Cancer science, made for everyone. We turn the research behind PDEOncology into interactive experiences you can actually feel — no equations, no textbooks.
Quick — what do you think?
Five things about cancer nobody told you
Why drugs fail
Good drugs can't always reach the tumor
Even the most effective chemotherapy drugs sometimes fail — not because they stop working, but because they physically cannot penetrate deep enough. We simulate this with real mathematics.
interactive simQuizEarly detection
Tumor size changes everything
A tumor found at 1 cm and at 5 cm are completely different problems. Drag a slider — and see exactly how much harder treatment becomes as tumors grow.
drag & exploreQuizLifestyle & risk
Your habits change how drugs work
Smoking and obesity don't just cause cancer — they change the tumor microenvironment in ways that make chemotherapy less effective. Get your personalised risk profile.
risk profilepersonalisedPrecision medicine
Why the same drug works differently for everyone
Two patients, same diagnosis, same drug — completely different outcomes. Genetics and tumor biology all play a role. See the difference with your own eyes.
compareQuizReading
Further reading: the journals behind the science on this site
The research on this site draws from the top peer-reviewed oncology journals. This tab links you directly to them — with a plain guide on how to read a scientific paper.
JournalsReading GuideWhy Drugs Fail
The most common reason chemotherapy fails isn't drug resistance — it's a physical problem. The drug simply cannot reach the cells it needs to kill.
Before we explain — what's your guess?
What's really happening inside
The tumor builds walls
Tumors actively create a hostile microenvironment that repels drugs:
- High interstitial fluid pressure — the tumor pushes fluid outward, physically repelling drugs
- Dense extracellular matrix — fibrous proteins slow drug movement
- Abnormal blood vessels — irregular and poorly distributed
The result: drug concentration drops dramatically moving from the tumor edge toward its center.
We can measure this
This is modelled by a reaction-diffusion equation used in PDEOncology:
Where D is how fast the drug diffuses. In pancreatic cancer, D is up to 75% lower than in breast cancer — because the stroma is so dense.
See it for yourself
Pick a drug and tumor. Run the simulation. Watch how far the drug actually gets.
Key takeaway
For pancreatic cancer, even the best-penetrating drugs cover less than 10% of the tumor volume at therapeutic concentrations. This is why pancreatic cancer has a 5-year survival rate of only ~12% — the biology makes it nearly impossible for current drugs to work. This is not a failure of chemistry. It's a failure of physics.
Frequently asked questions
If drugs can't penetrate tumors, why does chemotherapy still work at all?
Chemotherapy works by killing rapidly dividing cells — and it does reach the outer layers of a tumor effectively. The problem is the core. In small, early-stage tumors this matters less because the ratio of outer-to-inner cells is more favorable. In large, dense tumors, the unreachable core becomes a reservoir of surviving cancer cells that can seed recurrence.
What is IFP and why does it matter?
Interstitial Fluid Pressure (IFP) is the pressure of fluid within tumor tissue. Normal tissues have near-zero IFP. Tumors generate abnormally high IFP — sometimes 10–30 mmHg above normal — due to leaky blood vessels and compressed lymphatics. This outward pressure physically pushes drugs away from the tumor center, like trying to inject water into a balloon that's already pressurized.
Does tumor type really change how well drugs penetrate?
Dramatically. Pancreatic cancer is surrounded by dense stromal matrix that can reduce drug diffusion by up to 75% compared to breast cancer. Gliomas face a different challenge: the blood-brain barrier restricts large molecules entirely. This is why a drug that works in one cancer may be nearly useless in another — even if the cancer cells are equally sensitive to it.
Are there drugs designed to overcome these barriers?
Yes — this is an active research area. Approaches include: nanoparticle carriers exploiting the EPR effect; stromal-depleting agents that break down the collagen matrix; anti-VEGF agents that normalise tumor vasculature and reduce IFP; and ultrasound-mediated delivery that temporarily opens barriers.
What's the difference between drug resistance and drug penetration failure?
Drug resistance is biological — cancer cells evolve mutations that neutralise the drug. Penetration failure is physical — the drug never reaches those cells. Clinically the outcomes look identical (treatment failure), but the mechanisms are completely different. Penetration failure is often underappreciated because it doesn't appear in cell culture experiments.
