This chapter should be cited as follows:
Li JJ-X, Cheung AN-Y, Glob Libr Women's Med
ISSN: 1756-2228; DOI 10.3843/GLOWM.422023

The Continuous Textbook of Women’s Medicine Series – Gynecology Module

Volume 13

Gynecological cancer

Volume Editors: Professor Hextan Ngan , Department of Obstetrics and Gynaecology, The University of Hong Kong, Hong Kong
Professor Karen Chan, Department of Obstetrics and Gynaecology, The University of Hong Kong, Hong Kong

Chapter

HPV-Negative Cervical Cancer in the HPV-Vaccination Era: Pathology Perspective

First published: December 2025

AUTHOR(S)

Joshua Jing-Xi Li

Department of Pathology, School of Clinical Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China

Annie Nga-Yin Cheung

Department of Pathology, School of Clinical Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China

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INTRODUCTION

High-risk human papillomavirus (HPV) is recognized as the most important carcinogenic factor for cervical cancer (Figure 1), accounting for the great majority of cases. In the current era of increasing HPV-vaccine coverage and the widespread use of HPV testing for cervical cancer prevention and screening, HPV-negative cervical cancer has gained attention because of its potential clinical implications. With the use of molecular diagnostic techniques, pathological characterization of HPV-independent cervical carcinomas has been advancing, and several biologically and morphologically distinct entities have been identified. In this chapter, updated clinicopathological and molecular characteristics of significant HPV-independent cervical carcinomas, as well as the challenges associated with cytology-based screening and pathological diagnosis, are described.

Histological sections of HPV-associated carcinoma of the cervix. Squamous cell carcinoma (magnification ×40; a,b) and adenocarcinoma (magnification ×20; c,d), shown with H&E stain (a,c) and p16 immunohistochemistry (b,d).

HPV-NEGATIVE CERVICAL CANCER

HPV-negative cervical cancers are encountered for several reasons. First, some HPV-negative cervical cancers are not primary cancers but are metastatic from other organs, such as the endometrium, ovary, gastrointestinal tract, urinary bladder or breast.

Second, cervical carcinomas may be diagnosed after a negative HPV molecular test but, in fact, still be associated with HPV, i.e. due to false-negative HPV test results.¹ A study of cervical intraepithelial neoplasia (CIN) 2 or worse lesions that tested negative by the Cobas assay in the ATHENA study showed that a significant proportion were positive when tested with other HPV assays (Linear Array and Amplicor) indicating false-negative Cobas HPV test results.² There are several reasons that may underlie false-negative HPV results:³ the cervical cancer may be caused by an HPV type not covered by the test; the viral copy number may be low, or inhibitors may be present in the sample; heavy blood contamination or glycerol–acetic acid treatment may affect HPV test performance; loss of the PCR-targeted region during HPV integration, improper fixation and inadequate sampling may also reduce test accuracy.

Finally, some cervical adenocarcinomas and squamous cell carcinomas, as well as their precursors, are truly HPV-independent.

The clinical, morphological, genetic and biological features of these uncommon tumors, as well as their impact on prevention, diagnosis and management, will be discussed.

TYPES OF HPV-INDEPENDENT CERVICAL CANCER

HPV-independent carcinomas comprise approximately 14% of all cervical cancers,⁴ and are expected to increase in proportion due to the impact of HPV vaccine.⁵ HPV-independent cervical carcinomas encompass HPV-independent squamous cell carcinoma, clear cell adenocarcinoma, endometrioid adenocarcinoma, gastric-type adenocarcinoma and mesonephric type adenocarcinoma. While HPV-independent cervical squamous cell carcinomas constitute a small minority of all cervical squamous cell carcinomas, cervical adenocarcinomas are more frequently HPV-independent than are squamous cell carcinomas.⁴

HPV-independent squamous cell carcinoma

HPV-independent squamous cell carcinomas typically occur in older women and are more commonly seen in postmenopausal age groups.⁶ Most studies report a rate of around 10% for HPV negativity in squamous carcinomas of the cervix.⁴^,⁷^,⁸ A link with genital prolapse has been reported and is postulated to be a result of chronic inflammation and scarring leading to cancer development.⁹ These squamous cell carcinomas present at a higher disease stage with a propensity for lymph-node involvement, and subsequently worse disease outcomes.¹⁰ Histologically, keratinization, hyperkeratosis, parakeratosis and an absence of adjacent HPV-associated precursor lesions favor HPV-independent squamous cell carcinoma over its HPV-dependent counterpart, but the differentiation cannot be definitively made solely based on tumor morphology.⁹ The lack of p16 overexpression, among other negative results in ancillary molecular testing for HPV, is necessary for the diagnosis of HPV-independent squamous cell carcinoma. The P53 mutation is enriched in these tumors and can be demonstrated by p53 immunohistochemistry or DNA sequencing.⁹

