Almost all cervical cancers begin at the same site: the transformation zone of the cervix. And almost all share the same starting point: a high-risk HPV infection. But between this very common infection and a cancer, there are years, several stages, and as many opportunities to intervene.
Positive HPV test, abnormal smear, lesion identified on colposcopy: Dr Zeitoun reviews your results, places you in this pathway, and proposes, where needed, a conisation or oncological management at the Clinique Hartmann in Neuilly.
An abnormal screening result does not mean cancer; it prompts further investigation to clarify the situation before monitoring or treating.
Cervical cancer has a rare particularity: its origin is almost always known. In more than 99% of cases, it originates from a human papillomavirus (HPV) infection. But this infection is very common — most of us are exposed — and in the vast majority of cases, it leaves no trace.
What distinguishes high-risk infections is not simply the type of HPV (high-risk: predominantly types 16 and 18), but how the infection evolves: persistent, if the virus remains in the cells too long, or transforming, if the viral genome integrates into the cell's genetic material and initiates a process of malignant transformation.
And all of this begins at the same site: the transformation zone of the cervix. Over 95% of lesions and cancers originate there. Understanding this pathway — from infection to diagnosis — is understanding why the HPV test, screening and HPV vaccination genuinely protect, each at a different stage of the same process. This article follows the recommendations of the HAS and the INCa, and is part of the cervical cancer pathway.
Before discussing infection, we need to focus on the precise anatomical site where problems begin. The transformation zone is not an anatomical detail: it is the near-exclusive origin of cervical cancer.
The cervix is covered by two types of epithelium: a squamous epithelium (flat cells forming the visible part of the cervix) and a glandular epithelium (columnar cells lining the endocervical canal). Their meeting point is called the squamocolumnar junction, or transformation zone.
This zone is in permanent remodelling throughout life (particularly under hormonal influence). Its maturing cells are particularly vulnerable to the papillomavirus: this is where HPV takes hold, where lesions begin, and where 95% of cervical cancers arise.
What this means in practice: conisation targets this zone precisely. By removing the transformation zone in its entirety, it excises the lesion at its source — which is why it is so effective in treating high-grade 'so-called precancerous lesions' and carcinoma in situ.
HPV is ubiquitous. But between an infection that clears and one that leads to cancer, there is a considerable distance — and two distinct mechanisms to understand.
| Type of infection | What happens |
|---|---|
| Cleared | Most common scenario: the immune system eliminates the virus within 1 to 2 years — no consequences |
| Persistent | High-risk HPV remains detectable beyond 12 to 24 months: the HPV test stays positive, cells are disturbed but not yet transformed |
| Transforming | The viral genome integrates into the cell's chromosomes, dysregulating tumour suppressor genes: the cell begins to transform |
Among the approximately 14 high-risk HPV genotypes, types 16 and 18 account for around 70% of cervical cancers. They persist more readily, integrate their genome into cells more efficiently, and produce proteins (E6 and E7) that are particularly potent at neutralising the cell's natural protective mechanisms. This is why a positive HPV test for type 16 or 18 leads to closer surveillance.
Reduces local defences and promotes both HPV persistence and its progression towards a transforming infection.
A compromised immune system (immunosuppression, certain conditions) makes viral elimination more difficult and accelerates the evolution towards lesions.
Without regular screening, a persistent infection and its lesions progress undetected and untreated.
The key takeaway: having a high-risk HPV infection is not having cancer — nor a near-certainty of developing one. What distinguishes a benign infection from a dangerous one is persistence, then transformation. HPV vaccination acts precisely here: by preventing infection with types 16 and 18, it eliminates the starting point.
When the infection becomes transforming at the transformation zone, cells begin to display abnormalities. These abnormalities are described by several terms — dysplasia, CIN, intraepithelial lesions — all describing the same process: a progressive modification of cells, detectable and treatable — and precisely what an abnormal smear or a persistent positive HPV test reveals.
