common solid tumours

Management-focused companion to red-flag presentations of solid tumours. Covers receptor-directed treatment, staging workup, surveillance, and high-yield board pearls for the major solid tumours encountered by IM trainees.

breast cancer

diagnosis

diagnostic bilateral mammogram + axillary ultrasound + US-guided core needle biopsy
receptors evaluated: ER, PR, HER2 → drives all systemic therapy decisions

surgical management

mastectomy or lumpectomy (breast-conserving surgery) + lymph node evaluation (sentinel lymph node biopsy or axillary lymph node dissection)

occult breast cancer

isolated malignant axillary lymphadenopathy without a palpable breast mass → breast cancer is the leading differential
workup: bilateral diagnostic mammography + targeted breast ultrasound + breast MRI (highest sensitivity for occult primary) + core needle biopsy of axillary node for ER/PR/HER2
if imaging-negative: may proceed as cancer of unknown primary or treat as presumed breast primary based on receptor profile

staging imaging — when and when not

Scenario	Staging imaging
early-stage (T1–2, N0, asymptomatic)	not routinely indicated — low pretest probability of metastases; imaging leads to false positives, unnecessary biopsies, and patient anxiety
locally advanced (T3–4, N+) or symptomatic	CT chest/abdomen/pelvis ± bone scan or PET-CT
inflammatory breast cancer	always stage (CT + bone scan or PET-CT)

do not over-stage early breast cancer

Multiple guidelines (NCCN, ESMO, CCO) recommend against routine staging CT, bone scan, or PET-CT for asymptomatic early-stage breast cancer. A patient requesting staging imaging for T2N0 disease warrants a discussion about the harms of over-investigation.

systemic therapies — high-yield toxicity

Agent	Indication	Key toxicity
tamoxifen	pre- and post-menopausal ER+	VTE, endometrial cancer; maintains bone density and lowers CV risk vs. AIs
aromatase inhibitors (letrozole, anastrozole)	post-menopausal ER+ only	osteoporosis, arthralgias, increased CV risk vs. tamoxifen
anthracyclines (doxorubicin)	(neo)adjuvant	delayed, cumulative, irreversible cardiomyopathy
trastuzumab	HER2+	early-onset, reversible cardiomyopathy; monitor LVEF

anthracycline vs. trastuzumab cardiotoxicity

Anthracycline = irreversible, cumulative, dose-dependent. Trastuzumab = reversible, not dose-dependent, occurs during treatment. Do not give concurrently.

lung cancer

histology and associations

Type	Location	Associations
squamous cell	central	smoking, PTHrP → hypercalcaemia
small cell (SCLC)	central	smoking; very aggressive with rapid doubling time (expands over weeks–months); SIADH, LEMS (anti-VGCC antibodies), ectopic ACTH (Cushing syndrome)
adenocarcinoma	peripheral	common in non-smokers; targetable driver mutations (EGFR, ALK); hypertrophic osteoarthropathy

paraneoplastic syndromes

Lambert-Eaton myasthenic syndrome (LEMS)

Classic SCLC-associated paraneoplastic syndrome (anti-VGCC antibodies). Key exam features:

proximal weakness that improves with repeated effort (facilitation) — opposite of myasthenia gravis
reduced reflexes that augment after brief exercise
autonomic dysfunction: dry mouth, constipation, orthostatic hypotension
EMG: incremental response on repetitive nerve stimulation

Other key paraneoplastic associations:

SCLC → SIADH (most common), ectopic ACTH (Cushing syndrome), LEMS, limbic encephalitis (anti-Hu)
squamous cell → PTHrP → hypercalcaemia
adenocarcinoma → hypertrophic osteoarthropathy (clubbing, periostitis, arthralgia)

structural/compressive syndromes

Pancoast tumour (superior sulcus) → ipsilateral Horner syndrome (ptosis, miosis, anhidrosis) + brachial plexopathy (C8–T1 → hand weakness/pain) — usually squamous cell or adenocarcinoma
SVC syndrome → facial/upper extremity oedema, venous distension, dyspnoea — most commonly SCLC and lymphoma; requires urgent tissue diagnosis (biopsy before empiric treatment unless airway-compromised); see oncologic emergencies for full management

rapidly expanding mediastinal mass — differential

A mediastinal mass growing visibly over weeks is a narrow differential — all are potentially chemosensitive, making tissue diagnosis critical:

Tumour	Key features	Diagnostics
SCLC	heavy smoking history, central, very aggressive doubling time, paraneoplastic syndromes (SIADH, LEMS, ectopic ACTH)	CT-guided biopsy or EBUS; staging CT + brain MRI
lymphoma	younger patients, B symptoms, bulky lymphadenopathy; aggressive subtypes (DLBCL, Burkitt, lymphoblastic) expand rapidly	core biopsy (not FNA — need architecture for subtyping); PET-CT
germ cell tumour	young males; primary mediastinal or metastatic from testicular primary	β-hCG + AFP + LDH; testicular ultrasound; CT chest/abdomen/pelvis

germ cell tumours and tumour markers

Markedly elevated β-hCG or AFP in a young male with a mediastinal mass may be sufficient to initiate chemotherapy before biopsy results return — these markers are virtually diagnostic. Always examine the testes and order testicular ultrasound.