Early Detection
You've heard "catch it early." But do you know what that actually means in physical terms? First — a question.
Test your intuition
Drag to discover
Move the slider. Watch the numbers change. This is why early screening saves lives.
When should you screen?
| Cancer | Screening method | Start age | Why it matters |
|---|---|---|---|
| Breast | Mammogram | 40–45 | Stage I: 99% survival → Stage IV: 28% |
| Colorectal | Colonoscopy | 45 | Most cases preventable if polyps caught early |
| Cervical | Pap smear + HPV test | 21 | Near 100% preventable with screening |
| Lung | Low-dose CT | 50 (smokers) | Early finding triples survival rate |
| Pancreatic | No standard screening | — | Prevention is the only current strategy |
Cancer-by-cancer screening guide
Select a cancer type to see detailed screening recommendations and survival data.
Childhood cancer warning signs
Unlike adult cancers, childhood cancers are rarely caused by lifestyle factors. Parents and caregivers should know these warning signs — early detection dramatically improves outcomes.
Persistent fever · unexplained bruising · pallor · fatigue · bone or joint pain · swollen lymph nodes. ALL is the most common childhood cancer — and has a ~90% cure rate with early treatment.
Morning headaches · vomiting on waking · balance or gait changes · vision changes · personality change. Symptoms are often subtle and mistaken for other conditions.
Abdominal mass · dark circles around eyes (periorbital bruising) · bone pain · high blood pressure. Most common in children under 5.
White pupil reflex in photos (leukocoria) · squinting · red or swollen eye. If a flash photo shows one pupil glowing white, see a doctor immediately. Highly treatable when caught early.
These symptoms alone do not mean cancer — they are common in many childhood illnesses. But if symptoms are persistent, unexplained, or worsening, always consult a doctor promptly.
Lifestyle & Risk
Your lifestyle doesn't just affect your cancer risk — it affects how well treatment works if you do get cancer. Fill in the profile below to see your personalised result.
Build your microenvironment profile
Adjust the sliders to match your lifestyle. We'll show you how each factor affects drug penetration — and generate your personal profile.
Evidence-based actions
Smoking accounts for ~30% of all cancer deaths.
Obesity increases risk for 13 cancer types.
150 min/week reduces cancer risk by 10–20%.
Alcohol is a Group 1 IARC carcinogen.
Mediterranean diet reduces overall cancer risk 10–30%.
Chronic stress activates the HPA axis, elevating IFP.
Under 6 hrs/night is linked to elevated cancer mortality.
Precision Medicine
Two patients. Same cancer. Same drug. One responds — the other doesn't. This isn't bad luck. It's biology. First, a guess.
What do you think?
See the difference side by side
Questions to ask your oncologist
- Has my tumor been tested for biomarkers like HER2, KRAS, or EGFR?
- Is there a targeted therapy available for my specific mutation?
- Would genetic testing change my treatment plan?
Treatment approaches compared
Click any treatment to see how it works, its advantages, and its limitations.
Conventional chemotherapy
Targeted therapy (e.g. imatinib, trastuzumab)
Immunotherapy (checkpoint inhibitors)
CAR-T cell therapy
Antibody-drug conjugates (ADCs)
Childhood cancer: precision medicine success story
Acute Lymphoblastic Leukaemia (ALL)
In the 1960s, childhood ALL had a survival rate of under 10%. Today, with precision genetic subtyping and risk-stratified chemotherapy, it exceeds 90% in high-income countries — one of oncology greatest achievements, made possible entirely through precision medicine.
- BCR-ABL fusion — imatinib (targeted) added to chemo
- ETV6-RUNX1 fusion — lower intensity, excellent prognosis
- High hyperdiploid — high drug sensitivity, reduce toxicity
In low-income countries, survival remains 30-50% — not because the biology differs, but because genetic testing and treatment access are limited.
Childhood Cancer
Every year, around 400,000 children and adolescents aged 0–19 are diagnosed with cancer worldwide.
Who counts as a "childhood cancer" patient?