These terms all describe cellular abnormalities at the transformation zone caused by HPV. CIN 1, 2, 3 (cervical intraepithelial neoplasia) and LSIL/HSIL (low- and high-grade squamous intraepithelial lesions) are different readings of the same spectrum. We speak of 'so-called precancerous' lesions because their progression is never certain.
Low-grade lesions (CIN 1 / LSIL) regress spontaneously in the majority of cases, as the immune system eliminates the virus. They generally warrant surveillance by smear and HPV test, without immediate treatment, rather than immediate conisation.
High-grade lesions (CIN 2–3 / HSIL) carry a significant risk of progressing to carcinoma in situ then invasive cancer without treatment. They most often warrant conisation: removal of the abnormal transformation zone, which preserves the uterus and fertility. The decision accounts for age and reproductive wishes.
The progression from a transforming infection to high-grade lesions and then cancer takes several years. This slow timeline leaves ample time to act: this is the very principle of screening. An abnormal smear identifies precisely these intermediate stages.
The link with conisation: conisation removes precisely the transformation zone — the focus of these abnormalities. Fully analysed by the pathology laboratory, the surgical specimen confirms the grade, checks the margins and detects any potential micro-invasion. It is simultaneously a treatment and a definitive diagnosis.
CIN 2, CIN 3 or high-grade lesion confirmed on colposcopy: Dr Zeitoun reviews your results, explains the indication for conisation and how it is performed, and schedules the procedure at the Clinique Hartmann in Neuilly if required.
If high-grade 'so-called precancerous lesions' are neither detected nor treated, the disease progresses through two successive thresholds. These two stages do not carry the same prognosis nor the same treatment options.
Carcinoma in situ (= advanced CIN 3 / intraepithelial carcinoma) is the stage at which the full thickness of the epithelium of the transformation zone is invaded by abnormal cells — yet the basement membrane remains intact. The cells are malignant, the lesion does not invade the underlying tissues. This is the last stage before invasion.
This stage is still treatable by conisation in most cases, provided the margins are clear and there is no focus of micro-invasion in the surgical specimen. This is why meticulous pathological analysis of every conisation is essential.
Invasive cancer is defined by the breach of the basement membrane: abnormal cells invade the underlying tissues. At a very early stage (micro-invasion), treatment remains conservative in certain cases. Beyond this, management requires more extensive surgery, radiotherapy or their combination, decided through a multidisciplinary team (MDT) meeting.
Two main types exist according to the originating epithelium at the transformation zone: squamous cell carcinoma (80% of cases, arising from the squamous epithelium) and adenocarcinoma (arising from the glandular epithelium, harder to detect by smear alone).
The complete pathway: HPV 16/18 → infection of the transformation zone → persistence → transformation → 'so-called precancerous lesions' (CIN 1 → CIN 2–3) → carcinoma in situ → invasive cancer. Every step takes time. And at every stage — through to carcinoma in situ — conisation can interrupt this pathway. For the management of established invasive cancer, see the cervical cancer page.
Screening targets women with no symptoms. Its goal is not to find cancer, but to detect persistent infections and 'so-called precancerous lesions' — in other words, to intervene before the process crosses the threshold into cancer.
| Age | Recommended test (HAS, INCa) |
|---|---|
| 25 to 29 years | Cervical smear (cytology) |
| From 30 years | HPV test as first-line (high-risk virus detection) |
Detects directly the presence of high-risk virus (including types 16 and 18). More sensitive than the smear, it identifies persistent infection before cells become abnormal. A positive result for HPV 16 or 18 generally leads directly to colposcopy.
Examines the appearance of cells from the transformation zone under the microscope. It can detect changes suggestive of a lesion, but is less sensitive than the HPV test for detecting early infection. See the article on abnormal smear to understand the results.
Upstream of screening: vaccination. HPV vaccination (covering genotypes 16 and 18) acts well before screening, by preventing infection from taking hold. It is the only means of acting at the very first step of the process. Vaccination and screening are not mutually exclusive: their combination is the most effective strategy.
