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Common Solid Tumors

Four cancers — lung, breast, colorectal, and prostate — account for a large share of the world's cancer diagnoses and cancer deaths. If you understand these four well, you understand the working logic of clinical oncology: how a tumour is suspected, confirmed by tissue, staged, and then treated with some combination of surgery, radiation, chemotherapy, hormonal therapy, and targeted or immune agents. This page teaches those four tumours side by side so you can see both what they share and what makes each distinct.

The unifying theme is time. In solid tumours, a cancer caught while it is still local is often curable; the same cancer caught after it has spread is usually not. Almost everything interesting in this field — screening programs, staging systems, tumour markers, imaging — exists to move the diagnosis earlier in that timeline. Keep that in mind as we go.

Learning Objectives​

  • Recall the major risk factors, typical presentations, and screening strategies for lung, breast, colorectal, and prostate cancer.
  • Explain how the TNM staging framework guides prognosis and treatment across solid tumours.
  • Describe the evidence-based screening programs for breast, colorectal, and lung cancer and the ongoing controversy around prostate (PSA) screening.
  • Match each tumour to its first-line management approach by stage.
  • Distinguish curable-intent from palliative-intent treatment and recognise red-flag ("alarm") presentations.

Quick Answer​

Lung, breast, colorectal, and prostate cancers are the four most common solid tumours. Lung cancer is the leading cause of cancer death, strongly linked to smoking, often presents late, and is screened with low-dose CT in high-risk smokers. Breast cancer presents as a painless lump or is detected on mammographic screening; management combines surgery, radiation, and systemic therapy guided by hormone-receptor and HER2 status. Colorectal cancer arises from adenomatous polyps over years, is highly preventable by colonoscopy or stool-based screening, and presents with bleeding, altered bowel habit, or iron-deficiency anaemia. Prostate cancer is often indolent, detected by PSA testing and biopsy, and managed by active surveillance, surgery, radiation, or androgen deprivation depending on risk. Across all four, staging (TNM) drives whether treatment is curative or palliative.

Where It Came From​

For most of medical history, cancer was found only when it declared itself — a fungating breast mass, obstructive bowel symptoms, coughed-up blood. By then it was usually incurable. The central twentieth-century insight was that cancer has a pre-symptomatic window, and that finding disease during that window could save lives. This idea gave birth to cancer screening.

The story begins with the Pap smear. In the 1920s George Papanicolaou noticed that cervical cancer cells could be identified on a stained slide before invasive disease appeared; by the 1940s and 50s this became the first mass screening program, and cervical cancer mortality fell dramatically where it was adopted. That success became the template.

Breast cancer screening followed. The Health Insurance Plan (HIP) of New York trial in the 1960s was the first randomised trial to show mammography reduced breast cancer deaths, and by the 1980s–90s organised mammography programs spread across the developed world. Colorectal screening matured later: the recognition of the adenoma-to-carcinoma sequence (Vogelstein's molecular model in 1988) gave a biological rationale — remove the polyp, prevent the cancer — and randomised trials of faecal occult blood testing in the 1990s confirmed a mortality benefit. Lung cancer screening is the newest: the National Lung Screening Trial (NLST, 2011) finally showed that low-dose CT in heavy smokers reduced lung cancer deaths by about 20%, something older chest X-ray studies had failed to demonstrate.

Prostate screening is the cautionary tale. The PSA blood test, introduced in the late 1980s, could detect prostate cancer very early — but large trials (PLCO and ERSPC) later showed it also detected many cancers that would never have harmed the patient, leading to overdiagnosis and overtreatment. Prostate cancer taught oncology a humbling lesson: earlier is not always better. The motivation behind every program on this page is the same — buy time — but prostate cancer reminds us that screening must prove it does more good than harm.

The Shared Framework: How Any Solid Tumour Is Worked Up​

Before the individual tumours, learn the scaffold that applies to all of them.

  1. Suspicion — a symptom, a screening abnormality, or an incidental imaging finding.
  2. Tissue diagnosis — nothing is called cancer without a biopsy (histology). This also gives grade (how abnormal the cells look) and biomarkers.
  3. Staging (TNM) — T = size/local extent of the tumour, N = regional lymph node involvement, M = distant metastasis. These combine into stage groups I–IV. Roughly: stage I is small and local, stage IV has spread to distant organs.
  4. Treatment decision — curative intent (usually stages I–III: surgery and/or radiation, plus systemic therapy) versus palliative intent (usually stage IV: systemic therapy and symptom control).
  5. Surveillance — monitoring for recurrence.

The single most important prognostic factor for almost every solid tumour is stage at diagnosis. That is why screening matters.

