Evaluate and devise a management plan for a patient presenting with malignancy in pregnancy

In one line

Cancer in pregnancy is a multidisciplinary problem in which — for almost every tumour type — the mother receives stage-appropriate treatment without delay, using surgery and second/third-trimester chemotherapy to preserve the pregnancy where possible, and iatrogenic prematurity (not chemotherapy) is the dominant threat to the neonate.

This chapter assumes the diagnostic groundwork already taught at Intermediate — what an adnexal mass work-up is, how a breast lump is triaged, the basics of FIGO staging, and the SA cervical screening pathway — and spends its words on the consultant layer: how the tumour subtype and gestation together rewrite the plan, where the guidelines disagree, the named regimens and their exact differences, and the SA referral reality. The first-principles "is this malignant?" reasoning lives in the Intermediate oncology chapters and in cervical-premalignancy-colposcopy.

Assessment

The diagnostic task is to overcome the physiological camouflage that delays cancer diagnosis in pregnancy (breast nodularity, anaemia, fatigue, fundal-height "masses") and then to stage accurately while protecting the fetus. Pregnancy-associated cancer occurs in roughly 1 in 1000 pregnancies (FIGO cites 17–27 per 100 000); breast, haematological (lymphoma/leukaemia), melanoma and cervical cancers dominate. Incidence is rising with later childbearing and with incidental findings from cell-free DNA aneuploidy screening — an aberrant cfDNA result with multiple chromosomal imbalances should prompt maternal whole-body MRI, not reassurance.

• Tissue first. Biopsy is safe in pregnancy; never defer histological diagnosis. A breast lump still needs core biopsy, and a persistent or suspicious adnexal mass needs the standard work-up — that groundwork is assumed here, and the screening pathway that should have caught cervical disease earlier sits in SA cervical screening.
• Imaging — radiation is rarely the problem. Below ~50–100 mGy there is no measurable deterministic fetal harm. A chest radiograph delivers 0.001–0.01 mGy; CT abdomen/pelvis and whole-body PET/CT each deliver roughly 10–50 mGy (childhood-cancer risk 1 in 1000 to 1 in 200). MRI without gadolinium is the workhorse for staging — gadolinium crosses the placenta and is linked to rheumatological disease and neonatal death, so it is avoided. Use abdominal shielding and the lowest dose for any X-ray.
• Sentinel node mapping uses technetium-99m (cumulative pregnancy dose stays below 5 mGy); blue dyes are avoided (anaphylaxis) and indocyanine green is acceptable.
• Tumour markers mislead. CA-125, AFP, β-hCG, inhibin and LDH all shift in normal pregnancy — interpret only as trends, never as single-point staging tools.
• HIV. In the SA context every patient is offered/confirmed HIV testing; immunosuppression worsens cervical disease and complicates chemotherapy tolerance (see cervical-premalignancy-colposcopy). Apply SA HIV Consolidated Guidelines including PVT for the neonate.

The advanced assessment

Beyond "biopsy, stage, MDT", the work is reading three variables together — tumour biology, stage, and gestation — because each combination produces a different plan, and then handling the subtle presentations and the staging traps.

Gestation is the master variable, and it interacts with everything. The same diagnosis demands a different plan at 8, 18 and 32 weeks because gestation simultaneously fixes (a) whether termination is even on the table, (b) whether chemotherapy is permissible now or must wait for organogenesis to finish, (c) whether the surgical window is open (the second trimester is the operative sweet spot), and (d) how many weeks of fetal maturity can be bought before a delivery that is, in almost every case, the real treatment-limiting step. "Treat stage-appropriately" means nothing until every decision is anchored to the precise gestation.

Severity stratification is about urgency, not just stage. Stratify the presenting problem into three tiers because the tiers drive tempo:

• Oncological emergency (leukaemic blast crisis, spinal cord compression, superior vena cava obstruction from bulky mediastinal lymphoma, airway-threatening thyroid or head-and-neck disease): treat now, on the disease's own merits — pregnancy does not buy you time and rarely changes the immediate intervention. A first-trimester acute leukaemia is the sharpest version: the maternal disease is lethal in weeks untreated, induction chemotherapy in the first trimester is genuinely teratogenic, and the honest counselling is that continuing the pregnancy and deferring induction is not safe for the mother — most experts induce promptly and counsel on the fetal risk, or offer termination.
• Aggressive but not emergent (most invasive breast cancer, high-grade lymphoma, epithelial ovarian cancer): treat without delay but with time to convene the MDT, complete staging and time chemotherapy past organogenesis.
• Indolent / surveillable (microinvasive cervical disease, low-grade or early-stage tumours, some borderline ovarian tumours): the legitimate option to watch and bridge to fetal maturity exists, and choosing it is a defensible consultant judgement — but only with a documented surveillance plan and informed maternal consent.