HPV-independent cervical intraepithelial neoplasia (CIN)

HPV-independent CINs have recently been reported and may show verrucous, differentiated or basaloid patterns.¹¹^,¹² Koilocytes are usually absent. p16 expression is absent or of non–block-type. Mutation-type aberrant p53 expression may also be present.

Clear cell adenocarcinoma

Clear cell adenocarcinomas of the cervix follow a bimodal age distribution. The first peak is observed at late adolescence/early adulthood¹³^,¹⁴ and is associated with in-utero exposure to diethylstilbestrol (DES). The median age at presentation for clear cell adenocarcinoma not related to DES exposure is 48 years¹⁵ and constitutes the second peak. Its histological appearance resembles that of clear cell adenocarcinomas from other parts of the female genital tract (uterine corpus and ovaries), in particular tumor cells displaying overt nuclear atypia and a characteristic clear cytoplasm, arranged in variable destructive growth patterns¹⁶ (Figure 2a). Clear cell adenocarcinomas of the cervix share common immunophenotypic features with upper female genital tract carcinomas, notably PAX8 positivity and non-diffuse p16 expression¹⁷ (Figure 3a,b). Limited data from case series indicate that mutations in CMTM5 and WWTR1 are relatively frequently detected in clear cell adenocarcinomas of the cervix.¹⁸^,¹⁹

Histological sections of HPV-independent cervical carcinomas. (a) Clear cell adenocarcinoma. (b) Endometrioid adenocarcinoma. (c) Well-differentiated gastric-type adenocarcinoma. (d) Poorly differentiated gastric-type adenocarcinoma. H&E stain. Magnification ×20.

Immunohistochemical profile of HPV-independent cervical carcinomas. (a,b) Clear cell adenocarcinoma. (c,d) Gastric-type adenocarcinoma. HPV-independent cervical carcinomas do not show p16 diffuse expression (a,c) and are PAX8 positive (b,d). Magnification ×20.

Endometrioid adenocarcinoma

Primary cervical endometrioid adenocarcinomas are morphologically identical to endometrioid adenocarcinomas of the endometrium and ovaries¹⁷ (Figure 2b). The diagnosis can be made only when secondary involvement, particularly cervical involvement by endometrial endometrioid adenocarcinoma, is thoroughly excluded. These tumors are believed to arise from endometriosis of the cervix, which may occasionally be identified in proximity to the invasive adenocarcinoma component.¹⁷ In addition to PAX8 positivity, estrogen-receptor and progesterone-receptor immunoreactivity differentiates endometrioid adenocarcinomas from HPV-associated adenocarcinomas of the cervix. Genomic analyses have identified a subset of cervical carcinomas, mostly HPV-negative adenocarcinomas, that show enrichment for ARID1A, KRAS and PTEN mutations,²⁰ which correlate with these tumors.

Of note, the 2020 World Health Organization Classification of Tumours considers serous carcinomas identified in the cervix to represent metastasis or secondary involvement from ovarian or endometrial primaries,²¹ and therefore not a histotype compatible with a cervical primary.

Gastric-type adenocarcinoma

Peutz–Jeghers syndrome (germline STK11) and somatic STK11 mutations are detected in a significant proportion of cervical gastric-type adenocarcinomas.²² Among all HPV-independent cervical adenocarcinomas, the reported incidence of gastric-type adenocarcinoma is the highest,²³ thus clinicopathological and outcome data are relatively better defined for this entity.

