couppié, Mathieu Nacher and Catherine Thiéblemont. Tropical Hemato-Oncology. Springer International
Publishing, Switzerland. ISBN 978-3-319-18256-8. Part IV, Chapter 45, 443-448.
• Forman D, Bray F, Brewster DH et al (2014). Cancer incidence in five continents, vol. X (electronic version). IARC, Lyon. http://ci5.iarc.fr.
• de Martel C, Ferlay J, Franceschi S et al (2012). Global burden of cancers attributable to infections in 2008: a review and synthetic analysis.
Lancet Oncol 13:607-615.
• Bruni L, Barrionuevo-Rosas L, Serrano B et al (2014). ICO Information Centre on HPV and Cancer (HPV Information Centre).
HumanLaurentPapillomavirus and Related Diseases in World. Barcelona, Spain. Summary Report 2014-08-22.
• De Sanjosé S, Alemany L, Ordi J et al (2013). Worldwide human papilloma genotype attribution in over 2000 cases of intraepithelial and
invasive lesions of the vulva. Eur J Cancer 49:3450-3461.
• Del Pino M, Rodriguez-Carunchio L, Ordi J (2013). Pathways of vulvar intraepithelial neoplasia and squamous cell cancer. Histopathology 62
(1):161-175.
• Van der Avoort IA, Shirango H, Hoevenaars BM, Grefte JM, de Hullu JA, de Wilde PC, Bulten J, Melchers WJ, Massuger LF (2006). Vulvar
squamous cell cancer is a multifactorial disease following two separate and independent pathways. Int J Gynecol Pathol 25 (1):22-29.
• McCluggage WG (2013). Premalignant lesions of the lower female genital tract: cervix, vagina and vulva. Pathology 45(3):214-228.
• Massad LS, Xie X, Darragh T, Minkoff H, Levine AM, Watts DH, Wright RL, D’Souza G, Colie C, Strickler HD, Women’s Interagency HIV Study
Collaborative Study Group (2011). Genital warts and vulvar intraepithelial neoplasia: natural history and effects of treatment and human
immunodeficiency virus infection. Obstet Gynecol 118(4):831-839.
• Sobin LH, Gospodarowicz MK, Wittekind C (2019) UICC: TNM classification of malignant tumours, 7th edn. Wiley – Blackwell, Oxford. ISBN 978-
1-4443-3241-4.

References
• Pecorelli S (2009). Revised FIGO staging for cancer of the vulva, cervix, and endometrium. Int J Gynaecol Obstet 105(2):103-104.
• Tobian AA, Grabowski MK, Kigozi G, Gravitt PE, Eaton KP, Serwadda D, Nalugoda F, Wawer MJ, Quinn TC, Gray RH (2013). High-risk human
papillomavirus prevalence is associated with HIV Infection among heterosexual men in Rakai, Uganda. Sex Transm Infect. 2013
Mar;89(2):122-7. doi: 10.1136/sextrans-2012-050524. Epub 2012 May 24.
• Hampl M, Sarajuuri H, Wentzensen N, Bender HG, Kueppers V (2006). Effect of human papillomavirus vaccines on vulvar, vaginal, and anal
intraepithelial lesions and vulvar cancer. Obstet Gynecol 108(6):1361-1368.
• Chan JK, Sugiyama V, Pham H, Gu M, Rutgers J, Osann K, Cheung MK, Berman ML, Disaia PJ (2007). Margin distance and other clinic-pathologic
prognostic factors in vulvar cancer: a multivariate analysis. Gynecol Oncol 104(3):636-641.
• Oonk MHM et al (2021). Radiotherapy versus inguinofemoral lymphadenectomy as treatment for vulval cancer patients with micrometastases
in the sentinel node: Results of GROINSS-V II. J Clin Oncol.39(32):3623-3632.
• Te Grootenhuis NC et al (2016). Sentinel nodes in vulvar cancer: Long-term follow-up of the GROningen INternational Study on Sentinel nodes
in Vulvar cancer (GROINSS-V) I. Gynecol Oncol. 140(1):8-14.
• Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for
36 cancers in 185 countries. CA Cancer J Clin. 2018; 68: 394- 424.
• Olawaiye AB et al (2021). FIGO staging for carcinoma of the vulva: 2021 revision. Int J Gynecol Obstet. 155:43-47. https://doi.org/10.1002/ijgo.13880

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Vulval pre-cancer and Cancer-Diagnosis & Management.pptx

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