Cervical Carcinoma: A Clinical Review
Definition
Cervical carcinoma is a malignancy arising from the epithelial cells of the uterine cervix, specifically within a dynamic and vulnerable region known as the transformation zone. This area represents the junction where the glandular, columnar epithelium of the endocervical canal meets the stratified, squamous epithelium of the ectocervix (3). The constant physiological process of squamous metaplasia in this zone makes its cells uniquely susceptible to the oncogenic effects of human papillomavirus (HPV), establishing it as the primary site for neoplastic change.
The classification of cervical carcinoma is based on the histological cell of origin, leading to distinct subtypes with different clinical behaviours:
Squamous Cell Carcinoma (SCC): This is the most prevalent histological type, accounting for approximately 70-90% of all cervical cancers both globally and within Malaysia (1). Originating from the flat, skin-like squamous cells, these tumours are often exophytic (growing outwards) and are more readily detected by cytology (Pap smears) as they arise on the outer surface of the cervix.
Adenocarcinoma: Accounting for 10-25% of cases, this subtype arises from the mucus-producing glandular cells lining the endocervical canal (1). Adenocarcinomas are often more challenging to detect with traditional Pap smears as they grow within the canal. Their incidence has been reportedly increasing, particularly in younger women, underscoring the importance of screening methods that can effectively evaluate the endocervix, such as HPV testing and thorough colposcopic examination with endocervical sampling (6).
Other Rare Types: A small fraction of cervical cancers includes less common but often aggressive histologies such as adenosquamous carcinoma (containing both malignant squamous and glandular components) and small cell neuroendocrine carcinoma (7).
A crucial evolution in classification is the 2020 WHO system, which now sub-categorizes tumours based on their etiological link to HPV, distinguishing between HPV-associated and HPV-independent cancers (11). This distinction is not merely academic; it carries profound prognostic and therapeutic significance. HPV-associated cancers express viral antigens, making them potential targets for immunotherapies, whereas HPV-independent tumours may follow different molecular pathways and require alternative treatment strategies.
Epidemiology
National Incidence & Mortality
The epidemiological landscape in Malaysia is one of progress shadowed by persistent challenges. Cervical cancer now ranks as the 11th most common cancer among Malaysian women, with an age-standardised incidence rate (ASR) of 6.0 per 100,000 women for the 2017-2021 period (21). This represents a significant public health success, continuing a downward trend from an ASR of 7.6 in 2007-2011, largely attributed to the long-term impact of national screening efforts and the introduction of the HPV immunisation program in 2010 (13).
Despite this falling incidence, mortality remains alarmingly high. This paradox is explained by a deeply concerning counter-trend: an increase in the proportion of cancers detected at an advanced stage. The percentage of cases diagnosed at FIGO Stage III & IV rose from 63.7% in 2012-2016 to 65.1% in 2017-2021 (22). This critical statistic suggests that while primary prevention (vaccination) is successfully reducing the overall number of new cases, the benefits of early detection through screening are not effectively reaching a large segment of the population. These women present only when symptomatic, by which point the disease is often locally advanced and less curable, leading to poor outcomes.
Demographic and Ethnic Disparities
Age Distribution: The incidence of cervical cancer begins to rise after age 35, reaching its peak in women aged between 50 and 65 years. However, the disease has a devastating impact on younger women, ranking as the second most frequent cancer among Malaysian women in the 15 to 44 age bracket, striking during their prime reproductive and productive years (16).
Ethnic Disparities (The "Malaysian Cervical Cancer Paradox"): Malaysia's multi-ethnic population exhibits stark and complex disparities that underscore the impact of non-biological factors on cancer outcomes.
Incidence: Data consistently shows that Malaysian women of Chinese ethnicity have the highest incidence, followed by those of Indian ethnicity, with Malay women having the lowest incidence (26).
Survival: A striking paradox emerges when examining survival. Despite having the lowest risk of developing the disease, Malay women have the poorest 5-year relative survival rate (59.2%), significantly lower than that for Indian (69.5%) and Chinese women (73.8%) (28). This "paradox" strongly suggests that socioeconomic and healthcare system factors—such as health literacy, cultural beliefs influencing screening uptake, financial constraints, and geographical access to specialised treatment centres—are dominant drivers of poor outcomes, leading to delays in diagnosis and incomplete treatment.
