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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Curr Opin HIV AIDS. 2017 Jan;12(1):69–76. doi: 10.1097/COH.0000000000000332

Malignancies in Women with HIV Infection

Nora T Oliver 1, Elizabeth Y Chiao 2
PMCID: PMC5568069  NIHMSID: NIHMS875094  PMID: 27849632

Abstract

Purpose of Review

To review current knowledge of different cancer states affecting women with HIV infection.

Recent Findings

With improved survival of persons with HIV in the post-cART era, the landscape of malignancies in this population has greatly changed with fewer AIDS-defining malignancies (ADM) and a growing number of non-AIDS defining malignancies (NADM). Women, however, continue to represent a vulnerable population at risk for certain ADM and NADM such as cervical, anal, and breast cancer. Human papilloma virus-mediated cancers disproportionately burden women in resource-poor settings such as Subsaharan Africa. For cancers such as Kaposi’s Sarcoma, lung cancer, liver cancer, and colorectal cancer, women share a lower burden of disease compared to their male counterparts. However, there remains a dearth of evidence characterizing these disease states specifically among women.

Summary

Cancer in women with HIV continues to be a major source of morbidity and mortality worldwide, especially in low-income countries. Screening strategies, primary prevention through vaccination against human papillomavirus and viral hepatitis, and treatment for HIV with combined antiviral therapy remain cornerstones in cancer prevention.

Keywords: women, HIV, cancer, cervical cancer, breast cancer, human papillomavirus

Introduction

With the aging of the population of HIV-infected individuals due to combined antiretroviral therapy (cART), the landscape of malignancies has shifted. Classical AIDS-defining malignancies (ADM) have decreased; however, other non-AIDS-defining malignancies (NADMs) such as anal, lung, colorectal, and liver cancers continue to pose a significant health threat to patients with HIV [1, 2]. Women with HIV continue to be affected by gynecological and non-gynecological cancers at alarming rates. Cervical cancer, caused by human papillomavirus (HPV) continues to cause a significant burden of cancer and cancer-related deaths especially in resource limited setting such as Subsaharan Africa (SSA) [3]. Anal cancer has historically been a focus for men with HIV, especially those who have sex with men. However, anal cancer, another HPV-mediated state, has increasingly been recognized as a major health threat to women [4].

Herein, we review the following malignancies currently affecting women with HIV: cervical cancer, anal cancer, breast cancer, ovarian and uterine cancer, lung cancer, non-Hodgkin lymphoma (NHL), and Kaposi’s sarcoma (KS). Available research of colorectal and liver cancer indicates that HIV-infected women are less affected by these malignancies compared to HIV-infected men, and will not be included in detail in this review [5–8].

Cervical Cancer

Among reproductive malignancies, invasive cervical cancer (ICC) is the number one cause of new cancers in women and responsible for the most deaths in women world-wide [3]. Women residing in resource-limited settings bear the brunt of this disease with incidence rates >30.2/100,000 population compared to more industrialized nations where incidence rates are much lower, <7.9/100,000 population [3]. In the US where incidence is relatively low, cervical cancer in HIV-infected women the incidence still remains 66% higher than women without HIV [9]. However, in some areas of SSA, ICC incidence is much higher, nearly 168/100,000 women on cART [10]. Mortality from ICC has continued to be higher in HIV-infected women than HIV-uninfected women. Although mortality is not statistically significant in resource rich settings, [2] women living in resource-limited setting, suffer disproportionate mortality. For instance, in SSA mortality is >17.5/100,000 population, over 3-fold the morality of cervical cancer in the US [3].

HIV-infected women are known to be at high risk for human papillomavirus (HPV) infection, the virus responsible for genital warts, pre-cancerous lesions and ICC [11]. Globally, infection with one or multiple types of HPV virus, including high-risk HPV (hrHPV) strains, in HIV-infected women is common and as high as 91% in some SSA regions [12, 13]. In SSA, the six most common types of HPV are oncogenic types 16, 18, 35, 45, 33, and 52 [14]. Immunologic and virologic HIV control are significant co-factors in the persistence, and progression of HPV infection to pre-malignant lesions and ICC [11, 15, 16]. The use of cART, however, may not completely reverse the oncogenic potential of HPV especially if early malignant changes begin to take place while CD4 counts are low [15].

