Not every patient is the same. Neither is their cancer.
Tumours of the same name behave differently. Two patients with "breast cancer" can have opposite drug sensitivities, different surgical paths, and very different outcomes. POLEX brings chromosomal-fragility data into that decision.
Why it matters
One drug doesn't fit every patient.
Disease is heterogeneous. Cancer, neurodegeneration, ageing, gene therapy: response varies even when the diagnosis is identical. Oncology shows the principle most starkly. The numbers below are from cancer, but the same logic holds across disease.
30-50%of chemotherapy patients do not respond
15-20%of cancers are HRD, PARPi-sensitive
14%of solid tumors are MSI-H, IO-responsive
~3%of TP53 mutations change treatment
Genomic instability is heterogeneous across tumours. The same drug that cures one patient can be useless in another with the same histology diagnosis. Molecular context changes everything: which chromosomes, which breakpoints, which repair pathways.
The hypothesis
Chromosomes break where they were already fragile.
Cancers have distinct patterns of chromosomal instability. BRCA1/2-deficient tumours break around 17q21 and 13q12. Pancreatic cancers accumulate damage around KRAS on 12p and CDKN2A on 9p. Small-cell lung carcinomas destabilise RB1 on 13q and TP53 on 17p. Ewing sarcomas are defined by the EWSR1-FLI1 t(11;22) fusion.
When you map breaks at base resolution, not just at calling-panel hotspots, these patterns read as clean genomic fingerprints.
Fragile-site signatures
FRA3BFHIT · 60% of tumours
FRA16DWWOX · breast, prostate, lung
8p21-23Common deletion region
17p13 (TP53)Pan-cancer hotspot
3p21Renal, lung, head & neck
The break atlas
50 cancers, 50 break fingerprints.
Each card shows representative break-burden density, affected chromosomes and genes, drug-class sensitivity, treatment mix, and expected response. Click a category to filter.
Progeroid syndromes: DNA repair, broken at the source.
Helicase loss, NER defects, nuclear lamina disruption. When repair fails in every cell, the body ages decades early. 15 canonical progerias.
Restrictive dermopathy
High severity
0100break burden / Mb
Affected regions
ZMPSTE24 · LMNA · Nuclear lamina
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
40% Sym40% Prev20% Cure
Symptom control
8%
OnsetAt birth
ProgressionVery rapid
PrimarySupportive
Hutchinson-Gilford progeria
High severity
0100break burden / Mb
Affected regions
LMNA (1q22) · Nuclear lamina
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym30% Prev15% Cure
Symptom control
15%
Onset<2 yr
ProgressionVery rapid
PrimaryFarnesyl-TI
Nestor-Guillermo progeria
High severity
0100break burden / Mb
Affected regions
BANF1 (11q13) · Nuclear envelope
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym30% Prev15% Cure
Symptom control
15%
Onset<5 yr
ProgressionRapid
PrimarySupportive
Wiedemann-Rautenstrauch
High severity
0100break burden / Mb
Affected regions
POLR3A · RNA Pol III
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
60% Sym30% Prev10% Cure
Symptom control
15%
OnsetAt birth
ProgressionRapid
PrimarySupportive
Cockayne syndrome A
High severity
0100break burden / Mb
Affected regions
ERCC8 (5q12) · TC-NER
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
60% Sym30% Prev10% Cure
Symptom control
18%
Onset<2 yr
ProgressionRapid
PrimarySupportive
Cockayne syndrome B
High severity
0100break burden / Mb
Affected regions
ERCC6 (10q11) · TC-NER
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
60% Sym30% Prev10% Cure
Symptom control
18%
Onset<2 yr
ProgressionRapid
PrimarySupportive
Seckel syndrome
High severity
0100break burden / Mb
Affected regions
ATR (3q23) · CENPJ · DDR / rep stress
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
60% Sym30% Prev10% Cure
Symptom control
20%
OnsetAt birth
ProgressionProgressive
PrimarySupportive
Xeroderma pigmentosum A
High severity
0100break burden / Mb
Affected regions
XPA (9q22) · GG-NER
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
50% Sym40% Prev10% Cure
Symptom control
22%
Onset<5 yr
ProgressionProgressive
PrimaryPreventive
Nijmegen breakage syn.
High severity
0100break burden / Mb
Affected regions
NBN (8q21) · MRN / DSB
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym30% Prev15% Cure
Symptom control
22%
Onset<2 yr
ProgressionProgressive
PrimarySupportive
Werner syndrome
High severity
0100break burden / Mb
Affected regions
WRN (8p12) · HR / replication
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym30% Prev15% Cure
Symptom control
25%
Onset20-30 yr
ProgressionRapid
PrimarySupportive
Xeroderma pigmentosum C
High severity
0100break burden / Mb
Affected regions
XPC (3p25) · GG-NER
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
50% Sym40% Prev10% Cure
Symptom control
25%
Onset<10 yr
ProgressionProgressive
PrimaryPreventive
Bloom syndrome
High severity
0100break burden / Mb
Affected regions
BLM (15q26) · HR
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym30% Prev15% Cure
Symptom control
28%
Onset0-5 yr
ProgressionProgressive
PrimarySupportive
Rothmund-Thomson
High severity
0100break burden / Mb
Affected regions
RECQL4 (8q24) · Replication / HR
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym35% Prev10% Cure
Symptom control
30%
Onset<2 yr
ProgressionProgressive
PrimarySupportive
Trichothiodystrophy
Mid severity
0100break burden / Mb
Affected regions
ERCC2 · ERCC3 · GTF2H5 · NER
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
65% Sym25% Prev10% Cure
Symptom control
30%
Onset<1 yr
ProgressionProgressive
PrimarySupportive
Xeroderma pigmentosum V
Mid severity
0100break burden / Mb
Affected regions
POLH / XPV (6p21) · TLS
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
55% Sym35% Prev10% Cure
Symptom control
40%
Onset10-30 yr
ProgressionSlow
PrimaryPreventive
Immunodeficiency
When V(D)J breaks don’t resolve, immunity doesn’t form.