Primary Prevention: National HPV Immunisation Programme
Launched in 2010, this ambitious school-based program provides free HPV vaccination to all 13-year-old girls (Form 1 students) (29).
Success: The program was remarkably successful pre-pandemic, consistently achieving high coverage rates of 83-91% (24). The program initially used the quadrivalent vaccine (Gardasil), which protects against the highest-risk HPV types 16 and 18, as well as types 6 and 11 which cause genital warts. The 9-valent vaccine, available privately, offers even broader protection against other locally relevant strains like HPV-52 and HPV-58 (18).
COVID-19 Impact: The pandemic caused a catastrophic disruption, with school closures and resource diversion leading to a plummet in coverage to just 14.3% in 2021. This has created a significant "immunity gap" in an estimated 500,000 to 800,000 adolescent girls (16, 24). This gap will have predictable long-term consequences, likely leading to a future "echo wave" of increased pre-cancerous lesions and a subsequent rise in invasive cancer cases 15 to 25 years from now, threatening to reverse decades of progress.
Etiology
Primary Etiology
A persistent infection with a high-risk Human Papillomavirus (HR-HPV) strain is the necessary cause for over 95% of all cervical cancers (2). It is crucial to understand that HPV infection is extremely common, and most are transient, cleared by a healthy immune system within 1-2 years. Cancer only develops in the small fraction of cases where the virus evades immune clearance and establishes a long-term, persistent infection.
Key Oncogenic Strains: HPV-16 and HPV-18 are the most virulent types, collectively responsible for approximately 70% of all invasive cervical cancers globally and an even higher proportion—88.7%—of cases in Malaysia (16). Local data also highlights the significance of HPV-52 and HPV-58 among Malaysian women (18).
Key Cofactors and Promoters of Carcinogenesis
These risk factors do not cause cancer on their own but significantly increase the probability that an existing HR-HPV infection will persist and progress to malignancy.
Tobacco Smoking: This is a powerful, independent risk factor. Carcinogenic compounds from tobacco smoke, such as nicotine and cotinine, are absorbed into the bloodstream and become concentrated in the cervical mucus. Here, they exert a dual effect: directly damaging the DNA of cervical epithelial cells and suppressing the local immune response, making it more difficult for the body to clear the HPV infection (1).
Sexual and Reproductive History: A higher number of lifetime sexual partners increases the statistical probability of exposure to HPV. Initiating sexual activity at a young age is also a key risk factor, as the adolescent cervix is biologically more vulnerable to infection due to a larger, more exposed transformation zone (1, 2).
Immunosuppression: A competent immune system is critical for clearing HPV.
HIV Infection: This is one of the most significant cofactors. Women living with HIV are approximately six times more likely to develop cervical cancer (17). Immunosuppression dramatically accelerates the carcinogenic process, shortening the time from HPV infection to invasive cancer from a typical 15-20 years to as little as 5-10 years (20). This necessitates more frequent and rigorous screening for this patient group.
Other causes include iatrogenic immunosuppression in organ transplant recipients or from long-term corticosteroid use (33).
Other Factors: Prolonged use of combined oral contraceptives (for more than five years) is associated with a small but significant increase in risk (6). Co-infection with other STIs like Chlamydia can cause chronic inflammation that may facilitate HPV persistence (1). Lower socioeconomic status is a powerful overarching factor linked to many of the above risks as well as reduced access to screening and timely treatment (12).
Pathophysiology
The journey from a normal cervical cell to an invasive carcinoma is a multi-step process driven by the molecular hijacking of the cell's machinery by two viral oncoproteins, E6 and E7, following a persistent HR-HPV infection (3).
Infection and Persistence: HPV gains entry to the basal layer of the transformation zone epithelium. In most cases, the immune system clears the virus. However, in a minority of individuals, the virus evades immune clearance and integrates its genetic material into the host cell's DNA—a pivotal event in carcinogenesis (10).
Action of E6 Oncoprotein: The primary function of the E6 oncoprotein is to find and target the cell's "guardian of the genome," the p53 tumor suppressor protein, for destruction. By eliminating p53, E6 disables the cell's critical safety mechanism for inducing apoptosis (programmed cell death) in response to DNA damage, allowing genetically mutated cells to survive and proliferate (6).