Clinical presentation of ICC in women with HIV often occurs at younger ages, up to 15 years earlier in advanced HIV compared to HIV-uninfected women [17, 18], which may suggest a shorter latency period in HIV-infected women. Some studies have described women with HIV presenting with later, more advanced stage ICC than HIV-uninfected women [17]; however, other studies have found high rates of advanced ICC in both HIV-infected and HIV-uninfected populations alike in resource limited settings [19], suggesting the pervasive lack of cervical cancer screening.

Cervical cancer histology is most commonly squamous cell carcinoma (SCC), and treatment includes surgery, chemotherapy, and/or radiation [17, 19]. Treatment is challenging in many resource limited countries lacking appropriate facilities and equipment [20]‥ Treatment interruptions and incomplete cancer therapy have significant affects upon cancer outcomes, and women with HIV infection are at high risk of having residual tumor burden [18]. Interestingly, women treated with cART have higher likelihood of treatment completion [19], likely owing to improved treatment tolerance.

Screening for cervical cancer is a key component of primary care for women with HIV. However, wide spread cytology screening and hrHPV detection in low-income countries is difficult to implement due to lack of adequate facilities, resources, finances, and trained personnel, however [21]. The World Health Organization (WHO) has adopted an alternative approach using the “screen-and-treat” method for resource-limited settings. This encourages use of available screening methods, preferably HPV testing as first line, followed by immediate treatments (e.g. cryotherapy) for cervical abnormalities [22]. HPV testing in low-resource, high burden settings may be desirable because of its sensitivity for detecting pre-cancerous lesions as well as its convenience for self-testing [23, 24]; however, cost-effectiveness may preclude its widespread use [10].

Cervical cancer is a now a vaccine preventable disease. Widespread vaccination for HPV is critical in young girls and women with HIV in low-income and high-income settings alike. Most recently the 9-valent vaccine, containing a broader coverage of cancer-causing strains (additional types 31, 33, 35, 52, 58), was added to the armamentarium [25]. These are recommended for routine vaccination of females ages 11–26 years [26, 27]. Immunogenicity of the quadrivalent and bivalent vaccines in women with HIV but without evidence of HPV infection is good (>75%); however, like other vaccines in HIV-infected persons, robust CD4 counts confer better seroconversion response [28]. In 2014 only 58 countries had incorporated HPV vaccination into national immunization campaigns and mostly in high-income settings [27]. More recently, countries in SSA have begun to implement HPV vaccination nationwide with support from global health programs [29], which may have significant cost efficacy [30]. Unfortunately, the details of real-world vaccination uptake in HIV-infected girls and women remain difficult to accomplish [31].

Anal Cancer

The majority of anal cancers are composed of SCC and associated with the presence of hrHPV types in 90% of cases [32]. Incidence of anal SCC has continued to increase globally, and in developed countries incidence has increased 1–3% annually [32]. In the US, women are affected more than men with a rate of 1.8 versus 1.1/100,000 population [33]. Incidence of anal cancer in HIV-infected women in higher income countries is also high (3.9–30 per 100,000) [4]. Women with AIDS, in particular, have a nearly 15-fold higher risk of developing invasive anal SCC compared to the general population (SIR 14.5; 95% CI, 8.8–22.4) [34]. Risk factors for anal infection with HPV include tobacco use, perianal warts, and presence of cervical HPV infection [4].

Poor immune status with CD4 <200 cells/µL is a risk factor for anal HPV infection [4]; moreover, increased risk of HPV-associated neoplasia has been associated with increased duration after AIDS diagnosis [34, 35]. Immunosuppression may facilitate early viral-mediated oncogenesis which is irreversible despite CART-mediated immune restoration [34]. Interestingly, HIV viral load has not been associated with the presence of abnormal anal cytologic findings in HIV-infected women [4], but has been associated with an increased number of high-grade squamous intraepithelial lesions and anal condyloma [36, 37].

Practice of anal cancer screening using anal canal Dacron swab technique and liquid cytological evaluation has derived from cervical cytology testing. Classifying cellular histology of anal lesions also employs the revised Bethesda System for Reporting Cervical Cytology [38, 39]. Sensitivity of detecting high-grade anal neoplasia ranges from 69–93% in several studies [38], and abnormal anal cytology should be further investigated with high resolution anoscopy (HRA), which is analogous to the cervical colposcopy [40, 41]. HPV DNA testing is controversial given the high prevalence of hrHPV viral infection in HIV-infected persons [39, 42]. However, presence of hrHPV genotype 16 is associated with concurrent high-grade anal lesions in women with HIV [43, 44].