An abnormal screening result opens an investigation — it does not establish a diagnosis. The next step is designed to clarify the exact nature of the lesion at the transformation zone: is this a persistent infection without a lesion, a low- or high-grade 'so-called precancerous lesion', a carcinoma in situ, or an invasive cancer?
Examination of the cervix under a magnifying instrument, with application of stains (acetic acid, Lugol's iodine) that highlight abnormal areas — particularly at the transformation zone. Painless, quick, essential for targeting biopsies.
Taken during colposcopy, from the suspicious areas identified. The specimen is analysed by the pathology laboratory, which establishes the grade of the lesion (CIN 1, 2, 3, carcinoma in situ or invasive) and guides the decision: surveillance or conisation.
Low-grade lesions → close surveillance. High-grade lesions and carcinoma in situ → conisation. Invasive cancers → management through multidisciplinary team meeting (surgery, radiotherapy, or both).
'So-called precancerous lesions' and early-stage cancers most often produce no symptoms — which is why regular screening is indispensable. When a cancer has developed and progressed, certain signs may appear.
Signs that require prompt medical attention: intermenstrual bleeding, post-coital bleeding (a frequent and suggestive sign), unusual vaginal discharge (discoloured or malodorous), and at a more advanced stage, significant pelvic pain, sometimes radiating to the lower limbs. These signs do not necessarily indicate cancer — they are more often due to a benign cause — but they always warrant prompt medical assessment. After the menopause, any bleeding warrants investigation: see postmenopausal bleeding.
Depending on the stage of the process at which you present, the response differs. Dr Zeitoun intervenes whenever a surgical decision is required.
Positive HPV test (types 16 or 18 or other), abnormal smear, colposcopy or biopsy report: Dr Zeitoun reviews all your results and places you precisely in this pathway — persistent infection, low- or high-grade 'so-called precancerous lesion', carcinoma in situ, invasive cancer — before proposing the next step.
For high-grade 'so-called precancerous lesions' (CIN 2–3) and carcinoma in situ, Dr Zeitoun performs conisation: en-bloc removal of the transformation zone, organ-preserving (the uterus is kept), followed by close surveillance with co-testing. Pathological analysis of the specimen confirms the margins and excludes micro-invasion.
When an invasive cancer is confirmed, the strategy is defined through a multidisciplinary team (MDT) meeting with oncologists and radiotherapists. Dr Zeitoun coordinates surgical management according to the stage and the patient's situation.
Consultations at the 8th arrondissement practice (241 rue du Faubourg Saint-Honoré), procedures at Clinique Hartmann, Neuilly-sur-Seine. Secteur 2 non-OPTAM: fees above the national schedule, set out in a written estimate provided before any procedure.
No — and this is essential to understand. The vast majority of HPV infections clear spontaneously within one to two years. Only a minority, when a high-risk HPV (particularly types 16 and 18) persists and becomes transforming, can lead to 'so-called precancerous lesions' and, eventually, cancer. Having a positive HPV test is therefore neither having cancer, nor a near-certainty of developing one.
A persistent infection is one in which HPV remains detectable beyond 12 to 24 months without being eliminated — the HPV test stays positive. A transforming infection goes further: the viral genome integrates into cell chromosomes and dysregulates essential genes (notably tumour suppressors), initiating the progressive modification of cells at the transformation zone. Persistence is necessary, but it is transformation that truly drives the process towards 'so-called precancerous lesions'.
Among high-risk HPV types, genotypes 16 and 18 are responsible for approximately 70% of cervical cancers. They persist more readily, integrate their genome into cells more efficiently, and produce proteins that neutralise the cell's natural protective mechanisms. A positive HPV test for types 16 or 18 leads to surveillance — or even direct colposcopy — more rapidly than a positive test for other high-risk genotypes.