Action of E7 Oncoprotein: The E7 oncoprotein targets and inactivates the retinoblastoma protein (pRB). pRB acts as the primary "emergency brake" on the cell cycle. By inactivating pRB, E7 releases the brake, pushing the cell into a state of uncontrolled and continuous division (6).
Histological Progression: The combined actions of E6 and E7 drive a predictable sequence of changes visible under a microscope:
Low-Grade Squamous Intraepithelial Lesion (LSIL/CIN I): Represents a productive HPV infection with mild dysplasia confined to the lower third of the epithelium. Most of these lesions regress spontaneously without treatment (3).
High-Grade Squamous Intraepithelial Lesion (HSIL/CIN II-III): Represents a true pre-cancerous state with significant cell cycle deregulation. It is characterized by moderate-to-severe dysplasia involving the upper two-thirds or the full thickness of the epithelium. HSIL has a substantial risk of progressing to invasive cancer if left untreated and is the primary target of all cervical screening programs (3).
Invasive Carcinoma: The final step is the breach of the epithelial basement membrane. Once neoplastic cells invade the underlying cervical stroma, they can access lymphatic channels and blood vessels, enabling spread to regional lymph nodes and distant organs (6).
Clinical Presentation
Pre-invasive and Early-Stage Disease
High-yield point: The most crucial clinical feature of pre-invasive lesions (HSIL) and early-stage invasive cervical cancer is that they are typically asymptomatic. The absence of warning signs in the early, most curable phase of the disease is the fundamental rationale behind national screening programs. Symptoms generally do not manifest until the cancer has grown large enough to become invasive, disrupting the normal tissue architecture and blood vessels of the cervix (6).
Cardinal Symptoms of Early Invasive Cancer
Post-coital Bleeding: Bleeding after sexual intercourse is the classic, textbook red flag symptom. The friable, abnormal tissue of the tumor surface bleeds easily on contact. While benign conditions can also cause it, post-coital bleeding must always be considered a sign of malignancy until proven otherwise (2).
Other Abnormal Vaginal Bleeding: This is the most common presenting complaint and can manifest as intermenstrual bleeding, post-menopausal bleeding (which is always abnormal), or menorrhagia (periods that become significantly heavier or longer) (1).
Abnormal Vaginal Discharge: A persistent and unusual vaginal discharge is another common symptom. As the tumor grows and outstrips its blood supply, central necrosis can occur, leading to a characteristically foul-smelling (malodorous), often blood-tinged, discharge (1).
Pelvic Pain or Dyspareunia: As the tumor enlarges, it can cause a dull ache in the pelvic region or pain during deep sexual intercourse (1).
⚠️ Red Flag Signs & Symptoms of Advanced Disease
These signs indicate the cancer has progressed beyond the cervix to invade adjacent structures or spread to distant sites. They are signs of advanced disease and carry a poorer prognosis.
Urinary Tract Involvement:
Loin or Flank Pain: This is a highly significant red flag, often indicating that lateral tumor extension has compressed a ureter, leading to obstruction and hydronephrosis (swelling of the kidney). This finding automatically upstages the disease to at least FIGO Stage IIIB and mandates urgent intervention to preserve kidney function (2).
Other symptoms include urinary frequency, dysuria, or hematuria. In very advanced cases, a vesicovaginal fistula can form, resulting in the continuous, devastating leakage of urine from the vagina.
Bowel Involvement:
Posterior invasion into the rectum can cause pain on defecation, tenesmus, and rectal bleeding. A rectovaginal fistula, leading to the passage of feces from the vagina, is a catastrophic sign of late-stage disease (34).
Pelvic Sidewall and Lymphatic Involvement:
Severe Pelvic/Back Pain Radiating Down the Leg (Sciatica): This suggests tumor involvement of the pelvic sidewall and compression of the lumbosacral nerve plexus (2).
Unilateral or Bilateral Leg Swelling (Lymphedema): Results from the blockage of pelvic lymphatic channels and veins by the tumor, obstructing lymphatic drainage (2).
Constitutional Symptoms: Unexplained weight loss, loss of appetite (anorexia), and profound fatigue suggest the cancer has spread to distant organs like the liver, lungs, or bone (2).
Investigations
Screening (Malaysian National Programme)
The primary goal of screening is not to find cancer, but to detect and treat high-grade pre-cancerous lesions (HSIL) before they can progress. The 2023 Malaysian Ministry of Health guidelines reflect a global shift towards primary HPV DNA testing (13).