Due to lack of standardized guidelines on anal cancer screening, clinicians have been charged with creating local protocols to address this need. Determining which women are at high risk for anal cancer is of the utmost importance. Women with a history of cervical or vulvar neoplasias are more likely to have anal HPV-infection and abnormal anal cytology [4, 43, 45]. The presence of anal warts or condyloma acuminata may also be an indicator for HPV infection of the anal canal and may warrant further screening. A limitation of implementing anal cancer screening beyond a yearly digital rectal exam is the lack of readily accessible and trained personnel and equipment for performing HRA. If HRA is not available, anal cytology is discouraged [46].

Primary prevention of anal cancer has been more extensively studied in men due to high the high incidence rates of anal cancer in men who have sex with men (MSM). Women receiving the latest 9-valent HPV vaccine could potentially reap significant benefit and reduction of up to 87% of anogenital cancers globally [47]. Anal cancer prevention is an added benefit of early HPV vaccination in girls and women with HIV or in areas with high-endemic rates of HIV and HPV infection.

Breast Cancer

Breast cancer remains the most common cancer type (23% of total new cancer cases) in women living in industrialized and non-industrialized countries [3]. It also is the most common cause of cancer-related deaths among women, accounting for 15% of total cancer deaths [3]. Breast cancer has previously been described as occurring less frequently in women with AIDS compared to the general population [48–50]. One large retrospective US study of women with AIDS followed for 665,987 pys showed a SIR 0.69 (95% CI, 0.62–0.77); however, increases over the follow-up period of locally/regionally-disseminated disease approached that of the general population [51].

As HIV-infected women age, the incidence of breast cancer is likely going to increase. Previous case series have demonstrated that women present at younger ages, frequently with advanced disease, increased multifocality of disease, early metastasis, and poor outcomes [52–54]. Prior studies have not demonstrated significant association with low CD4 counts or AIDS diagnoses with the development of breast cancer [54]. The links between HIV, the immune response, and natural history of breast cancer are unclear based on the limited, available data. Larger studies are needed to identify HIV-specific risk factors in the acquisition and progression of breast cancer.

Breast cancer treatment in HIV-infected women remains challenging because chemotherapeutic agents can also pose significant drug interactions with anti-retroviral therapies. Standard guideline-based therapies based on stage at diagnosis should be implemented for eligible HIV-infected women[54]. Rates of estrogen, progesterone, or HER-2/neu receptor status of breast tumors in HIV-infected women are not well established, but estrogen-receptor positivity has been reported in nearly 50% of cases [54, 55]. Close attention should be paid to drug interactions between breast cancer therapies, including hormonal therapies and antiretroviral therapies. Cancer-specific mortality in women with HIV in the post-cART era remains higher than in the general population (HR 3.43, 95% CI, 2.35–5.01) [2]. In one case series, progression free-survival at 5 years was 50% and median overall survival was 52 months [54, 55].

Screening and prevention of breast cancer are of the utmost importance in women with HIV infection. Current US Preventive Service Task Force (USPSTF) screening guidelines recommend for the general population biennial mammography for women ages 50–74; however, more frequent screening can be used in patients who may be at increased risk [56]. For HIV-infected women, this level of screening is the acceptable practice [57] until further risk factors (e.g. HIV-specific or genetic markers) beyond family history can be firmly established and in practice to better identify women at high risk for breast cancer. Despite these recommendations, screening for breast cancer in women with HIV remains challenging with historically low screening rates (30–50%) compared to the general population [58, 59].

Ovarian and Uterine Cancer

Uterine and ovarian cancers account for about 4% of new cancer diagnoses in women [60, 61]. While relatively less common, ovarian malignancies are responsible for are large burden of annual deaths (age-standardized rate 3.8%) with poor survival often less than 50% when compared to other gynecological cancers [3, 60].

