National Cancer Prevention Policy - Tobacco Control Supersite

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epithelial carcinomas of the bladder, oesophagus and lung is being studied (Persing & Prendergast 1999). The role of HPV infection in the aetiology of a range of anogenital and other cancers has been demonstrated. However, the HPV vaccines currently available have principally been tested for and aimed at reducing cervical cancer incidence. The following summary will focus on HPV infection and cervical cancer. HPV and cervical cancer The association between HPV and cervical cancer was not determined until the 1970s, and it wasn’t until the mid-1990s that the primary role of HPV in the development of cervical cancer was definitely confirmed (Eurogin 2003). Research has now distinguished between high-risk (oncogenic) and low-risk (non-oncogenic) types of HPV, and persistent infection with high-risk types of HPV is now recognised to be a necessary precursor to the development of cervical cancer (Nobbenhuis et al. 1999). Oncogenic and non-oncogenic HPVs cause low-grade squamous intraepithelial lesions (LSIL) of the cervix (Baseman & Koutsky 2005). It was believed that the development of cervical cancer involved progression from low to moderate to high-grade intraepithelial lesions (HSIL). However, natural history studies suggest that low and high-grade cervical lesions are distinct HPV processes (Baseman & Koutsky 2005). LSIL represent the transient appearance of viral infection where the HPV-infected epithelium undergoes differentiation and maturation and displays minor cellular abnormalities (Baseman & Koutsky 2005). Longitudinal studies were conducted in Brazil (Schlecht et al, 2003) and the Netherlands (Nobbenhuis et al. 2001) to examine the natural history of low grade cervical neoplasia. Schlecht et al. (2003) reported that, in the absence of intervention, only a minority of LSIL progressed to HSIL (mean progression time 86.4 months, 95% CI, 81.9 to 90.9), with the majority (78%) of LSIL regressing in less than one year (mean regression time 10.5 months, 95% CI, 8.1 to 12.9). The regression rates reported by the Dutch (Nobbenhuis et al, 2001) were slightly lower, 37.2% (95% CI, 24.8 to 49.6) at 12 months, and 54.9% (95% CI, 41.9 to 67.9) at 24 months, which probably reflects their stricter definition of regression (two negative follow-up Pap tests). HSIL occurs when HPV infects immature cells and prevents maturation and differentiation, resulting in the replication of immature cells and the accrual of genetic changes that can lead to cervical cancer (Baseman & Koutsky 2005). Cervical screening data shows the incidence of HSIL is 0.7% (VCCR 2005) and is most commonly found amongst women in their twenties, declining rapidly with age (NHMRC 2005). In an unscreened population, it is estimated that between one third and two thirds of women will develop cervical cancer after HSIL, although the time to development of cancer is variable. (Schiffman & Kjaer 2003) The world age standardised incidence rate of cervical cancer is 26.9 per 100,000, peaking at age 54 years (Gustafsson et al. 1997). It is estimated that it takes an average of 10 years from HPV infection to malignant progression (Schiffman & Kjaer 2003). The steps involved in HPV-induced cervical carcinogenesis include HPV infection, HPV persistence, progression to precancer and invasion (Schiffman & Kjaer 2003). Most HPV infections are transient and clearance of HPV infection and regression of precancerous changes can occur (Schiffman & Kjaer 2003). The majority of type-specific HPV infection clears within two years (Richardson et al. 2003). The mean time for regression of precancerous changes is longer in women infected with high-risk HPV types (mean duration of regression 13.8 – 17.1 months) compared to low-risk HPV types (mean duration of regression 7.7 – 8.9 months) (Schlecht et al. 2003). Precancerous changes also persist longer and progress faster in women infected with high-risk HPVs (Schlecht et al. 2003), and those with HIV infection (Ferenczy et al. 2003). National Cancer Prevention Policy 2007 – 09 1 H u m a n p a p i l l o m a v i r u s
The impact About 70% of invasive cervical cancers are caused by HPV 16 and 18 (Munoz et al. 2003) and about 90% of genital warts are caused by HPV 6 or 11 (Von Krogh 2001). Cervical cancer is the second most common cancer, and the third most common cause of cancer deaths in women worldwide (Figure 3.1). Eighty per cent of cervical cancer cases occur in the developing world (Jones 1999). Figure 3.1 Female cancer incidence and mortality worldwide: leading sites of new cancer and cancer death 2002 Breast Cervix uteri Colon and rectum Lung Stomach Ovary etc. Corpus uteri Liver Oesophagus Leukaemia Non-Hodgkin lymphoma Pancreas Thyroid Oral cavity Melanoma of skin Brain, nervous system Kidney etc. Bladder Multiple myeloma Nasopharynx Other pharynx Hodgkin lymphoma Larynx Mortality Incidence 0 5 10 15 20 25 30 35 40 Age-standardised rate per 100,000 women Source: Ferlay et al. 2004 In 2005 in Australia, there were 610 estimated cases of cervical cancer (AIHW 2006) and there were 212 deaths in 2004 (AIHW 2005), making cervical cancer the 12th most common cause of cancer in women and 16th most common cause of cancer death (AIHW & AACR 2004). Approximately 80% of cervical cancers occur in less developed countries and this is largely attributable to the absence of organised population-based cervical cancer screening programs (Monsonego et al. 2004). HPV has been identified in 99.7% of cervical cancer specimens (Walboomers et al. 1999). The estimated lifetime risk for women of one or more genital HPV infection is 75%. Worldwide there are estimated to be 326 million adult women who are infected with HPV. In comparison, there are approximately 450,000 new cases of cervical cancer worldwide each year (Bosch 2000); thus, HPV is considered necessary but not sufficient for the development of cervical cancers. 1 Section Three: Immunisation
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National Cancer Prevention Policy 2
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The Cancer Council Australia Member
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Overweight and obesity 86 Introduct
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A b b r e v i a t i o n s AACR Aust
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T h e N a t i o n a l C a n c e r P
