Clinical overview
Cancer complicates roughly one in a thousand pregnancies, and the question the exam wants you to answer is bidirectional: what does pregnancy do to the neoplasm, and what does the neoplasm — and its treatment — do to the pregnancy. In South Africa this is not an academic curiosity. We are a young, high-fertility population superimposed on the world's largest HIV epidemic, and the commonest cancer diagnosed during pregnancy here is cervical cancer, precisely because HPV-driven disease is accelerated by immunosuppression and our screening coverage remains below the WHO 90-70-90 targets. Breast cancer, thyroid cancer, melanoma, lymphoma/leukaemia and ovarian neoplasms make up most of the remainder. A registrar will meet the abnormal smear in the antenatal clinic, the adnexal mass on the dating scan, and the persistently raised βhCG after a "miscarriage" that turns out to be a molar pregnancy.
The central teaching point is that pregnancy is rarely the cause of a worse cancer outcome — stage-for-stage, prognosis is usually equivalent to the non-pregnant patient — but it powerfully modifies detection, investigation and treatment. Physiological breast and pelvic changes mask early signs and delay diagnosis; ionising radiation and many cytotoxics threaten the fetus, especially in the first trimester; and the emotional and ethical weight of balancing two lives demands genuine multidisciplinary, patient-centred decision-making. The skill being tested is the ability to hold maternal oncological benefit and fetal safety in the same frame and arrive at a defensible plan.
Core knowledge
How pregnancy might influence tumour biology
Figure D15.1 — How pregnancy affects neoplasia: hormone-sensitive growth, immune tolerance, vascular/lymphatic boost, diagnostic masking, and placental/fetal metastasis (melanoma).
Several physiological features of pregnancy are theoretically pro-neoplastic, and you should be able to reason through them rather than memorise a verdict.
- Hormonal milieu. Oestrogen, progesterone and prolactin rise enormously. For hormone-receptor-positive tumours (a subset of breast cancer, low-grade endometrial-type lesions, some ovarian sex-cord tumours) this is a plausible growth stimulus, though pregnancy-associated breast cancers are more often receptor-negative and high-grade — partly a biological feature of younger women rather than a hormonal effect.
- Immune modulation. Pregnancy induces a tolerogenic state (shift toward regulatory T cells, altered Th1/Th2 balance) that protects the semi-allograft fetus but may also blunt anti-tumour surveillance. This matters most for immunogenic and virally-driven tumours.
- Angiogenesis and vascular permeability. Pregnancy is a pro-angiogenic, hyperdynamic state (rising VEGF, increased plasma volume and cardiac output), which could theoretically support tumour growth and dissemination.
- Mechanical and lymphatic changes. Increased pelvic and breast vascularity and lymphatic flow are invoked to explain occasional rapid progression, but the evidence that pregnancy genuinely accelerates metastasis is weak for most tumours.
Against this, large series and the ESGO/ESTRO/ESP cervical guideline (Update 2023) — which contains a dedicated cancer-in-pregnancy section — conclude that stage-matched survival is not demonstrably worse for cervical cancer diagnosed in pregnancy. The dominant clinically observable effect is delayed diagnosis, not accelerated biology.
Cervical neoplasia — the SA-relevant centrepiece
Figure D15.2 — Pregnancy-associated cancers and the cervical-cancer-in-pregnancy pathway (ESGO/ESTRO/ESP 2023): individualised by stage, gestational age and the woman's wishes.
Pregnancy is, for many women, their only sustained contact with the health system, making the antenatal visit a screening opportunity that the SASOG/BetterGyn 2024 guideline and NDoH cervical screening policy explicitly endorse. Use WHO 2020 / LAST terminology: LSIL (≈ CIN 1) and HSIL (≈ CIN 2–3), HPV-associated.
Key biological facts:
- HSIL does not progress to invasion during the pregnancy interval. Cytological "regression" postpartum is well described and partly reflects sampling and the transformation-zone eversion of pregnancy rather than true cure.
- Decidualisation of the cervical stroma can mimic dysplasia or invasion both cytologically and colposcopically — a classic pitfall. The transformation zone is everted and more accessible, which aids colposcopy but increases bleeding.
- HIV (high local prevalence) drives both higher HPV-HSIL incidence and faster progression; HIV-positive pregnant women warrant a low threshold to evaluate. The HIV-positive screening rule — screen at diagnosis and approximately 3-yearly regardless of age — is unchanged by pregnancy.