Subtle and atypical presentations the camouflage hides. Pregnancy-associated breast cancer is more often diagnosed at a higher stage and is more frequently triple-negative or HER2-positive — the "nodularity is normal" reflex delays it, and a discrete, dominant or enlarging mass in a lactating or pregnant breast is cancer until a core biopsy says otherwise; never settle for fine-needle aspiration cytology here, because the proliferative gestational background degrades cytological interpretation. Cervical cancer presenting as antepartum bleeding is mislabelled as a placental or "show" bleed; a speculum-and-cervix examination is mandatory for unexplained bleeding, and a friable or bulky cervix is biopsied, not just cytologically screened. An adnexal mass found on the dating scan that persists beyond ~16 weeks, is >5–6 cm, solid or with the standard malignant ultrasound morphology, is not a corpus-luteum cyst and needs IOTA/O-RADS characterisation and a surgical plan.

Where the staging tools mislead in pregnancy:

• Tumour markers are the classic trap. CA-125 peaks physiologically in the first trimester and at delivery; AFP rises throughout; β-hCG and inhibin are gestational hormones; LDH rises with haemolysis and the placenta. A single elevated value cannot stage, and a "rising" marker may simply be a maturing pregnancy. Use them only as within-patient trends after a baseline, and never to decide between continuation and termination.
• Lymph-node assessment loses fidelity as the uterus grows. Surgical pelvic lymphadenectomy in cervical cancer is feasible only up to roughly 20–22 weeks, beyond which uterine volume collapses the nodal yield and the operation becomes hazardous. PET/CT (high background uptake, fetal dose) and the gravid uterus both degrade radiological nodal staging. This is why the cervical-cancer plan hinges on gestation at diagnosis.
• Restaging imaging is constrained. Gadolinium and high-dose CT/PET are limited, so the staging you can obtain antenatally is often less complete than you would accept outside pregnancy — and the consultant judgement is to act on the best feasible staging rather than to delay treatment chasing a perfect one.

Management

Decisions run immediate → ongoing → long-term and are owned by a tumour board (oncology, gynae-oncology, MFM, neonatology, radiology, pathology, anaesthesia, psychology) — convening this MDT is the first step.

Immediate

• Confirm gestation precisely (drives every threshold) and establish maternal wishes regarding continuation versus termination — a permitted choice under the SA Choice on Termination of Pregnancy Act and central where treatment cannot proceed alongside pregnancy.
• Stabilise oncological emergencies (cord compression, SVC obstruction, leukaemic crisis) on their own merits — pregnancy does not change that calculus.

Ongoing (the operative core)

• Surgery is safe in any trimester; the second trimester is optimal for major abdominal/pelvic surgery.
• Chemotherapy is deferred past organogenesis — never in the first trimester (malformation risk ~14% single-agent, up to 25% combination), but after ~14 weeks the major-malformation rate falls to roughly background (~1.3%). Standard regimens (anthracyclines, cyclophosphamide, carboplatin + paclitaxel, cisplatin, 5-FU, vincristine) are used at full, weight-adjusted dose.
• Stop chemotherapy by ~33–35 weeks and leave a 3-week washout before delivery (1–2 weeks for weekly/fortnightly regimens) so fetal marrow and placental clearance recover — neonatal myelosuppression is the avoidable harm.
• Absolute drug exclusions: methotrexate and other antimetabolites (aminopterin embryopathy), trastuzumab/anti-HER2 (oligohydramnios, fetal death), tamoxifen (defer to postpartum), and daunorubicin.
• Radiotherapy to the pelvis is contraindicated; supradiaphragmatic RT with shielding is occasionally feasible but usually deferred.