Lymphocyte diversity depends on programmed double-strand breaks. Cells break the DNA deliberately and rejoin it. Failures in NHEJ, class-switch, or ICL repair produce severe immune phenotypes. 15 cases.
Ataxia-telangiectasia
High severity
0100break burden / Mb
Affected regions
ATM (11q22) · DSB signalling
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
50% Sym35% Prev15% Cure
Symptom control
30%
Onset<5 yr
ProgressionProgressive
PrimarySupportive
Bloom syndrome
High severity
0100break burden / Mb
Affected regions
BLM (15q26) · HR / replication
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
45% Sym35% Prev20% Cure
Symptom control
35%
Onset<5 yr
ProgressionProgressive
PrimarySupportive
Fanconi anaemia
High severity
0100break burden / Mb
Affected regions
FANC-A/C/G/D2 · ICL (FA)
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
40% Sym35% Prev25% Cure
Symptom control
38%
Onset<10 yr
ProgressionProgressive
PrimaryBone-marrow-Tx
Nijmegen breakage syn.
High severity
0100break burden / Mb
Affected regions
NBN (8q21) · MRN / DSB
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
30% Sym35% Prev35% Cure
Symptom control
40%
Onset<2 yr
ProgressionProgressive
PrimarySupportive
ATLD (MRE11 def.)
High severity
0100break burden / Mb
Affected regions
MRE11A (11q21) · MRN
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
30% Sym40% Prev30% Cure
Symptom control
40%
Onset2-5 yr
ProgressionProgressive
PrimarySupportive
RIDDLE syndrome
High severity
0100break burden / Mb
Affected regions
RNF168 (3q29) · Ubiquitin DSB
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
30% Sym40% Prev30% Cure
Symptom control
42%
Onset<5 yr
ProgressionProgressive
PrimarySupportive
Ligase IV syndrome
High severity
0100break burden / Mb
Affected regions
LIG4 (13q33) · NHEJ ligation
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
25% Sym35% Prev40% Cure
Symptom control
45%
Onset<2 yr
ProgressionProgressive
PrimarySupportive
Cernunnos/XLF def.
High severity
0100break burden / Mb
Affected regions
NHEJ1 (2q35) · NHEJ ligation
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
20% Sym35% Prev45% Cure
Symptom control
50%
Onset<2 yr
ProgressionProgressive
PrimaryBone-marrow-Tx
DNA-PKcs deficiency
High severity
0100break burden / Mb
Affected regions
PRKDC (8q11) · NHEJ / DNA-PK
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
20% Sym30% Prev50% Cure
Symptom control
55%
Onset<1 yr
ProgressionRapid
PrimaryBone-marrow-Tx
Artemis SCID
High severity
0100break burden / Mb
Affected regions
DCLRE1C (10p13) · NHEJ hairpin
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
15% Sym25% Prev60% Cure
Symptom control
65%
Onset<1 yr
ProgressionRapid
PrimaryBone-marrow-Tx
SCID — RAG1 deficiency
High severity
0100break burden / Mb
Affected regions
RAG1 (11p13) · V(D)J
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
10% Sym25% Prev65% Cure
Symptom control
70%
Onset<1 yr
ProgressionRapid
PrimaryBone-marrow-Tx
SCID — RAG2 deficiency
High severity
0100break burden / Mb
Affected regions
RAG2 (11p13) · V(D)J
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
10% Sym25% Prev65% Cure
Symptom control
70%
Onset<1 yr
ProgressionRapid
PrimaryBone-marrow-Tx
XLP / SH2D1A
Mid severity
0100break burden / Mb
Affected regions
SH2D1A (Xq25) · Immune signalling
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
25% Sym40% Prev35% Cure
Symptom control
65%
OnsetChildhood
ProgressionVariable
PrimaryBone-marrow-Tx
Hyper-IgM Type 5 (UNG)
Mid severity
0100break burden / Mb
Affected regions
UNG (12q24) · BER
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
20% Sym35% Prev45% Cure
Symptom control
72%
Onset2-5 yr
ProgressionSlow
PrimaryIgG replacement
Hyper-IgM Type 2 (AID)
Mid severity
0100break burden / Mb
Affected regions
AICDA (12p13) · Class-switch
Therapeutic approach
Gene-RxBMTTargetedSupportive
Care pattern
20% Sym30% Prev50% Cure
Symptom control
75%
Onset2-5 yr
ProgressionSlow
PrimaryIgG replacement
Signal → diagnosis
POLEX as a diagnostic marker.
Our output is not a disease label. It is a quantitative fingerprint that places a tumour on a continuous axis of chromosomal fragility. Where on that axis a patient sits informs which drugs, which dose, which monitoring cadence.
PREDICT
HRD probability
From per-read break signatures, estimate homologous-repair deficiency in minutes. No reflex panel wait.
STRATIFY
Drug sensitivity score
A single score per drug class (PARPi, platinum, IO, targeted) from the fragility fingerprint.
MONITOR
Repair kinetics
Track break accumulation across time points. Early signal for resistance, progression, or repair failure.
STAGE
Chromosomal fragility index
A reproducible, quantitative marker that can stratify clinical trials and standardise cross-study comparisons.
Want to pilot POLEX in your clinic or study?
We run sample pilots with clinical investigators and pharmaceutical partners. Typical turnaround from sample to break atlas is seven days.