Target Population: Women aged 30 to 65. For younger women (25-29), cytology remains the method of choice.
Screening Methods:
HPV DNA Testing (Preferred): This molecular test is more sensitive than cytology for detecting HSIL. A key strategy being adopted in Malaysia is self-sampling, where a woman can collect her own vaginal sample. This has been shown to improve screening uptake by overcoming cultural, personal, or logistical barriers to a clinician-performed examination (13). If the HPV test is negative, the recommended screening interval is 5-10 years (15).
Cervical Cytology (Pap Smear): This method examines cells for morphological abnormalities. It remains a vital tool, especially where HPV testing is unavailable. The standard interval is every 3 years, following two consecutive negative annual tests (12).
Diagnostic Workup
This is performed after an abnormal screening result or if a clinician observes a suspicious lesion on the cervix.
Colposcopy: A magnified visual examination of the cervix. The application of acetic acid causes abnormal areas with high nuclear density to turn white (acetowhite lesions), and Lugol's iodine highlights glycogen-depleted abnormal areas, allowing the clinician to identify suspicious regions for biopsy (12).
Directed Biopsy: This is the gold standard for diagnosis. A small piece of tissue is taken from the most abnormal-appearing area identified during colposcopy and sent for histological analysis (12).
Endocervical Curettage (ECC): This procedure scrapes cells from the endocervical canal. It is essential when the entire transformation zone is not visible (an "unsatisfactory colposcopy") or when adenocarcinoma is suspected, as this cancer type originates within the canal (12).
Staging Investigations
Once invasive cancer is confirmed, staging is crucial to determine the extent of the disease and guide management.
FIGO Staging System: Malaysia uses the FIGO clinical staging system. It is critical to understand that this is a clinical system, based on findings from physical examination (often an Examination Under Anesthesia, or EUA), colposcopy, and a specific set of allowed basic investigations. The FIGO stage is NOT changed by findings on advanced imaging like MRI or PET scans (12). This allows for consistent staging worldwide, even in resource-limited settings.
Imaging for Treatment Planning: While imaging does not alter the official FIGO stage, it is indispensable for detailed treatment planning.
MRI Pelvis: Superior to CT for evaluating the local extent of the primary tumor, including its size, depth of stromal invasion, and invasion into the parametrium, bladder, or rectum (12).
CT Chest/Abdomen/Pelvis: The workhorse for assessing lymph node involvement outside the pelvis and screening for distant metastases to organs like the liver and lungs (40).
PET/CT Scan: This is the most sensitive imaging modality for detecting lymph node metastases (both pelvic and para-aortic) and distant disease. It is particularly valuable in planning radiotherapy for locally advanced cases to ensure all affected areas are included in the treatment field (41).
Management
The optimal management of cervical cancer requires a collaborative, Multidisciplinary Team (MDT) approach. All cases must be discussed in an MDT meeting comprising a Gynaecological Oncologist, a Clinical/Radiation Oncologist, a Radiologist, and a Pathologist to formulate a consensus treatment plan (40).
Definitive Therapy
Early-Stage Disease (Stage IA - IIA1)
For early-stage disease confined to the cervix, surgery is the primary treatment. It offers survival outcomes equivalent to radiotherapy but has the significant advantages of preserving ovarian function in young women and avoiding the long-term effects of radiation on vaginal tissue (40).
Fertility-Sparing Surgery (for selected young patients):
Stage IA1: A cervical conisation (cone biopsy) that achieves clear surgical margins is considered adequate curative treatment.
Stage IA2 & small IB1: A radical trachelectomy is the procedure of choice. This complex surgery removes the cervix, upper vagina, and surrounding parametrial tissue, while preserving the uterine body, which is then reattached to the vagina. It is always combined with a pelvic lymph node dissection (PLND) (40).
Non-Fertility-Sparing Surgery (Standard of Care):
Stage IA1: A simple or extrafascial hysterectomy is sufficient.
Stage IA2, IB1, IIA1: The standard operation is a radical hysterectomy (Wertheim's hysterectomy), which involves a more extensive removal of the uterus, cervix, upper vagina, and parametrial tissues, combined with a bilateral PLND (40).