The transformation zone (squamocolumnar junction) is the area of the cervix where squamous epithelium (the surface of the cervix) meets glandular epithelium (the endocervical canal). Its cells, in permanent remodelling, are particularly vulnerable to HPV. This is where 95% of cervical lesions and cancers arise — and it is precisely this zone that conisation removes in its entirety when treating high-grade lesions.
These are cellular abnormalities at the transformation zone caused by a transforming HPV infection. They are also described as CIN 1, 2 or 3, or as LSIL (low grade) and HSIL (high grade). They are not cancer, but some can become so without treatment. Low-grade lesions (CIN 1) often regress spontaneously. High-grade lesions (CIN 2–3) most often require conisation. The term 'so-called precancerous' reflects that progression is never certain.
Carcinoma in situ (advanced CIN 3 / intraepithelial carcinoma) is the stage at which the full thickness of the epithelium of the transformation zone is invaded by malignant cells — but without breach of the basement membrane. The cells are malignant, but the lesion remains confined to the surface of the cervix, without invasion of the underlying tissues. This is the last stage before invasive cancer, and is still treated by conisation in most cases, provided the margins are clear.
The process is generally very slow: it most often takes ten to fifteen years, sometimes longer, between a persistent HPV infection and a potential invasive cancer. It is this slow progression that makes screening effective — it leaves ample time to detect and treat 'so-called precancerous lesions' and carcinoma in situ well before the stage of invasion.
Yes. High-grade lesions (CIN 2–3) and carcinoma in situ are most often treated by conisation: en-bloc removal of the abnormal transformation zone, by loop diathermy or laser, as a day procedure. The uterus is preserved, as is fertility in the vast majority of cases. Close surveillance (co-testing at 6 months) is organised after the procedure.
'So-called precancerous lesions' and early-stage cancers are most often asymptomatic — which is why screening is indispensable. When a cancer has developed, possible signs include: intermenstrual bleeding, post-coital bleeding, unusual vaginal discharge, and at a more advanced stage, significant pelvic pain, sometimes radiating to the lower limbs. These signs should prompt prompt medical assessment, without necessarily indicating cancer.
Yes. HPV vaccination (see our dedicated article on vaccination) protects against genotypes 16 and 18, responsible for approximately 70% of cervical cancers, by preventing infection from taking hold at the transformation zone. Acting at the very first link in the process — before infection — it eliminates the starting point. It does not replace screening but complements it: together, both strategies target the elimination of cervical cancer.
Dr Zeitoun is a gynaecological oncology surgeon: he treats high-grade 'so-called precancerous lesions' and carcinoma in situ by conisation, and manages invasive cervical cancer surgery through a multidisciplinary team (MDT) meeting. He consults at his 8th arrondissement practice in Paris and operates at the Clinique Hartmann in Neuilly-sur-Seine. He charges fees above the national schedule (secteur 2 non-OPTAM), set out in a written estimate provided before any procedure.
To go deeper into each stage of this pathway — from the virus to surgery.
The reference page: staging, surgery and management of established invasive cervical cancer, from diagnosis.
TreatmentThe procedure that removes the abnormal transformation zone: indications, technique, fertility, aftercare and follow-up.
Screening resultWhat a positive HPV test means, what to do next, and why it is not a cancer diagnosis.
Screening resultUnderstanding a smear report: ASC-US, LSIL, HSIL, and the examinations that follow.
PreventionThe vaccine against HPV 16 and 18: who, when, and why it acts at the very first link in the process.
The virusHow the papillomavirus is transmitted, why it is so common, and what this means in practice.
Positive HPV 16/18 test, high-grade 'so-called precancerous lesion', carcinoma in situ or invasive cervical cancer: Dr Jérémie Zeitoun consults at his 8th arrondissement practice in Paris and operates at the Clinique Hartmann in Neuilly-sur-Seine. Please bring your colposcopy and biopsy reports.
This article is for information only and does not replace a medical consultation; screening and follow-up are coordinated with your gynaecologist, GP or midwife.