workup and management

tissue diagnosis: CT-guided biopsy (peripheral) or EBUS/bronchoscopy (central)
if tissue unavailable → circulating tumour DNA (ctDNA / liquid biopsy) can identify driver mutations and guide therapy
staging: CT chest/abdomen/pelvis + brain MRI
NSCLC EGFR+ adenocarcinoma → osimertinib (EGFR TKI)
SCLC → chemotherapy + immunotherapy; limited stage may receive concurrent chemoradiation

always test for driver mutations in NSCLC

EGFR, ALK, ROS1, BRAF, KRAS G12C, PD-L1 — results change first-line therapy. If insufficient tissue, consider ctDNA.

colorectal cancer

diagnosis and staging

full colonoscopy + biopsy → staging CT chest/abdomen/pelvis + serum CEA

management by stage

Stage	Approach
1–3	surgical resection ± adjuvant chemotherapy (stage 3, select stage 2)
4 — oligometastatic (isolated liver/lung, <4 lesions)	potentially curable with metastasectomy + systemic therapy
4 — widespread	palliative systemic therapy

surveillance (stage 1–3, post-resection)

clinical follow-up every 6 months × 3 years
CT chest/abdomen/pelvis at year 1 and year 3
colonoscopy at 1 year post-resection

prostate cancer

histology — adenocarcinoma, androgen-driven; metastasises as sclerotic/osteoblastic bone lesions (vs. most solid tumours → lytic)
diagnosis — DRE, serum PSA, prostate biopsy (Gleason score)
staging — CT chest/abdomen/pelvis + bone scan (detects sclerotic lesions; bone scan does not reliably detect lytic lesions — contrast with RCC, thyroid)
hypercalcaemia in prostate cancer — uncommon; when present, typically indicates very advanced disease; still requires standard workup to exclude primary hyperparathyroidism

management

Setting	Approach
localised	active surveillance, radical prostatectomy, or radiation
metastatic	androgen deprivation therapy (ADT: GnRH agonists/antagonists) + anti-androgens or CYP17 inhibitor (abiraterone)

osteoblastic metastases

Prostate cancer is the classic exception — most solid tumour bone metastases are lytic. Osteoblastic lesions on bone scan in a male → think prostate.

testicular cancer

types — germ cell tumours: seminoma vs. non-seminoma
markers — β-hCG, AFP, LDH

never transscrotal biopsy

Risk of tumour seeding and altered lymphatic drainage. Perform radical inguinal orchiectomy for diagnosis and treatment.

AFP is never elevated in pure seminoma — if AFP↑, treat as non-seminoma regardless of histology
bleomycin-containing regimens (BEP) → risk of pulmonary fibrosis

renal cell carcinoma

“the internist’s tumour” — often incidental; classic triad (flank pain, haematuria, palpable mass) in <15%
paraneoplastic associations:
- erythrocytosis (EPO production)
- hypercalcaemia (PTHrP)
- hypertension
- Stauffer syndrome — non-metastatic hepatic dysfunction (elevated ALP, transaminases; resolves with nephrectomy)
management: nephrectomy for localised disease; immunotherapy/TKIs for metastatic

bone metastases — lytic vs sclerotic

Pattern	Classic tumours	Mechanism
lytic (osteoclast-driven)	RCC, thyroid, lung, multiple myeloma	tumour factors (PTHrP, RANKL, IL-6) stimulate osteoclast resorption
sclerotic/osteoblastic	prostate, carcinoid	tumour factors (endothelin-1, BMPs) stimulate osteoblast activity; sclerotic lesions store excess calcium in bone matrix
mixed	breast (lytic, sclerotic, or mixed), lung	both pathways active

most solid tumour bone mets are lytic — prostate is the classic exception (purely sclerotic)
RCC and thyroid produce typically lytic lesions — bone scan may underestimate disease burden (bone scan detects osteoblastic reaction, not lysis itself)
breast can produce any pattern — lytic, sclerotic, or mixed; do not assume lytic
multiple myeloma produces purely lytic lesions (bone scan may be falsely negative → use skeletal survey or low-dose whole-body CT)
hypercalcaemia is more common with lytic lesions (bone resorption releases calcium)

Trousseau syndrome

migratory superficial thrombophlebitis and unprovoked VTE associated with occult or known malignancy
classically linked to pancreatic adenocarcinoma and other mucinous adenocarcinomas (gastric, ovarian, lung)
mechanism: tumour-derived mucins and tissue factor activate coagulation
unexplained recurrent VTE (especially if warfarin-resistant or unusual sites — splanchnic, upper extremity) should prompt malignancy workup