There is no universally agreed upper age limit. The World Health Organization defines childhood and adolescent cancer as affecting those aged 0–19 years. Most national cancer registries split this further: 0–14 ("childhood") and 15–19 ("adolescent"). The broader Adolescent and Young Adult (AYA) category — widely used in clinical research — extends to age 39.
The 400,000 annual WHO figure covers the full 0–19 range. Restricting to 0–14 gives approximately 280,000–300,000 new cases per year. [WHO Childhood Cancer Fact Sheet, 2021] [Steliarova-Foucher et al., Lancet Oncol 2017]
Teenagers with cancer occupy an uncomfortable middle ground between paediatric and adult oncology — and outcomes reflect this. An adolescent with ALL treated on a paediatric protocol has significantly better survival than the same patient treated on an adult protocol, despite identical biology. [Barry et al., JCO 2012]
In many countries, 15–19 year olds are routinely admitted to adult wards and treated by adult oncologists with less experience of adolescent cancer types. Studies show paediatric oncology units achieve 10–20% better survival for shared cancer types. [Fidler et al., Lancet Oncol 2016]
Additional challenges specific to adolescents: lower clinical trial enrolment rates than younger children or adults; fertility preservation becoming relevant from puberty; treatment adherence difficulties; and distinct psychosocial needs (body image, school, peer isolation) that paediatric teams are better equipped to address.
Prevention & early detection
The honest answer: most cases are not preventable
Because the majority of childhood cancers result from random developmental mutations or inherited genetic conditions — not lifestyle choices — there is no meaningful primary prevention programme comparable to adult cancer prevention (smoking cessation, sunscreen, diet). Parents should not search for a cause they could have changed. [WHO, 2021]
What CAN reduce risk
HPV vaccination (adolescents)
The HPV vaccine prevents cervical cancer, and emerging evidence suggests it also reduces oropharyngeal and anal cancers caused by HPV. Given before sexual debut (recommended age 9–14 in most countries), it is >90% effective against the HPV strains that cause most HPV-related cancers. This is the single most impactful cancer prevention measure available to adolescents. [Lei et al., Lancet 2020]
Avoid unnecessary ionising radiation
Medical imaging radiation (CT, X-ray) is a weak but real risk. This does not mean avoiding necessary investigations — clinical benefit always outweighs risk. It does mean: CT scans should not be used when ultrasound or MRI would answer the clinical question equally well; dental X-rays should use the minimum necessary views; and paediatric CT protocols should use child-appropriate dose settings. [Pearce et al., Lancet Oncol 2012]
Genetic counselling for high-risk families
Families with Li-Fraumeni syndrome (TP53), hereditary retinoblastoma (RB1), BRCA1/2 carriers, neurofibromatosis (NF1), or Beckwith-Wiedemann syndrome have significantly elevated childhood cancer risk. Genetic counselling + surveillance programmes (regular MRI, ultrasound) can detect tumours at earlier, more treatable stages. If there is a strong family history of cancers across multiple family members at young ages, referral to a clinical geneticist is appropriate. [Ripperger et al., NEJM 2017]
Lifestyle — relevant from adolescence
For teenagers: not smoking, limiting alcohol, and maintaining a healthy weight are relevant because these behaviours begun in adolescence compound over decades. Alcohol is a Group 1 carcinogen at any age. Tobacco begun in teenage years is associated with higher lifetime risk than adult-onset smoking. Sunscreen use from childhood meaningfully reduces melanoma risk. These are not causes of most childhood cancers — but they matter for adult cancer risk being set during teenage years. [Sung et al., CA Cancer J Clin 2021]
Early detection: know the warning signs
Early detection is achievable — and it saves lives. The challenge is that childhood cancer symptoms often mimic common illnesses. The CCLG "HeadSmart" and ICCC campaigns use a mnemonic to help parents and GPs recognise warning signs. [CCLG UK]
Why do children get cancer?
Unlike most adult cancers, childhood cancers are almost never caused by lifestyle factors like smoking, diet, or alcohol. This is a critical distinction — parents should never feel that their child's cancer was preventable through different choices.
The causes are mostly related to genetic changes that occur during the rapid cell division of childhood development. In most cases, no specific cause can be identified.