Gastric-type adenocarcinomas frequently present at a late stage (parametrial involvement, ovarian and lymph node metastasis) with unfavorable histopathological features (lymphovascular invasion and positive peritoneal cytology) and significantly worse disease-free and overall survival compared to HPV-associated endocervical adenocarcinomas.²⁴ Macroscopically, these tumors have been associated with a ‘barrel-shaped’ cervix, attributed to deep invasion and induction of desmoplasia, leading to diffuse enlargement and thickening of the cervix.²⁵ The histological appearance of these tumors is diverse. Well-differentiated forms (Figure 2c) can be difficult to distinguish from non-lesional cervical glands, which is reflected in the older terminology ‘adenoma malignum’ and ‘minimal deviation adenocarcinoma’. These historically referred to gastric-type adenocarcinomas that exhibit bland morphological features.²² In contract, poorly differentiated tumors can display variable architectural patterns, ranging from irregular incomplete, glands to solid nests or single cells in which glandular differentiation is not readily evident²⁶ (Figure 2d).

Gastric-type adenocarcinoma of the cervix produces neutral mucin and is termed ‘gastric-type’ because neutral mucin is commonly found in gastric adenocarcinomas.²⁷ Its phenotypic resemblance to gastric adenocarcinoma can also be seen in its clear-to-pale eosinophilic, abundant cytoplasm²⁸ and expression of HIK1083 (gastric O-glycan),²⁹ MUC6 (gastric mucin)³⁰ and TFF2 (gastric mucosal peptide).³¹ As compared to other HPV-independent adenocarcinomas, PAX8 expression is variable in gastric-type adenocarcinomas³² (Figure 3c,d). Mutations in TP53, CDKN2A, KRAS, ERBB2 and ERBB3 (≥10%)³³^,³⁴ are found in gastric-type adenocarcinomas.

Mesonephric adenocarcinoma

Mesonephric adenocarcinomas are derived from mesonephric duct remnants.³⁵ Mesonephric duct remnants are vestiges from the regressed mesonephric ducts that form the male reproductive organs during embryonic development, and are located along the female genital tract, particularly along the lateral wall of cervix.³⁵ Although associated with embryonic remnants, mesonephric adenocarcinomas classically present in postmenopausal women.³⁵ The outcomes of mesonephric adenocarcinomas of the cervix, endometrium and ovary are similarly poor, with an increased incidence of lung metastasis.³⁶ These tumors are morphologically distinct, exhibiting a mixed architectural pattern with tubular structures, intraluminal eosinophilic secretions and papillary thyroid carcinoma-like nuclear features (nuclear angulation, grooves and pseudoinclusions).³⁷ Adjacent mesonephric remnants or mesonephric hyperplasia may be present. Mesonephric adenocarcinomas display a unique immunoprofile with reciprocal expression of GATA3 and TTF1, and luminal CD10 positivity³⁷ PAX8 is also frequently positive in mesonephric lesions.³⁸ KRAS mutation is nearly ubiquitous in mesonephric adenocarcinomas and serves both as a diagnostic and targetable therapeutic marker³⁹ (Table 1).

HPV-independent adenocarcinoma in situ

The relatively more commonly reported HPV-independent adenocarcinoma in situ refers to non-invasive gastric-type adenocarcinoma in situ or atypical lobular endocervical glandular hyperplasia (LEGH) featuring gastrointestinal differentiation and absence or non-block p16 expression.⁴⁰^,⁴¹ Aberrant p53 mutant type expression and Claudin 18 immunoreactivity may help in the diagnosis.⁴² They are often found adjacent to invasive gastric-type adenocarcinoma and the independent clinical outcome of such lesions is still not clear. Some may be associated with synchronous mucinous metaplasia and neoplasia of the female genital tract and Peutz–Jeghers syndrome.⁴³

Highlighted features of HPV-independent carcinomas.⁹^,¹⁵^,²²^,³⁴^,³⁶^,³⁷^,⁴⁴^,⁴⁵

Carcinoma type	Pathogenesis	Histology	Molecular features
Squamous cell carcinoma (HPV-independent)	Postmenopausal age Association with prolapse	Keratinization Hyperkeratosis Parakeratosis	p53 overexpression P53 mutation
Clear cell adenocarcinoma	DES-related cases present early DES-independent cases present later	Similar to clear cell adenocarcinoma of the uterine corpus and ovaries
Endometrioid adenocarcinoma	Association with endometriosis	Similar to endometrioid adenocarcinomas of the uterine corpus and ovaries	ARID1A, KRAS and PTEN mutations
Gastric-type adenocarcinoma	Peutz–Jeghers syndrome	Clear to pale eosinophilic and abundant cytoplasm	STK11 mutation
Mesonephric type adenocarcinoma	Arise from mesonephric duct remnants	Tubular pattern Intraluminal eosinophilic secretions Papillary thyroid carcinoma-like nuclei Adjacent mesonephric components	KRAS mutation

DES, diethylstilbestrol.