The named regimens — exact composition, dosing logic, and how they differ

Beyond "give chemo after the first trimester", what matters is which regimen, why that one in pregnancy, and where the pharmacokinetics of pregnancy bite. The mechanistic principle that unifies the whole list: cytotoxics damage the fetus through the same anti-proliferative mechanism that fights the tumour, so the period of maximal harm is organogenesis (weeks ~2–8 post-conception) — after the major organs are formed, the residual fetal targets are growth and the marrow, which recover with a delivery washout. That single mechanism→consequence link explains every timing rule below.

Breast — anthracycline backbones. The standard pregnancy-compatible regimens are AC (doxorubicin + cyclophosphamide), EC (epirubicin substituted) and FAC/FEC (adding 5-fluorouracil). Anthracyclines have the largest in-pregnancy safety dataset of any cytotoxic class, which is precisely why they anchor the breast regimen. Doxorubicin is preferred over epirubicin and emphatically over idarubicin/daunorubicin — the latter are more lipophilic, cross the placenta more readily and carry more fetal cardiotoxicity signal. Taxanes (paclitaxel weekly, or docetaxel) are added from the second trimester and the accumulated registry data (Cardonick's Cancer and Pregnancy Registry; INCIP) show no excess malformation over anthracyclines alone. The two named drugs you do not give: trastuzumab/pertuzumab (anti-HER2 → fetal renal hypoplasia, oligohydramnios, pulmonary hypoplasia, death — the fetal kidney expresses HER2 and depends on it) and endocrine therapy (tamoxifen → craniofacial and genital malformation; defer to postpartum). HER2-positive and hormone-receptor-positive disease therefore have their targeted component deferred until after delivery, and the antenatal treatment is the cytotoxic backbone only.

Cervical and ovarian — the platinum–taxane doublet. Carboplatin + paclitaxel is the in-pregnancy workhorse for epithelial ovarian cancer and for neoadjuvant bridging of cervical cancer. Carboplatin is preferred over cisplatin in pregnancy — both are used, but cisplatin carries more ototoxicity and nephrotoxicity signal in exposed neonates, and carboplatin's dosing (AUC-based, Calvert formula) is more forgiving. The judgement call is dosing in the expanded plasma volume and increased renal clearance of pregnancy: doses are calculated on actual weight and not capped, because under-dosing to "protect the fetus" is a silent failure that under-treats the mother — the discipline of giving the full, weight-appropriate dose is the same principle as never narrowing a treatment to dodge a theoretical harm.

The antimetabolite exclusion — the mechanism. Methotrexate (and aminopterin, its parent) is an absolute contraindication because folate-antagonism in organogenesis produces the recognised aminopterin/methotrexate embryopathy — cranial dysostosis, limb defects, growth restriction. This is the clean mechanism→teratology link: the drug's anti-folate action is identical to the mechanism that makes it abortifacient, so there is no safe gestational window for it as an anticancer agent. (Its single-dose use for ectopic pregnancy is a different, deliberate context.)

Worked contrast — why the regimens differ. Set side by side:

The single transferable rule across all of them: the cytotoxic backbone is given antenatally at full dose; the targeted/endocrine/radiation components that have no safe gestational window are sequenced to the postpartum period.

Subtype-specific management — how the plan forks by tumour and gestation

Cervical cancer — the sharpest gestation-dependent fork.

• Microinvasive (IA1, no lymphovascular space invasion): treat as if low-risk — diagnostic cone/large-loop biopsy if needed, colposcopic surveillance through pregnancy, definitive management deferred ≥6 weeks postpartum. Vaginal delivery is permissible for true microinvasive disease.
• IA2–IB1 with desire to continue: the modern option is neoadjuvant carboplatin–paclitaxel to hold the disease while buying fetal maturity, ideally after pelvic lymphadenectomy if gestation permits (≤20–22 weeks) to confirm node-negativity. Reported disease progression on neoadjuvant chemotherapy during pregnancy is low (on the order of ~3%), but the evidence is observational.
• Bulky IB3+/node-positive disease: standard of care is chemoradiation, which is incompatible with continuing the pregnancy. If the fetus is previable, most experts recommend termination plus definitive chemoradiation; if viable, deliver (classical caesarean) then treat. Continuing a previable, node-positive pregnancy on neoadjuvant chemotherapy is the most contested scenario and demands fully informed maternal autonomy.
• Delivery mode is non-negotiable for invasive disease: classical caesarean. Vaginal delivery risks catastrophic tumour haemorrhage, obstructed labour and the named, do-not-miss complication — implantation metastasis at the episiotomy or laceration site, which is almost uniformly fatal.