Genetic predispositions
Certain inherited gene mutations significantly increase risk. Examples include BRCA1/2 (breast/ovarian), RB1 (retinoblastoma), TP53 (Li-Fraumeni syndrome), and NF1 (neurofibromatosis). These account for roughly 10% of childhood cancers. [Ripperger et al., NEJM 2017]
Random DNA copy errors
The majority of childhood cancers result from random mutations during DNA replication — unavoidable errors that accumulate during the extraordinarily rapid cell division of early development. These are not heritable and not preventable.
Chromosomal abnormalities
Down syndrome (trisomy 21) increases the risk of leukaemia by 10–20×. Other chromosomal conditions including Turner syndrome and Klinefelter syndrome are also associated with elevated cancer risk. [Hunger & Mullighan, NEJM 2015]
Environmental exposures (rare)
High-dose ionising radiation (including previous radiotherapy) increases risk. Some childhood cancer clusters near nuclear sites have been studied but causal links are not definitively established for most. Unlike adult cancers, environmental exposure plays a minor role overall.
Common childhood cancers
Click any cancer type to learn what it is, who it affects, how it's treated, and why drug delivery is particularly challenging.
Acute Lymphoblastic Leukaemia (ALL) — Most common, ~25% of cases
What it is: A cancer of the blood and bone marrow where immature white blood cells (lymphoblasts) multiply uncontrollably, crowding out normal blood cells. It progresses rapidly and requires urgent treatment. [Hunger & Mullighan, NEJM 2015] [Inaba & Pui, Nat Rev Cancer 2021]
Who gets it: Peak incidence is ages 2–5. ALL accounts for ~75% of all childhood leukaemia. Boys are slightly more affected than girls. Children with Down syndrome have a 20× higher risk.
Warning signs: Persistent fever · unexplained bruising or bleeding · pallor · extreme fatigue · bone/joint pain · swollen lymph nodes · recurrent infections.
Treatment: Chemotherapy in three phases — induction (remission), consolidation (eliminate remaining cells), maintenance (2–3 years). CNS prophylaxis prevents brain spread. Targeted therapy (imatinib) added for BCR-ABL fusion subtype. CAR-T for relapsed cases. Bone marrow transplant in high-risk or relapsed disease.
Brain & CNS tumours — 2nd most common, ~20% of cases
What it is: A broad category including medulloblastoma (most common malignant brain tumour in children, arising in the cerebellum), gliomas (astrocytoma, glioblastoma), ependymoma, and DIPG (diffuse intrinsic pontine glioma — one of the most treatment-resistant cancers known).
Who gets it: Brain tumours can occur at any childhood age. Medulloblastoma peaks at 3–8 years. DIPG almost exclusively affects children aged 5–10. Together, brain tumours are the leading cause of cancer-related death in children. [Pollack et al., Nat Rev Clin Oncol 2019]
Warning signs: Morning headaches (worse on waking) · vomiting without nausea · balance/gait changes · vision changes · personality or behaviour change · new seizures. These are often subtle and initially misdiagnosed.
Treatment: Surgery (where accessible) + radiation + chemotherapy. Medulloblastoma: molecular subgrouping now guides treatment intensity. DIPG has no effective standard treatment — radiation buys time, but median survival remains ~11 months despite decades of research. [Vanan & Eisenstat, Front Oncol 2015] Convection-enhanced delivery (CED) is being trialled to bypass the blood-brain barrier.
Neuroblastoma — ~8% of cases, most common solid tumour in infants
What it is: A cancer of immature nerve cells (neuroblasts), most commonly arising in the adrenal glands (above the kidneys) or along the sympathetic nervous system. Biologically unique: some tumours spontaneously regress, while others are among the most aggressive childhood cancers.
Who gets it: Almost exclusively children under 5 (median diagnosis age: 17 months). Around 40% of cases have metastasised at diagnosis. MYCN gene amplification identifies high-risk cases. [Matthay et al., JCO 2023]
Warning signs: Abdominal mass or swelling · dark circles around eyes (periorbital bruising, "raccoon eyes") · bone pain · lump in neck or chest · high blood pressure · persistent diarrhoea · unusual eye movements (opsoclonus).