Only few studies have characterized ovarian and uterine cancers in women with HIV infection. Interestingly, one large study following 85,268 women for 665,987 pys found significantly lower incidence of uterine cancer compared to the general population with only 31 cases (SIR 0.57; 95% CI 0.39–0.81) [51]. After stratifying groups based on menopausal status, women <50 years had a uterine cancer SIR 0.86 (05% CI, 0.54–1.32), and women >50 years had a SIR of 0.33 (95% CI, 0.4–1.68). Within this same study only 42 cases of ovarian cancer were identified (SIR 1.05; 95% CI, 0.75–1.42) [51]. With regard to immune status, there was also no significant relationship between onset of AIDS diagnosis or CD4 count for uterine or ovarian cancer. However, infertility and poor ovarian function are also more common in women with HIV than in the general population [62]; thus, the impact of HIV infection upon ovarian cancer development is unclear.

Data on mortality due to ovarian and uterine cancers specifically in the HIV population is limited likely due to the relative infrequency of these cancers. One Italian study, mortality from uterine cancer accounted for 4% of cancer-specific deaths from 2006–2011 [63]. Standardized mortality ratio of women with AIDS and uterine cancer was 52.5 (95% CI, 14.3–134.5) compared to those without AIDS in the same study [63].

Lung Cancer

Lung cancer, primarily non-small cell lung cancer (NSCLC), is a leading cause of cancer death among persons with HIV infection and poses a major threat to morbidity and mortality in the HIV population globally [2, 63]. Over time from the pre-cART era to post-cART, the number of lung cancer cases has risen more than 2-fold in the US, especially in people >50 years, which is likely due to both high rates of tobacco use and aging in the HIV-infected population [64]. Even after carefully controlling for smoking prevalence, HIV itself has been described as an independent risk factor for lung cancer [65], and women with HIV have nearly 4-fold higher incidence than the general population [66]. Recurrent bacterial pneumonias among persons with HIV also has been implicated as a risk factor for lung cancer development due to persistent tissue inflammation [67]. Mortality continues to remain higher among patients with HIV in the post-cART era compared to HIV-uninfected patients (HR 1.38, 95% CI 1.21–1.56) [2].

Lung cancer patients with HIV tend to present at younger ages (54.1 v 60.5 years) compared to those without HIV, and a South African study found no statistical gender difference between HIV-infected and uninfected lung cancer cases [68, 69]. Several studies have found that HIV-infected patients commonly present with advanced disease (stage III/IV) [65, 68–70]. In addition, HIV-infected patients with NSCLC have worse 5-year overall survival compared to those without HIV (9% versus 23%) [71]. Robust CD4 count (>200 cells/µL) carry improved survival compared to those with low CD4 counts (median survival 11.5 months compared to 3.4 months) [69].

Tobacco smoking prevalence among HIV-infected men and women is significant with rates nearly 2–3 times higher than in the general population [72, 73]. Among persons with HIV and lung cancer, current smokers (aIRR 6.3, 95% CI, 4.7–8.4) and former smokers (aIRR 3, 95% CI 2.2–4.1) have higher risk of lung cancer than never smokers [65]. Tobacco smoking cessation should be a key component of primary care and for lung cancer prevention for HIV-infected women, pharmacologic-aides may be useful during cessation attempts [74].

Because of improved mortality benefit, lung cancer screening with low-dose computed tomography (LDCT) is recommended for people aged 55–80 in the general population with at least a 30 pack-year smoking history and currently smoke or who have quit within 15 years, regardless of gender [75]. Some caution must be taken in screening HIV-infected patients, especially those with poor CD4 count, as they are likely to have false positive LDCT findings due to prior lung infections [76]. These may lead to unnecessary testing, surgery, and patient anxiety.

Non-Hodgkin Lymphoma

The post-cART era has experienced an overall decline in incidence of NHL; however, incidence of NHL among HIV-infected persons continues to be significantly higher (>10-fold) than the general population [1, 77]. Gender-specific incidence rates of NHL favor women, who have a lower incidence of this malignancy across high and low-income regions. French and Swiss data have shown fewer HIV-infected women are at risk of acquiring NHL compared to HIV-infected men (16% v 18%, respectively) [5, 66]. In Southeast Asia, North Africa, and SSA, NHL affects women less than men as well. [77].

NHL remains the largest cause death among the ADMs [2, 63, 78]; however, NHL-specific death in the post-cART era affects women much less frequently than men (3–22% versus 15.2–78%, respectively) [78, 79]. Furthermore, with the widespread implementation of cART, 5-year survival across genders has improved dramatically compared to pre-cART eras in France (65% v 15% 5-year survival, respectively) and in the US (54% to 9% 5-year, respectively) [5, 79]. In addition, increased uptake of standard, more dose-intensive chemotherapeutic treatment strategies has helped improve complete remission and survival rates in the HIV-infected population regardless of low CD4 counts and AIDS diagnoses [80, 81].