Lung Cancer​

Epidemiology and risk. Lung cancer is the leading cause of cancer death worldwide. Smoking causes roughly 85–90% of cases; other factors include radon, asbestos, air pollution, and prior radiation. Risk rises with pack-years and falls (but never to baseline) after quitting.

Two big categories. Lung cancer splits into non-small-cell lung cancer (NSCLC), about 85% (subtypes: adenocarcinoma — now the most common, including in never-smokers; squamous cell; large cell), and small-cell lung cancer (SCLC), about 15%, which is aggressive, strongly smoking-related, and usually disseminated at diagnosis.

Presentation. Often late and non-specific: persistent cough, haemoptysis, dyspnoea, chest pain, recurrent pneumonia, weight loss. Watch for characteristic syndromes:

  • Pancoast tumour (apical) — shoulder/arm pain, Horner syndrome (ptosis, miosis, anhidrosis).
  • SVC obstruction — facial/arm swelling, distended neck veins.
  • Paraneoplastic syndromes — SIADH and Lambert-Eaton (SCLC); hypercalcaemia from PTHrP (squamous cell).

Screening. Annual low-dose CT (LDCT) for high-risk adults (broadly, ages 50–80 with a significant smoking history, e.g. 20+ pack-years, currently smoking or quit within 15 years). Chest X-ray does not work as a screening test.

Management (by stage).

  • Early NSCLC (I–II): surgical resection (lobectomy) is the curative mainstay; stereotactic radiation if inoperable.
  • Locally advanced NSCLC (III): concurrent chemoradiation, often followed by immunotherapy.
  • Metastatic NSCLC (IV): treatment is now biomarker-driven — test for EGFR, ALK, ROS1 mutations (targeted oral drugs) and PD-L1 expression (immunotherapy such as pembrolizumab). This is oncology's precision-medicine flagship.
  • SCLC: chemotherapy plus immunotherapy is the backbone (± radiation); it responds well initially but relapses quickly.

Breast Cancer​

Epidemiology and risk. The most common cancer in women worldwide. Risk factors: increasing age, female sex, family history, BRCA1/BRCA2 mutations, early menarche/late menopause, nulliparity, obesity, alcohol, and hormone replacement therapy.

Presentation. Classically a painless, hard, irregular, fixed lump, most often in the upper outer quadrant. Also: skin dimpling, nipple retraction, bloody nipple discharge, peau d'orange (inflammatory carcinoma), or an axillary node. Increasingly, though, it is found on screening before any lump is palpable.

Screening. Mammography, typically every 1–2 years for women roughly 40/50–74 (exact age varies by guideline). High-risk women (e.g. BRCA carriers) add MRI and start earlier.

The triple assessment. A breast lump is evaluated by (1) clinical examination, (2) imaging (mammogram and/or ultrasound), and (3) core-needle biopsy. This is a classic exam favourite.

Biology drives treatment. Every breast cancer is tested for three receptors:

  • ER/PR (oestrogen/progesterone receptors) → hormone therapy (tamoxifen; aromatase inhibitors in post-menopausal women).
  • HER2 → anti-HER2 therapy (trastuzumab).
  • Triple-negative (ER/PR/HER2 all negative) → chemotherapy-dependent, more aggressive.

Management.

  • Surgery: breast-conserving surgery (lumpectomy) + radiation, OR mastectomy. Survival is equivalent between the two for suitable candidates — a landmark finding.
  • Sentinel lymph node biopsy to stage the axilla and avoid unnecessary full axillary dissection.
  • Systemic therapy: chemotherapy, endocrine therapy, and/or HER2-targeted therapy based on receptor status and stage. Radiation after lumpectomy is standard.

Colorectal Cancer (CRC)​

The prevention story. CRC is the textbook example of a preventable cancer because it arises through the adenoma–carcinoma sequence: a benign adenomatous polyp accumulates mutations (APC → KRAS → p53 pathway) over roughly 10 years before becoming invasive. Remove the polyp and you prevent the cancer. This is why colonoscopic screening reduces both incidence and mortality.

Risk factors. Age, family history, hereditary syndromes (FAP, Lynch/HNPCC), inflammatory bowel disease, low-fibre/high-red-meat diet, obesity, smoking.

Presentation (differs by side):

  • Left-sided/rectal: change in bowel habit, fresh rectal bleeding, tenesmus, obstruction (narrower lumen, solid stool).
  • Right-sided: often silent until it causes iron-deficiency anaemia and fatigue (wider lumen, liquid stool). Any older adult with unexplained iron-deficiency anaemia needs the colon investigated.