Treatment: Low-risk: surgery alone or observation. High-risk: intensive chemotherapy + surgery + radiation + high-dose chemo with stem cell rescue + immunotherapy (anti-GD2 antibody dinutuximab) + isotretinoin. Despite aggressive treatment, high-risk neuroblastoma has only ~50% long-term survival. [Matthay et al., JCO 2023]
Wilms Tumour (Nephroblastoma) — most common kidney cancer in children
What it is: A kidney tumour arising from embryonic kidney cells (metanephric blastema) that failed to differentiate normally. One of oncology's great success stories — survival has risen from under 30% in the 1960s to over 90% today through multimodal treatment. [Dome et al., ASCO Ed Book 2019]
Who gets it: Peak age 3–4 years. Usually presents as a painless abdominal mass. Associated with WAGR syndrome, Beckwith-Wiedemann syndrome, and Denys-Drash syndrome. Bilateral (both kidneys) in ~5–10% of cases.
Warning signs: Painless abdominal swelling or mass (often discovered by a parent during bathing) · abdominal pain · blood in urine (haematuria) · high blood pressure · fever.
Treatment: Surgery (nephrectomy) + chemotherapy (vincristine, actinomycin D, doxorubicin depending on stage) ± radiation for advanced stages. The SIOP (European) protocol uses pre-operative chemo to shrink the tumour before surgery. Overall survival exceeds 90% — a benchmark for what childhood cancer treatment can achieve.
Retinoblastoma — most common eye tumour in children
What it is: A malignant tumour of the retina, caused by mutation or deletion of both copies of the RB1 tumour suppressor gene. Around 40% of cases are hereditary (germline RB1 mutation) — these children have bilateral disease and are at lifelong risk of other cancers. [Dimaras et al., Nat Rev Dis Primers 2015]
Who gets it: Almost exclusively infants and young children — median diagnosis age 18 months. Bilateral in ~40% of hereditary cases. One of the most treatable childhood cancers when caught early.
Warning signs: White pupil reflex in photographs (leukocoria) — the single most important sign. If a flash photo shows one pupil glowing white instead of red, see a doctor immediately. Also: squinting (strabismus) · red or swollen eye · vision loss.
Treatment: Depends on stage. Small tumours: laser photocoagulation or cryotherapy. Moderate: intra-arterial chemotherapy (direct injection into the ophthalmic artery), intra-vitreal chemotherapy. Advanced: systemic chemotherapy + enucleation (eye removal) as last resort. Survival >95% in high-income countries; eye salvage rates now >80% with modern techniques. [Dimaras et al., Nat Rev Dis Primers 2015]
Bone tumours: Osteosarcoma & Ewing sarcoma — ~5% of cases
What they are: Osteosarcoma is the most common primary bone cancer, arising from bone-forming cells (osteoblasts), most commonly in the metaphysis of long bones near the knee or shoulder. Ewing sarcoma arises from primitive neuroectodermal cells, can occur in any bone, and is characterised by the EWS-FLI1 chromosomal translocation. [Luetke et al., Skeletal Radiol 2014]
Who gets it: Both peak during adolescence (10–20 years) — coinciding with puberty-driven bone growth spurts, which may explain the association. Osteosarcoma is more common in males. Ewing sarcoma disproportionately affects white children.
Warning signs: Persistent localised bone pain (especially at night) · swelling near a bone · unexplained limb pain · fracture from minor injury. Often initially misdiagnosed as growing pains.
Treatment: Both: neoadjuvant chemotherapy (before surgery) + surgical resection (limb-sparing where possible) + adjuvant chemotherapy. Ewing: often radiation as well. Key drugs: osteosarcoma uses MAP regimen (methotrexate, doxorubicin, cisplatin); Ewing uses VIDE/VAI regimens. Histological response to neoadjuvant chemo is the strongest prognostic factor.