Kaposi’s Sarcoma

Human herpesvirus-8 (HHV-8) infection has a significant geographic variance ranging from 1–8% in Western nations and 40–80% in SSA [82]. People with HIV infection are more likely (OR 1.99, 95% CI, 1.7–2.34) to have HHV-8 infection than the general population [83]. This parallels the trends of AIDS-related KS, and in the US, for example, the incidence of KS within the HIV population is exceedingly high compared to the general population (130/100,000 py versus 0.2/100,000 py, respectively) [1]. HIV-infected men carry the largest burden of these conditions among persons with HIV due to the high prevalence of HHV-8 infection among MSM [84]. A recent systematic review comparing HHV-8 prevalence between men and women found that after excluding studies with MSM, heterosexual men in SSA had a increased risk of HHV-8 infection (OR 1.21, 95% confidence interval (CI) 1.09–1.34), but this was not true for men from other localities [85]. In resource-rich countries, KS represents a small fraction (2–3%) of all ADM in women [5, 86, 87]; however, in low-income regions such as SSA, incidence of KS in women with HIV seems to be elevated, especially in untreated groups (1,214/100,000 py) [88].

Comprehensive data on clinical presentation of KS in women are limited; however, women may present at younger ages (second and third decades) and may have more disseminated skin disease compared to men [89, 90]. Treatment of HIV with cART is the cornerstone of prevention and treatment of KS owing to improved immunological control [91]. Additionally, systemic chemotherapeutic agents such as taxanes and anthracyclines for progressive KS may be beneficial [92].

Survival data in women compared to men is mixed in studies from SSA regions. Furthermore, treatment outcomes specifically for HIV-infected women are limited likely due to lower burden of disease in this gender class, especially in Western regions. In one small study from Uganda, sex was not a risk factor for KS-associated mortality [93]. However, another study from South Africa found women were twice as likely to die from KS compared to their male counterparts [88].

Key Points

  • Cervical cancer disproportionately affects women with HIV likely due to high prevalence and persistence of HPV infection.

  • Lack of primary prevention programs, screening infrastructure, and treatment resources have contributed to high mortality in low-income countries.

  • HPV vaccination has been shown to be beneficial and cost-effective in preventing cervical and anal cancer in women.

  • Treating underlying HIV with cART is a critical component of cancer prevention, treatment, and survival for HIV-infected women with cancer.

Conclusion

At the cornerstone of all prevention strategies for cancer in HIV-infected women is engagement in healthcare and effective treatment with cART. Cancer prevention is critical to curb morbidity and mortality in HIV-infected women, especially because many neoplastic states present at younger ages and at more advanced stages than in the general population. In addition, HIV-infected women are especially at risk for HPV-mediated disease due to persistent HPV infection, especially in low-income settings with high HPV infection prevalence. Thus, primary prevention with vaccination strategies for HPV-related neoplasias is of utmost importance. Furthermore, implementation, access, and affordability of breast and lung cancer screening are also key components for decreasing cancer morbidity and mortality among HIV-infected women. Finally, differences in the incidence and mortality of non-female specific cancers, such as: colorectal, liver, KS, and lymphoma are needed to better clarify the potential effect of gender specific differences, including sex hormones and other gender specific biologic and behavioral risk factors on the incidence and outcomes of these cancers in HIV-infected women.

Acknowledgments

Nora T. Oliver was the primary author of the manuscript. Elizabeth Y. Chiao provided content, writing and editorial supervision.

Disclosures: Dr. Elizabeth Chiao received research funding for this project through a 2011 developmental grant from the Baylor-UT Houston Center for AIDS Research (CFAR), a NIH-funded program (NIH P30 CA125123), the AIDS Malignancy Consortium (NIH 2U01CA121947), and NIH R01 CA163103. This work was also supported in part by the Center for Innovations in Quality, Effectiveness and Safety (#CIN 13-413).

Footnotes

Disclaimer: The views expressed in this article are those of the author(s) and do not necessarily represent the views of the Department of Veterans Affairs.

Conflicts of Interest

Neither author has any conflicts of interest to declare.

Reference and recommended reading

Papers of particular interest, published within the period of review have been highlighted as:

* of special interest

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