CLINICAL IMPLICATIONS

HPV-independent cervical carcinoma poses challenges with regards to detection, pathological diagnosis and clinical management owing to its unique repertoire of clinicopathological characteristics. For one, HPV-independent carcinomas occur mostly in postmenopausal women, with DES-associated clear cell adenocarcinomas presenting as early as in teenagers.¹⁴ These populations are socioeconomically more vulnerable than are independent adults, in which HPV-associated carcinomas most commonly present.⁴⁶ There is conflicting evidence on the effect of age on the outcomes of cervical cancer depending on the cut-off adopted for analysis.⁴⁷^,⁴⁸^,⁴⁹ However, results from Barben et al. defining older women as ≥ 70 years demonstrated worse short-, medium- and long-term overall survival with advanced age.⁴⁷ Regardless, outcomes of HPV-independent cervical carcinomas, including recurrence-free, disease-free and overall survival, are inferior to those of HPV-associated cervical carcinoma.⁵⁰

LIMITATIONS OF HPV TESTING FOR CERVICAL CANCER

In terms of epidemiology, HPV-associated precancerous lesions and HPV-associated cervical carcinomas are preventable by HPV vaccination,⁵¹ and decreases in incidence and mortality related to cervical carcinomas have been observed in regions in which effective population-level HPV vaccination has been adopted.⁵² As a result, the incidence of HPV-independent carcinomas is gaining increased clinical significance.⁵³ Because these carcinomas are relatively uncommon and morphologically diverse, encompassing multiple morphologically distinct subtypes of adenocarcinomas with a wide variation in degree of differentiation,⁵³ diagnosis by cervical cytology is challenging⁵⁴ (Figure 4). Even so, cytomorphological assessment may allow the detection of HPV-independent cervical carcinomas, particularly morphologically high-grade tumors such as HPV-independent squamous cell carcinomas and clear cell adenocarcinomas.⁵⁵ On the other hand, the absence of detectable precursor lesions on cytologic specimens, the subtle or non-HPV-related cytologic features of these tumors, and potential false reassurance from negative HPV testing can make HPV-independent adenocarcinomas more difficult to recognize microscopically. Consequently, the false-negative rate for cervical cytology in HPV-independent adenocarcinomas may be higher than that in HPV-associated adenocarcinomas.⁵⁶

Gastric-type adenocarcinoma on cervical cytology.

In an HPV testing standalone approach, without cytological evaluation, HPV-independent cervical carcinomas would likely not be detected on screening. It has also been reported that a proportion of girls receiving HPV vaccination and their parents might erroneously assume that the vaccine entirely removes the risk of developing cervical cancer and that further cervical screening is not required.⁵⁷ Such factors contribute to HPV-independent cervical carcinoma presenting at more advanced stages than HPV-associated cervical carcinomas.⁴⁴

DIAGNOSTIC CONSIDERATIONS

The pathological diagnosis of HPV-associated cervical carcinoma is relatively uncomplicated, as its clinicopathological features are well defined.⁵⁸ A previous positive cervical cytology or HPV test result is useful in supporting the diagnosis. The histological features of HPV-associated cervical carcinoma are well studied, with a much narrower spectrum consisting mostly of squamous cell carcinomas and a minority of adenocarcinomas.⁵⁹ The presence of concurrent precursor lesions (squamous intraepithelial lesion and adenocarcinoma in situ) in histological sections serves as another helpful diagnostic feature. Finally, diffuse overexpression of p16 is a robust and sensitive immunohistochemical marker that identifies HPV-associated precancerous lesions and carcinomas, and often sees use in the diagnosis of these lesions in small biopsies.⁶⁰

In contrast, HPV-independent cervical carcinoma, despite a trend in increasing incidence, remains uncommon and relatively unfamiliar to the general pathologist and gynecologist. The diverse morphological appearance of HPV-independent cervical carcinomas leads to a multitude of diagnostic considerations.⁶¹ Diagnosing early and well-differentiated HPV-independent cervical carcinomas requires extensive experience in gynecologic pathology, with challenging pitfalls such as differentiating mesonephric adenocarcinoma from florid mesonephric hyperplasia³⁵ and recognizing well-differentiated gastric-type adenocarcinomas that radiologically mimic Nabothian cysts and histologically resemble normal structures.⁶² The absence of HPV-positive test results and identifiable precursor lesions reduces diagnostic certainty. The differential diagnosis of HPV-independent cervical carcinomas includes non-malignant cervical lesions, HPV-positive cervical carcinomas, endometrial and ovarian neoplasms and extragenital tumors.⁶³ HPV testing, p16 and PAX8 immunohistochemistry can aid in distinguishing between HPV-associated and HPV-independent cervical carcinomas; however, they do not reliably separate HPV-independent cervical carcinomas from benign or malignant lesions of the upper female genital tract or from extragenital tumors³⁷^,³⁸ (Table 2).