Hodgkin Lymphoma — highly treatable, >95% survival
What it is: A cancer of the lymphatic system characterised by the presence of Reed-Sternberg cells. Hodgkin lymphoma (HL) is one of the most curable cancers — it represents one of the earliest examples of chemotherapy curing a cancer. Non-Hodgkin lymphoma (NHL) in children is a distinct group with different biology and treatment. [Castellino et al., JCO 2014]
Who gets it: Two peaks — adolescence/young adulthood and >55 years. EBV (Epstein-Barr virus) infection is associated with some subtypes. More common in males. Immunosuppressed children (HIV, organ transplant) have higher risk.
Warning signs: Painless enlarged lymph nodes (neck, armpit, groin) · "B symptoms" — drenching night sweats, unexplained fever, unintentional weight loss >10% · itching without rash · shortness of breath (mediastinal mass).
Treatment: ABVD chemotherapy regimen (adriamycin, bleomycin, vinblastine, dacarbazine) ± radiation. Modern protocols use response-adapted therapy (PET scan after 2 cycles guides whether radiation is needed). 5-year survival >95% for early stage, ~85% for advanced. Long-term side effects (cardiac, pulmonary, secondary cancers) from radiation are now a major focus of treatment reduction research. [Castellino et al., JCO 2014]
How childhood cancer is diagnosed
Early and accurate diagnosis is the single most important factor in childhood cancer outcomes. The diagnostic pathway typically involves several steps.
Blood tests & bone marrow biopsy
Full blood count (FBC) is usually the first test — leukaemias often show abnormal white cell counts, anaemia, or thrombocytopenia. A bone marrow biopsy (aspirate + trephine) is required to confirm leukaemia diagnosis, assess blast percentage, and collect material for genetic testing. Results typically within 24–48 hours for FBC, 1–2 weeks for full genetic panel.
Imaging (CT, MRI, PET, ultrasound)
CT scans show tumour location, size, and whether it has spread to lymph nodes or organs. MRI provides better soft tissue detail — essential for brain tumours. PET scans (using radiolabelled glucose) show metabolically active cancer tissue and are standard in lymphoma staging. Ultrasound is first-line for abdominal masses — quick, no radiation, readily available.
Biopsy & histopathology
Tissue biopsy is required for most solid tumours — a small sample is removed (needle biopsy or surgical) and examined under a microscope by a pathologist. This confirms the cancer type, grade, and growth rate. Results typically take 1–2 weeks. In DIPG, biopsy has historically been avoided due to surgical risk, but is now increasingly performed at specialist centres.
Genetic & molecular testing
This is where precision medicine transforms outcomes. FISH, PCR, and next-generation sequencing (NGS) identify specific chromosomal translocations, gene fusions (BCR-ABL, EWS-FLI1), copy number variations (MYCN amplification), and point mutations. These results determine risk group, treatment intensity, and eligibility for targeted therapies. Takes 2–4 weeks but is now standard of care in high-income countries.
Lumbar puncture (spinal tap)
Used in leukaemia and brain tumours to check whether cancer cells have entered the cerebrospinal fluid (CSF). A needle is inserted into the lower spine under local anaesthetic. If CNS disease is confirmed, additional intrathecal chemotherapy (injected directly into the CSF) is added to treatment.
How childhood cancer is treated
Most children receive a combination of treatments. The specific regimen depends on cancer type, genetic subtype, stage, and the child's age and general health. Treatment decisions are always made by a multidisciplinary team.
The backbone of most childhood cancer treatment. Drugs are given in cycles — periods of treatment followed by recovery. Common regimens: ABVD (lymphoma), MAP (osteosarcoma), VIDE (Ewing), multidrug protocols for ALL. Children generally tolerate chemotherapy better than adults due to greater bone marrow reserve and organ resilience, but long-term side effects (growth, fertility, cardiac, secondary cancers) remain a serious concern.
Aims to remove the primary tumour while preserving as much function as possible. Limb-sparing surgery has replaced amputation for most bone tumours. Tumour surgery is ideally performed at specialist centres with paediatric surgical expertise. Pre-operative (neoadjuvant) chemotherapy is often used first to shrink tumours and improve surgical outcomes.
Uses high-energy X-rays to destroy cancer cells. Essential for brain tumours, Ewing sarcoma, and some lymphomas. Modern techniques (proton therapy, stereotactic radiosurgery) target tumours precisely, minimising radiation to surrounding developing tissue. Avoided or minimised in very young children when possible due to effects on brain development.