Breast cancer. Surgery (breast-conserving or mastectomy) is safe in any trimester; axillary staging uses technetium-only sentinel-node mapping (blue dye contraindicated). Cytotoxic chemotherapy from the second trimester as above; targeted and endocrine therapy postpartum. Pregnancy itself does not worsen stage-for-stage prognosis (see the evidence section), so the plan mirrors the non-pregnant pathway with the targeted components time-shifted.

Epithelial ovarian cancer. Surgical staging/debulking is best in the second trimester; if diagnosed too late for primary surgery, neoadjuvant carboplatin–paclitaxel bridges to a postpartum interval cytoreduction. Borderline tumours and early germ-cell tumours are frequently managed with fertility-sparing unilateral salpingo-oophorectomy plus staging.

Haematological malignancy. Hodgkin lymphoma (ABVD) and aggressive non-Hodgkin lymphoma (R-CHOP) are treated promptly, deferring past the first trimester where the disease tempo allows; indolent disease can sometimes be watched to delivery. Acute leukaemia is the exception that proves the rule — it cannot wait, so a first-trimester diagnosis forces the hardest counselling in the whole field: induction is teratogenic, deferral is maternally lethal, and termination is openly discussed.

Melanoma — the placental/fetal-transmission tumour. Melanoma is the malignancy most likely to metastasise to the placenta and the fetus. The placenta of any woman with metastatic melanoma must be examined histologically; when placental metastasis is documented, the reported risk of fetal/neonatal metastasis is on the order of ~22% (CLAUDIUS and earlier case series), and neonatal melanoma metastasis is almost always fatal — so a placenta positive for melanoma mandates paediatric oncology referral and neonatal surveillance, not reassurance.

Long-term / delivery

• Aim for term (≥37, ideally ≥38 weeks) — planned prematurity, not chemo exposure, is the strongest predictor of impaired neurocognitive outcome.
• Mode: vaginal birth is default; caesarean (classical incision) is mandatory for invasive cervical cancer — vaginal delivery risks tumour haemorrhage, obstruction and lethal episiotomy/laceration-site implantation metastasis.
• Examine the placenta histologically (microscopic metastasis — especially melanoma).
• Resume full oncological therapy (RT, trastuzumab, endocrine therapy) postpartum. Breastfeeding withheld during chemo; safe ~3 weeks after the last non-platinum dose.

Differential diagnosis and the mimics that change management

The "is this even cancer, and is it the cancer I think it is?" reasoning changes the plan as much as the staging does.

• Adnexal mass: the dominant benign mimic early is the corpus luteum / functional cyst (resolves by ~16 weeks), and the malignant differentials — epithelial cancer, germ-cell tumour, borderline tumour, and the metastatic Krukenberg (signet-ring gastric/breast deposits, often bilateral) — each carry a different operation. Decidualised endometriomas in pregnancy mimic malignancy on ultrasound (papillary projections with flow) and are a notorious false-positive that has driven unnecessary surgery — MRI characterisation and serial follow-up, not a reflex laparotomy, is the consultant move.
• Breast mass: the benign mimics — lactating adenoma, galactocele, fibroadenoma, mastitis/abscess — are common and reassuring, but the rule is core biopsy of any dominant or persistent mass, because the cost of mislabelling cancer as "pregnancy nodularity" is a stage shift.
• Cervical mass / antepartum bleeding: distinguishing invasive cervical cancer from a cervical ectropion, polyp, decidual reaction or placenta praevia is a speculum-and-biopsy decision, not a cytology decision.
• Gestational trophoblastic neoplasia sits in its own category — a wildly elevated β-hCG, a "snowstorm" or co-existing molar picture, and a different (highly chemosensitive, methotrexate-based) management entirely; do not fold it into the solid-tumour algorithm.
• Pancytopenia / blasts on the film in pregnancy must separate physiological gestational changes and pre-eclampsia with severe features/HELLP-related cytopenias from acute leukaemia — the bone-marrow and the smear, not the platelet count alone, make that call, and getting it wrong delays a treatment measured in days.