Clinicopathological comparison between HPV-associated and HPV-independent cervical carcinomas.¹^,⁵^,¹²^,²⁴^,³⁵^,⁵²

	HPV-associated cervical carcinoma	HPV-independent cervical carcinoma
Demographics	Reproductive age	More commonly postmenopausal
Epidemiology	Preventable by HPV vaccination Decreasing incidence	Not preventable by HPV vaccination Increasing relative incidence among cervical cancers
Screening	Higher detection rate Detectable by HPV testing	Lower detection rate Undetectable by HPV screening
Presentation	Earlier stage, particularly with screening	More often later stage
Diagnosis	Well understood histomorphology and clinicopathological features	Morphologically diverse and challenging to diagnose Well-differentiated carcinomas resemble normal structures
Histology	Vast majority squamous cell carcinomas	Adenocarcinomas more common than squamous cell carcinomas Specific entities with specific histomorphology
Outcome	Better disease-specific and overall survival	Shorter disease-specific and overall survival

OPPORTUNITIES FOR TREATMENT

Other than surgery, traditional chemotherapy and radiotherapy, the options for targeted therapy for HPV-associated cervical carcinomas are limited. Approved agents, such as the HER2 antibody-drug conjugate trastuzumab deruxtecan⁶⁴ and PD-1/PD-L1 inhibitors⁶⁵ are indicated for pan solid tumors, thus cannot be considered as specific treatments for HPV-associated cervical carcinomas. However, targeted therapy tailored to specific cancers often exhibits excellent efficacy, as evidenced by tyrosine kinase inhibitors acting on EGFR, ROS1 and ALK mutations in non-small cell lung carcinomas.⁶⁶

Because HPV-independent cervical carcinomas encompass a broad range of subtypes, the pathogenesis and subsequent immunophenotypic and genotypic features of each entity differ and may represent potential targets for personalized treatment. KRAS mutations are defining features of mesonephric adenocarcinoma,³⁹ and are also common in endometrioid carcinomas,⁶⁷ including the targetable KRAS G12C mutation,³⁷ which can be treated with adagrasib or sotorasib.⁶⁸ Inhibitors targeting other KRAS mutations are currently under active investigation and the arsenal against KRAS mutated carcinomas may be expanded in the future.⁶⁹ Another potential targeted therapy is zolbetuximab, a monoclonal antibody against claudin 18.2.⁷⁰ Claudin 18.2 is aberrantly expressed primarily in pancreatic, gastric (including gastroesophageal) and biliary carcinomas,⁷¹^,⁷² thus a specific target for drug action. With their similarity to gastric carcinomas, gastric-type adenocarcinomas of the cervix have also been reported to express claudin 18.2, providing a potential basis for targeted treatment.⁷³

Among HPV-independent cervical carcinomas, clear cell adenocarcinomas have been reported to more frequently exhibit mismatch-repair protein deficiency and high PD-L1 expression, both of which are favorable predictors of response to immune checkpoint inhibitors.⁷⁴ HER2 overexpression and amplification are also reported in gastric-type and clear cell adenocarcinomas at greater rates than in HPV-associated cervical adenocarcinomas, but supporting data are limited to a small number of cases.⁷⁵

PRACTICE RECOMMENDATIONS

The clinical significance of HPV-independent cervical carcinomas is increasing with the relative decrease of HPV-associated cervical carcinomas due to HPV vaccination.
HPV-independent cervical carcinomas encompass a wide range of subtypes, each with individual pathogenesis, clinical associations, and histological and molecular features.
Screening, detection and histological diagnosis of HPV-independent cervical carcinomas are difficult, and patients often present at later stages with worse outcomes.
Specific molecular aberrations and biomarker profiles of certain HPV-independent cervical carcinomas offer promising opportunities for targeted therapy.

CONFLICTS OF INTEREST

The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.

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