Imatinib for BCR-ABL+ ALL · Anti-GD2 (dinutuximab) for neuroblastoma · CAR-T (tisagenlecleucel/Kymriah — FDA-approved for paediatric ALL) · Checkpoint inhibitors in some lymphomas. Targeted therapies are only effective when the specific molecular target is present — reinforcing the importance of genetic testing at diagnosis.
The global survival gap
The same childhood cancer has dramatically different outcomes depending on where a child is born. This is not biology — it is access to diagnosis, treatment, and expertise.
The gap exists because of three interconnected problems. First, late diagnosis — in low-income settings, children present at far more advanced stages because access to imaging and laboratory testing is limited and awareness among primary care doctors is lower. Second, treatment abandonment — families cannot afford prolonged hospital stays, drug costs, or travel. Around 30–60% of children in some LMICs abandon treatment before completion. [Gupta et al., Lancet Oncol 2015] Third, drug availability — even where treatment is theoretically affordable, supply chain failures mean critical chemotherapy agents are frequently unavailable.
Organisations working to close this gap focus on improving diagnostic capacity, training local oncologists, subsidising treatment costs, and ensuring drug supply reliability. The science is largely solved — the challenge is delivery. [Lam et al., Nat Med 2022]
We are proud to support: World Child Cancer
Our Vision is a world where every child with cancer, wherever they live, has timely access to the highest quality treatment, care and support to allow them to survive and thrive.
Our Mission is to improve survival rates, care and quality of life for children with cancer and their families in low and middle-income countries. We will do this through evidence-led programmes, impactful collaborations, and influencing policy change.
Learn more about World Child Cancer and their global collaborators at worldchildcancer.org.
Your donation could support early and accurate diagnosis, by helping train healthcare workers to spot the early warning signs of cancer.
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Patient stories
Further Reading
Want to go deeper? Here are the journals where the science on this site comes from. All are freely accessible in some form — either open access, or via your local library.
The journals we use
How to read a scientific paper if you're not a scientist
Start with the Abstract (one paragraph summary at the top) and the Discussion section at the end — skip the Methods entirely on first read. In the Results section, look at the figures rather than the text. If a number seems important, check the confidence interval or p-value nearby; if either looks uncertain, the finding is probably preliminary.
Be sceptical of single studies, especially in cancer biology where replication is often difficult. The highest-quality evidence comes from systematic reviews and meta-analyses, which pool data from many studies. If something is described as "shown in a mouse model" or "in vitro" (in a dish), it hasn't yet been tested in humans — which matters a lot in oncology.
About PDEOutreach
PDEOutreach is a free cancer science education platform built by students, for everyone. We turn the research behind PDEOncology — using partial differential equations to simulate how drugs move through tumours — into interactive experiences that anyone can understand. No medical degree required.
Who we are
我们都是17岁。癌症治疗背后的科学，不该只属于买得起期刊的人，或坐在大学课堂里的学生。无论身在何处，患者、家属和任何感到好奇的人，都应当有机会了解肿瘤内部究竟发生了什么，以及为什么治疗有时有效，有时却不奏效。
A charity we're proud to support
We chose World Child Cancer because their mission directly mirrors what this site is about: the survival gap between high-income and low-income countries is not a biological problem — it is an access problem. The science is largely solved. WCC works on the delivery.
Every article on this site is free because we believe knowledge shouldn't be gated. Every donate button points to WCC because knowledge, without action, isn't enough. If what you've read here has moved you — please consider donating.
我们为何建立这个平台
研究人员掌握的知识与公众对癌症的认知之间，存在巨大的落差。大多数人不知道，化疗失败往往不是因为药物失效，而是它在物理层面根本到不了目标细胞。同样的诊断、同样的药，两个患者却可能因肿瘤生物学的差异走向截然不同的结局——这一点，大多数人同样不了解。
我们希望尽一份力，缩小这个落差。PDEOutreach 是 PDEOncology.com 的公众科普平台——PDEOncology 是一个用偏微分方程模拟实体肿瘤药物渗透过程的研究工具。