The evidence & the controversy

The contemporary anchor is the FIGO 2025 Best Practice Advice (Nanda et al.) alongside the ESGO/INCIP 2025 guidelines — both built substantially on the INCIP registry, whose central finding is that infants exposed to chemotherapy after the first trimester have congenital malformation, growth and cardiac outcomes no different from controls, with cognitive scores driven by gestational age at birth, not cytotoxic exposure. This reframed the field: the historic reflex to deliver early "to start real treatment" actively harms the child. Population data temper the optimism — a 2025 JNCI cohort signalled small increases in some paediatric outcomes after in-utero chemotherapy — so the honest position is "reassuring but not zero-risk; minimise prematurity and follow children up."

The sharpest controversy is early-stage cervical cancer with the desire to continue pregnancy. Neoadjuvant platinum–taxane to bridge to fetal maturity is now an established option — reported disease progression during pregnancy on neoadjuvant chemotherapy is low (~3%) — yet evidence is observational, optimal nodal assessment (lymphadenectomy loses feasibility beyond ~20–22 weeks, when uterine volume sharply reduces nodal yield) is contested, and node-positive disease still pushes most experts toward recommending termination plus standard chemoradiation. Both sides are defensible, and the decision centres on informed maternal autonomy.

A second live debate is sentinel node biopsy in breast cancer: FIGO/ESGO now endorse technetium-only mapping as safe, reversing older blanket prohibitions — but blue dye remains contraindicated, a distinction that still catches clinicians out.

A third, quieter controversy is the platinum/taxane growth signal. The INCIP registry's own data link antenatal chemotherapy to small-for-gestational-age birth, and the signal is strongest for exactly the platinum and taxane agents that the cervical and ovarian regimens depend on (see the de Haan row below for the odds ratios). The consultant reconciliation is not to withhold or dose-reduce the chemotherapy — that under-treats the mother — but to add serial growth and Doppler surveillance to any platinum/taxane pregnancy and to factor a higher baseline SGA rate into delivery planning. This is the same discipline as everywhere else in the chapter: treat the mother fully, surveil the fetus closely, and let gestational age at birth — not drug avoidance — be the lever you pull for the baby.

The unspoken Final-level point is equity: the SA author contribution to FIGO 2025 (Adam, Pretoria; Bergman, Stellenbosch) reflects that most evidence is high-income, while SA carries a high-incidence, HIV-driven cervical cancer burden (women living with HIV have roughly three-fold higher cervical cancer risk) and constrained access to MRI, neonatal ICU and multi-agent chemo. A realistic district-to-tertiary referral plan is part of the management.

The South African delivery system — what the international plan assumes that SA does not have

Every international algorithm in this chapter silently assumes resources that a SA district hospital does not have, and the consultant answer names the gap and the workaround:

• MRI and PET are tertiary-only and queued. The whole-body MRI that the FIGO advice treats as routine is, in much of SA, a referral and a wait. Stage on the best feasible imaging — ultrasound, a shielded chest radiograph, and tertiary MRI when reachable — and do not let an unobtainable scan delay treatment.
• Multi-agent chemotherapy lives at regional/tertiary oncology units, not at district level. A pregnant woman with a new cancer diagnosis is a referral up the chain — district stabilises and refers, regional/tertiary delivers the regimen and houses the MDT. The NDoH referral pathway, not a textbook, decides where she is treated.
• Neonatal ICU is scarce and unevenly distributed. The "buy fetal maturity to term" strategy presupposes a neonatal unit that can rescue a preterm infant if the plan fails. Where there is none, the delivery must be located where neonatal care exists — an antenatal transfer, planned early, not an emergency one.
• HIV is the dominant local modifier. SA's cervical cancer burden is HIV-driven; women living with HIV have ~3-fold higher risk. Every plan starts with HIV status, ART optimisation, and PVT (Prevention of Vertical Transmission) for the neonate under the SA HIV Consolidated Guidelines — and immunosuppression both worsens the cervical disease and reduces chemotherapy tolerance, so the oncology and the HIV plans are not separable.
• SAMF/EML availability constrains the regimen. The named agents above are broadly available through the oncology services, but the targeted drugs (trastuzumab/pertuzumab) and some newer agents are access-limited — another reason the antenatal plan leans on the cytotoxic backbone and sequences the targeted component postpartum, where the access question is at least separable from the pregnancy.