Screening options (typically start at age 45–50):

  • Colonoscopy every 10 years — the gold standard; both diagnostic and therapeutic (polyps removed).
  • Faecal immunochemical test (FIT) annually — detects occult blood.
  • Stool DNA (FIT-DNA) every 3 years; CT colonography every 5 years. A positive stool or CT test must be followed by colonoscopy.

Management.

  • Localised colon cancer: surgical resection with regional lymphadenectomy; adjuvant chemotherapy (FOLFOX) for node-positive (stage III) disease.
  • Rectal cancer: often neoadjuvant chemoradiation before surgery (total mesorectal excision) to reduce local recurrence.
  • Metastatic (IV): chemotherapy plus targeted agents based on biomarkers — anti-EGFR (cetuximab) only if RAS wild-type; anti-VEGF (bevacizumab); immunotherapy if MSI-high/mismatch-repair-deficient. Selected liver-only metastases can be resected for cure.

Prostate Cancer​

Epidemiology. The most common non-skin cancer in men. Risk rises with age, family history, and is more common and aggressive in men of African ancestry. Most prostate cancers are adenocarcinomas arising in the peripheral zone.

The overdiagnosis problem. Many prostate cancers are so slow-growing that a man dies with them, not of them. This is central to the screening controversy.

Presentation. Early disease is usually asymptomatic (peripheral zone, away from the urethra). Advanced disease: obstructive urinary symptoms, haematuria, and — a classic clue — bone pain from osteoblastic (sclerotic) metastases to the axial skeleton.

Screening — the controversy. PSA (prostate-specific antigen) is a blood test. It is not cancer-specific (also raised by BPH, prostatitis, instrumentation). Trials showed PSA screening prevents relatively few deaths while causing substantial overdiagnosis and treatment harm (incontinence, erectile dysfunction). Current guidance favours shared decision-making: discuss risks and benefits, typically for men aged 55–69, rather than blanket screening. Diagnosis is confirmed by biopsy, increasingly guided by multiparametric MRI.

Risk stratification. Uses PSA level, clinical T stage, and the Gleason score / Grade Group (histological grade). This sorts men into low-, intermediate-, and high-risk disease.

Management.

  • Low-risk / low-grade: active surveillance — monitoring with periodic PSA, MRI, and biopsy, treating only if it progresses. Avoiding overtreatment is itself good medicine here.
  • Localised intermediate/high-risk: radical prostatectomy OR radiation therapy (external beam or brachytherapy), often with androgen deprivation.
  • Advanced/metastatic: androgen deprivation therapy (ADT) — medical or surgical castration — because these tumours are androgen-driven; plus newer agents (abiraterone, enzalutamide) and chemotherapy for castration-resistant disease.

Real-World Applications​

  • Primary care is where most of these cancers are first suspected — recognising alarm symptoms (rectal bleeding, a breast lump, haemoptysis, unexplained anaemia or weight loss) and ordering the right test saves lives.
  • Screening program design is a core public-health activity: who to invite, how often, at what cost, and with what harms.
  • Smoking cessation counselling prevents more lung (and bladder, and many other) cancers than any treatment cures — the highest-yield intervention you can offer.
  • Genetic counselling: a young woman with breast cancer or a family clustering of colon cancer should trigger consideration of BRCA or Lynch testing, which changes screening for the whole family.

Common Mistakes​

  1. "A painful breast lump is more worrying than a painless one." Wrong — most breast cancers are painless. Pain more often suggests a benign cyst or mastitis, but any discrete lump still needs triple assessment. Never dismiss a lump because it hurts or because it doesn't.

  2. "Chest X-ray is a good way to screen smokers for lung cancer." Wrong. Randomised trials showed chest X-ray does not reduce lung cancer mortality; only low-dose CT does. Screening the right way matters as much as screening at all.

  3. "A high PSA means cancer; a normal PSA rules it out." Wrong on both counts. PSA rises with BPH, prostatitis, and even ejaculation or a recent exam, and significant cancers can occur with "normal" PSA. PSA is a prompt for shared decision-making and possible biopsy, not a diagnosis.

  4. (Bonus) "Iron-deficiency anaemia in an older adult just needs iron tablets." Wrong — in an older adult it is right-sided colon cancer until proven otherwise; investigate the GI tract.