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increase their understanding of man
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T o b a c c o Introduction 12 Secti
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Figure 1.1 Number of Australians wh
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(16.3%) continues the trends observ
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in the longer-term future, when hea
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Tobacco products are among the top
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In 2007, given estimated costs of $
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improved regulation, by collectivel
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Tobacco control strategy for Aborig
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Australian National Tobacco Strateg
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Regulation of products Possible reg
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• • parents/carers and children
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Australia in partnership with a num
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What needs to be achieved How The C
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——— 2005. 2004 National Drug
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Schofield PE, Borland R, Hill DJ, P
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In adult life, recreational (interm
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ehaviours as a result of public edu
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Screening for melanoma There is ins
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Autier P 2004. Issues about solaria
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N u t r i t i o n Introduction 52 S
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Table 1.4 Conclusions of the major
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It may be possible that different t
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Table 1.5 Current trends in consump
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key stakeholders (Sorensen et al. 1
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A large scale randomised controlled
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• The International Union Against
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References Nutrition Agency for Hea
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Kushi L & Giovannucci E 2002. Dieta
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Strategic Inter-Governmental Nutrit
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How physical activity is measured U
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There is consistent epidemiological
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• • Moderate-intensity physical
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to help them achieve greater and mo
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Populations Aboriginal and Torres S
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An increased capacity to monitor be
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McTiernan A, Kooperberg C, White E,
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O v e r w e i g h t a n d o b e s i
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Table 1.9 Proportion of cancer attr
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were $107.3 million in 2005, with 7
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Obese children have a 25% to 50% ch
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Table 1.10 Summary of the strengths
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more than moderately effective. The
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a screening approach particularly f
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References Overweight and obesity A
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Gebel K, King L, Bauman A, Vita P,
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——— 2004. SNAP: A population
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(the highest level of evidence in t
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How the amount of disease caused by
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The challenge Adults Alcohol is a s
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and healthy drinking cultures in Au
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ook’) (RACGP 2006) assists in dev
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English DR, Holman CDJ, Milne E, Hu
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Section Two: Screening to detect ca
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early detection improves health out
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false positive faecal occult blood
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Page 130 and 131: Breast self-examination Breast self
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Page 136 and 137: References Breast cancer Australian
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Page 148 and 149: could focus on: how to use this tim
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Page 154 and 155: likely to do so if reinvited, espec
Page 156 and 157: What we want to achieve How The Can
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Page 168 and 169: have lower levels of free PSA than
Page 170 and 171: • • a monitoring mechanism be p
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Page 174 and 175: Klein EA 2004. Selenium and vitamin
Page 176 and 177: Section Three: Immunisation www.can
Page 180 and 181: The challenge Stigmatisation of cer
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Page 184 and 185: Brinkman JA, Caffrey AS, Muderspach
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Page 196 and 197: The policy context The bleak outcom
Page 198 and 199: Aims What needs to be achieved How
Page 200 and 201: Chen DS 2005. Long-term protection
Page 202 and 203: Williams A 2002. Reduction in the h
Page 204 and 205: Authors Dr Cleola Anderiesz BSc (Ho
Page 206 and 207: Associate Professor John Kelly MDBS
Page 208 and 209: A alcohol 107 - 119 aims of The Can
Page 210 and 211: east cancer (post-menopause) 87, 88
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