Landmark trials & key evidence

These are the studies behind the principle that maternal cancer is treated stage-appropriately and the fetus protected by reaching term — not by curtailing treatment. The field has no randomised trials (it would be unethical); the evidence base is observational cohorts and registries, chiefly the INCIP registry, which is itself the central limitation to weigh.

The honest caveat: the Metcalfe 2025 population cohort found a real (if preterm-mediated) excess of severe neonatal morbidity, so the defensible position is "reassuring but not zero-risk — minimise prematurity and follow the child up," not a blanket "chemotherapy is harmless."

Reading the numbers

• The cleanest causal claim in the whole field is the gestation→IQ slope. Amant 2012's +11.6 IQ points per additional month in utero (95% CI 6.0–17.1) is the number that justifies "aim for term." The arithmetic: a baby delivered electively at 34 instead of 38 weeks loses roughly a month of gestation — by this estimate, on the order of ~11–12 IQ points of avoidable cost, for no oncological gain in a mother already on stage-appropriate treatment. That is the quantified case against engineering prematurity.
• Metcalfe 2025 closes the loop at population scale. The crude signal — severe neonatal morbidity aRR 1.67 (95% CI 1.13–2.46) with antenatal chemotherapy — looks alarming until you read the mediation: preterm birth explained 100% of it, and the neurodevelopmental hazard with the drug itself was null (aHR 0.93, 95% CI 0.71–1.22). The honest synthesis is that the apparent "chemotherapy harm" is overwhelmingly a prematurity harm wearing a cytotoxic costume.
• The SGA signal is the one real drug-attributable harm, and it is graded. From the INCIP data, ~21% of chemotherapy-exposed neonates are born SGA (vs ~10% expected by definition), and the de Haan analysis attributed the excess specifically to platinum and taxane exposure. This is why the consultant adds growth surveillance to every platinum/taxane pregnancy rather than treating "chemo in pregnancy" as uniformly safe.
• Pregnancy does not worsen breast-cancer prognosis stage-for-stage. Amant 2013's disease-free-survival HR of 1.34 (95% CI 0.93–1.91) crosses 1 — the CI includes no difference — so the defensible statement is "no proven prognostic penalty after adjustment," which removes the historic excuse for advising termination on prognostic grounds.

Worked viva — how to structure the answer

Take a stem such as "a 31-year-old, 19 weeks pregnant, presents with a 4 cm hard right breast mass; core biopsy is grade 3, ER-negative, HER2-positive invasive ductal carcinoma." The answer runs:

1. Frame it — "This is pregnancy-associated breast cancer at 19 weeks; she is past organogenesis, the mass needs full locoregional staging, and the HER2-positive biology means the targeted component will have to be sequenced postpartum."
2. Convene and stage — name the tumour-board MDT (oncology, gynae-oncology/breast surgery, MFM, neonatology, radiology, pathology, anaesthesia, psychology); stage with MRI without gadolinium, shielded chest radiograph, liver ultrasound; confirm HIV status; establish maternal wishes and document informed consent.
3. Treat without delay, sequenced to gestation — surgery (BCS or mastectomy) safe now; technetium-only sentinel-node mapping (no blue dye); start AC/EC ± weekly paclitaxel in the second trimester at full weight-adjusted dose; withhold trastuzumab and endocrine therapy until postpartum (HER2-targeting causes oligohydramnios and fetal renal/pulmonary hypoplasia).
4. Protect the fetus by reaching term — stop chemotherapy by ~33–35 weeks, honour a 3-week washout before delivery (avoid neonatal myelosuppression), serial growth/Doppler surveillance (taxane SGA signal), antenatal steroids only if preterm birth is anticipated, and aim for term (≥37–38 weeks), not early delivery.
5. Justify from evidence — Amant 2012 (+11.6 IQ points per month of gestation), Metcalfe 2025 (harm is preterm-mediated, drug hazard null), Amant 2013 (no prognostic penalty for treating in pregnancy), de Haan/INCIP (the SGA signal that justifies surveillance).
6. Anticipate the SA reality — refer to a regional/tertiary oncology unit with the MDT and neonatal ICU; the targeted therapy is access-limited and postpartum anyway; plan an antenatal transfer to where the baby can be delivered safely.
7. Close the loop — resume trastuzumab and endocrine therapy postpartum, withhold breastfeeding during chemotherapy, examine the placenta, and arrange long-term oncological follow-up.