Comparison and Connections​

FeatureLungBreastColorectalProstate
Main risk factorSmokingAge, hormones, BRCAAge, polyps, diet, LynchAge, ethnicity, family
Screening testLow-dose CT (high-risk)MammographyColonoscopy / FITPSA (shared decision)
Typical early signOften none / coughPainless lumpBleeding / anaemiaUsually none
Key biomarkersEGFR, ALK, PD-L1ER, PR, HER2RAS, MSI/MMRPSA, Gleason grade
Curative mainstaySurgery (early NSCLC)Surgery + radiationSurgerySurgery or radiation
Systemic driver therapyTargeted / immunoEndocrine / anti-HER2Chemo + targetedAndrogen deprivation

Connections worth noting. All four use the same TNM staging logic and the same curative-versus-palliative decision. Breast and prostate are both hormone-driven cancers — one blocks oestrogen, the other blocks androgen — a nice parallel. Lung and colorectal both showcase biomarker-guided targeted therapy in the metastatic setting.

Practice Questions​

Recall​

Q: Which screening test reduces lung cancer mortality in high-risk individuals, and who qualifies? A: Annual low-dose CT, for roughly ages 50–80 with a heavy smoking history (e.g. 20+ pack-years, current or quit within 15 years). Chest X-ray does not work.

Understanding​

Q: Why does right-sided colon cancer typically present with anaemia rather than obstruction, while left-sided presents with change in bowel habit? A: The right colon has a wide lumen and liquid contents, so tumours grow large and bleed chronically before obstructing — producing iron-deficiency anaemia. The left colon is narrower with solid stool, so lesions cause altered habit, visible bleeding, and obstruction earlier.

Application​

Q: A 62-year-old woman has a 2 cm firm breast lump. Core biopsy shows invasive ductal carcinoma, ER-positive, HER2-negative, one positive sentinel node. Outline the treatment approach. A: Surgery (breast-conserving lumpectomy + radiation, or mastectomy) with axillary staging; adjuvant endocrine therapy (aromatase inhibitor, as post-menopausal) given ER-positivity; consider chemotherapy based on stage and genomic recurrence-risk score. HER2 therapy is not indicated (HER2-negative).

Analysis​

Q: Prostate and breast cancer screening are viewed very differently — mammography is broadly recommended, PSA is not. Explain the reasoning. A: Both detect early disease, but the balance of benefit to harm differs. Mammography detects cancers that meaningfully benefit from early treatment with acceptable harms. PSA detects many indolent cancers that would never cause harm (overdiagnosis), and treating them causes real morbidity (incontinence, impotence) while preventing relatively few deaths. Hence PSA is offered through shared decision-making rather than as a blanket program.

FAQ​

Is finding a cancer early always better? Not always. Early detection helps when the cancer is destined to progress and early treatment changes the outcome. When a cancer is indolent (many prostate cancers), "early" detection just leads to overtreatment. Good screening proves it reduces mortality, not just that it finds more cancer.

What is the difference between grade and stage? Grade describes how abnormal the tumour cells look under the microscope (how aggressive the biology). Stage describes how far it has spread anatomically (TNM). Both matter, but stage is usually the stronger driver of prognosis and treatment intent.

Why do we biopsy before treating — can't imaging tell us it's cancer? Imaging can strongly suggest cancer but cannot reliably confirm it or provide grade and biomarkers. Nearly all solid-tumour treatment decisions require tissue diagnosis. Treating without histology risks treating a benign or unexpected condition.

What does "metastatic" mean for prognosis? Metastatic (stage IV) means spread to distant organs. For most solid tumours this shifts treatment from curative to palliative intent — controlling the disease and symptoms and prolonging life rather than eliminating it. Some exceptions (e.g. limited colorectal liver metastases) can still be cured.

How does immunotherapy fit into these cancers? Immunotherapy (checkpoint inhibitors like pembrolizumab) unleashes the patient's own T-cells against the tumour. It is now central in metastatic lung cancer, triple-negative breast cancer, and MSI-high colorectal cancer, and is used in many others. Biomarkers (PD-L1, MSI status) help predict who benefits.

Quick Revision​

  • Lung — top cancer killer; smoking; presents late; screen with low-dose CT; NSCLC vs SCLC; metastatic care is biomarker-driven (EGFR/ALK/PD-L1).
  • Breast — painless lump; triple assessment; test ER/PR/HER2; surgery + radiation ± systemic therapy.
  • Colorectal — adenoma-carcinoma sequence (preventable); colonoscopy/FIT; right = anaemia, left = bleeding/obstruction; surgery ± chemo; check RAS/MSI.
  • Prostate — often indolent; PSA = shared decision (overdiagnosis risk); Gleason grade; active surveillance vs surgery/radiation; advanced = androgen deprivation.
  • Universal: tissue diagnosis first; TNM staging; stage at diagnosis is the dominant prognostic factor; curative (I–III) vs palliative (IV).

Prerequisites​

Next Topics​

  • Principles of chemotherapy and radiation therapy
  • Cancer staging and tumour markers in depth
  • Palliative and supportive care in oncology