Adjuvant Therapy: If the post-operative pathology report reveals high-risk features (positive lymph nodes, positive surgical margins, or parametrial invasion), post-operative concurrent chemoradiotherapy (CCRT) is required to reduce the risk of recurrence (40).
Locally Advanced Disease (Stage IB2/IIA2 - IVA)
For women with larger tumours or disease that has spread beyond the cervix, surgery is generally not the primary treatment.
Standard of Care: Concurrent Chemoradiotherapy (CCRT): The definitive standard of care is a combination of radiation and chemotherapy given together. This approach is superior to radiation alone, significantly improving both local control and overall survival (40).
Radiotherapy: This is delivered in two phases: External Beam Radiotherapy (EBRT) to the entire pelvis to treat the primary tumour and at-risk lymph nodes, followed by a brachytherapy boost. Brachytherapy involves temporarily placing a radioactive source directly into the cervix, delivering a very high, targeted dose of radiation to the tumour's epicentre while minimizing dose to the bladder and rectum. The brachytherapy boost is an essential, non-negotiable component of curative treatment.
Chemotherapy: The chemotherapy acts as a radiosensitizer, making cancer cells more vulnerable to radiation. The worldwide standard is weekly Cisplatin (40 mg/m²) administered concurrently with EBRT.
The entire course of treatment should be completed within 8 weeks to maximize biological effectiveness (40).
Emerging Paradigms:
Neoadjuvant Chemotherapy (INTERLACE Trial): This trial showed that giving 6 weeks of induction chemotherapy (Carboplatin/Paclitaxel) before standard CCRT resulted in a significant improvement in 5-year survival for high-risk cases, likely by treating distant micrometastases early (44).
Adjuvant Immunotherapy (KEYNOTE-A18 Trial): This trial demonstrated that adding the immune checkpoint inhibitor Pembrolizumab to the standard CCRT regimen also improved survival, likely by enhancing the anti-tumour immune response triggered by radiation (46).
Management of Recurrent & Metastatic Disease
When cancer recurs or is diagnosed at Stage IVB, the intent shifts from curative to palliative. The goals are to prolong survival, manage symptoms, and maintain quality of life.
First-Line Systemic Therapy: The choice of regimen depends on tumour characteristics, specifically PD-L1 expression.
For patients with PD-L1 positive tumours, the current standard is a combination of Pembrolizumab (immunotherapy) + Chemotherapy (Cisplatin/Paclitaxel) +/- Bevacizumab (an anti-angiogenic agent that inhibits tumour blood vessel growth) (41).
Palliative Radiotherapy: Radiation plays a vital role in palliating symptoms. It is highly effective for controlling problematic vaginal bleeding, relieving severe pelvic pain from local recurrence, and treating painful bone metastases.
Supportive & Symptomatic Care
This is a critical, parallel component of management, focusing on preventing and relieving suffering.
Pain Management: Follow the WHO analgesic ladder. Neuropathic pain from nerve involvement is common and often requires adjuvant agents like gabapentin or amitriptyline in addition to opioids.
Malignant Fistulae (Vesicovaginal/Rectovaginal): These are among the most distressing complications. Management is complex and may require surgical diversion (e.g., colostomy, ureteric stents, or percutaneous nephrostomy tubes) to redirect waste and medical management with anti-secretory drugs like octreotide (40).
Ureteric Obstruction: Urgent relief with ureteric stents or percutaneous nephrostomy (PN) tubes is necessary to prevent irreversible renal failure (40).
Vaginal Bleeding/Discharge: Palliative radiotherapy is highly effective for bleeding. For the foul odour associated with necrotic tumours, topical application of metronidazole gel can be very helpful (40).
When to Escalate
A house officer must call for senior help (MO/Specialist) for any of the following clear, actionable triggers:
Any new neurological signs (e.g., confusion, new-onset weakness, seizure), which could indicate brain metastases.
Signs of ureteric obstruction (e.g., new-onset loin pain, rising creatinine, anuria, or new hydronephrosis on imaging).
Uncontrolled vaginal bleeding (e.g., soaking more than one pad per hour) or hemodynamic instability.
Severe, uncontrolled pain not responding to initial analgesia.
Signs of sepsis (fever, tachycardia, hypotension) in a patient who may be neutropenic from chemotherapy.
Any sudden, unexplained deterioration in clinical status.
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