For a cervical presentation, the structure is the same but the fork is gestation-and-stage: microinvasive → surveil and treat postpartum; early-stage continuing → lymphadenectomy if ≤20–22 weeks then neoadjuvant carboplatin–paclitaxel; node-positive/bulky → chemoradiation, which forces the termination-versus-deliver conversation; and classical caesarean for any invasive disease with the episiotomy-implantation risk named explicitly.

Exam traps & red flags

• Do not delay diagnosis or treatment for "the pregnancy." Deferring a biopsy or stage-appropriate chemotherapy to protect the fetus is the classic error.
• Never give chemotherapy in the first trimester, and never methotrexate, trastuzumab or tamoxifen at any gestation.
• Do not engineer iatrogenic prematurity to "complete treatment sooner" — outcomes track gestational age, not chemo timing. Aim for term.
• Do not dose-reduce chemotherapy to "spare the fetus." Pregnancy expands plasma volume and renal clearance; dose on actual weight. Under-dosing silently under-treats the mother — surveil the fetus instead of shrinking the dose.
• Invasive cervical cancer → classical caesarean. Allowing vaginal delivery risks fatal recurrence at the episiotomy/laceration site — a named, do-not-miss error.
• FNA, not core biopsy, of a breast mass — gestational proliferation degrades cytology; a dominant or persistent mass needs core histology.
• Mistaking a decidualised endometrioma or corpus luteum for ovarian cancer — and operating — when MRI characterisation and serial follow-up were the answer.
• Don't over-rely on radiation fear — most diagnostic imaging is well below the harm threshold; withholding necessary MRI/CT mis-stages the mother. Conversely, gadolinium is the one to avoid.
• Stopping chemo too close to delivery causes neonatal myelosuppression and maternal/neonatal sepsis — honour the 3-week washout and the ~33–35 week ceiling.
• Forgetting the placenta: omitting histology misses melanoma metastasis — and when the placenta is positive, the ~22% fetal-metastasis risk means the neonate needs paediatric-oncology surveillance, not reassurance.
• Treating tumour markers as valid in pregnancy — CA-125/AFP/β-hCG physiology makes single values uninterpretable.
• Missing the leukaemia in the cytopenia — attributing pancytopenia or blasts to HELLP/pre-eclampsia and losing the days that acute leukaemia does not give you.
• Ignoring HIV/PVT and the SA referral reality — an internationally "correct" plan that the patient cannot access is not a complete answer.

Evidence anchors

• Nanda S, et al. Cancer in pregnancy: FIGO Best practice advice and narrative review. Int J Gynaecol Obstet 2025;171(1):131–151. DOI
• Amant F, et al. ESGO/INCIP Guidelines for the management of patients with gynecological cancers during pregnancy. Int J Gynecol Cancer 2025;35(9):101975. DOI
• Maxwell C, et al. Pregnancy after cancer: FIGO Best practice advice. Int J Gynaecol Obstet 2025;169(3):1119–1126. DOI
• de Haan J, Cardonick E, et al. Chemotherapy against cancer during pregnancy: a systematic review on neonatal outcomes. PMC5044906
• de Haan J, Verheecke M, Amant F, et al. Oncological management and obstetric and neonatal outcomes for women diagnosed with cancer during pregnancy: a 20-year international cohort study of the INCIP. Lancet Oncol 2018;19(3):337–346. DOI
• Cordeiro CN, et al. Cervical cancer in pregnancy (review). PMC10281765
• According to PubMed, the FIGO and ESGO/INCIP guidance above is indexed under PMIDs 40704672 and 40707270 respectively.
• South African data: women living with HIV carry an ~3-fold higher risk of cervical pre-cancer/cancer — Fernández Villalobos et al. Int J Cancer 2024. Apply SA NDoH Maternity Care Guidelines, SA HIV Consolidated Guidelines (PVT) and SAMF for drug availability (plain text — no single stable guideline URL).