• The "traditional" adenoma-carcinoma sequence as described above (Vogelstein model)
• Characterised by aneuploidy (abnormal chromosome numbers) and loss of heterozygosity (LOH) at tumour suppressor loci (APC, TP53, SMAD4)
• Higher risk in large (> 2.5 cm), villous, sessile adenomatous polyps ^[3]
• Predominantly left-sided tumours
• Tends to have KRAS mutations and be microsatellite stable (MSS)

• Caused by defective DNA mismatch repair (MMR) system ^[1][7][10]
• MMR genes (MLH1, MSH2, MSH6, PMS2) normally correct errors during DNA replication — specifically insertion-deletion loops at microsatellite repeats (short tandem repeat sequences)
• When MMR is defective → errors accumulate at microsatellites → "microsatellite instability"
• Two mechanisms of MMR deficiency:
  • Germline mutation in MMR genes → Lynch syndrome (HNPCC) ^[7]
  • Sporadic epigenetic silencing of MLH1 by promoter hypermethylation (CpG island methylator phenotype, CIMP) → accounts for ~12% of sporadic CRC
• Predominantly right-sided tumours
• Often poorly differentiated, mucinous, with dense lymphocytic infiltration (because the high mutation burden generates neoantigens that attract immune cells)
• Better stage-for-stage prognosis than MSS tumours
• MSI-high tumours respond well to immune checkpoint inhibitors (e.g. pembrolizumab/nivolumab) ^[4][5] — this is because the high neoantigen load makes them immunogenic
• BRAF V600E mutation is common in sporadic MSI-H tumours (but NOT in Lynch syndrome) — this is a useful distinguishing feature ^[1][4][5]

• Autosomal dominant; germline mutation in APC gene (chromosome 5q21) ^[7]
• Hundreds to thousands of adenomatous polyps throughout the colon — classically > 100 polyps
• Virtually 100% lifetime risk of CRC if untreated (average age of cancer development ~39 years)
• Extracolonic manifestations: duodenal adenomas (most common extracolonic malignancy), desmoid tumours, osteomas (mandible), congenital hypertrophy of retinal pigment epithelium (CHRPE), epidermoid cysts, supernumerary teeth
  • Gardner syndrome: FAP + osteomas + desmoid tumours + epidermoid cysts
  • Turcot syndrome: FAP + CNS tumours (medulloblastoma in FAP variant; glioblastoma in Lynch variant)
• Management: prophylactic colectomy (usually proctocolectomy with ileal pouch-anal anastomosis) recommended by age 20-25, or when polyps become numerous
• Attenuated FAP (AFAP): < 100 polyps, later onset, similar genetics but different mutation location on APC gene

• Autosomal dominant; germline mutations in DNA mismatch repair (MMR) genes: MLH1, MSH2, MSH6, PMS2 ^[7]
• Most common hereditary CRC syndrome (~3-5% of all CRC)
• Lifetime CRC risk: 40-80% (lower than FAP but still very high)
• Right-sided predominance, younger onset (mean age ~45)
• Associated extracolonic cancers: endometrial (most common, 40-60% lifetime risk), ovarian, gastric, urinary tract (renal pelvis/ureter), small bowel, hepatobiliary, brain (Turcot variant), sebaceous skin tumours (Muir-Torre variant)
• Characterised by MSI-high, better prognosis stage-for-stage, responds to immunotherapy
• Amsterdam II is a family-history suspicion rule, not a molecular diagnosis or a prerequisite for universal tumour testing (3-2-1 rule):
  • 3 or more relatives with CRC, endometrial, small-bowel, ureteric or renal-pelvis cancer (the specific Amsterdam II list)
  • 2 or more successive generations affected
  • 1 or more diagnosed before age 50
  • One should be a first-degree relative of the other two
  • FAP should be excluded and tumours verified pathologically

All newly diagnosed CRC should undergo universal MMR/MSI testing (by IHC for MMR proteins or PCR for MSI) to screen for Lynch syndrome and guide immunotherapy decisions ^[4][5][7]

• MUTYH-Associated Polyposis (MAP): autosomal recessive, 10-100 adenomatous polyps, resembles attenuated FAP
• Peutz-Jeghers Syndrome (PJS): autosomal dominant, STK11/LKB1 mutation, hamartomatous polyps + mucocutaneous pigmentation (lips, buccal mucosa, fingers), increased risk of GI and extra-GI cancers
• Juvenile Polyposis Syndrome (JPS): hamartomatous polyps, increased CRC risk
• Serrated Polyposis Syndrome: multiple serrated polyps, increased CRC risk

Why does the right side present later?

• The caecum and ascending colon have a large diameter (~7.5 cm) and distensible walls → tumours can grow to a large size before causing symptoms
• Stool content is still liquid at the right colon → does not obstruct
• Bleeding is slow and chronic (tumour surface oozes) → iron deficiency develops insidiously → patients present with anaemia symptoms (fatigue, pallor, dyspnoea) rather than obvious bleeding
• Pain is vague and dull (stretching of the visceral peritoneum) — often misdiagnosed as "IBS" or "functional pain"

Why does the left side present earlier?

• The descending colon and sigmoid have a narrower calibre (~2.5-3 cm)
• Stool is solid and formed → annular constricting lesion narrows the lumen → change in bowel habit (alternating constipation and diarrhoea), tenesmus, and eventually complete obstruction
• Bleeding is frank because solid stool rubs against the tumour surface

• Alternating diarrhoea and constipation ^[2][11] — the tumour causes partial obstruction; stool accumulates proximally, then is forced through → diarrhoea-like episode
• Reduced stool calibre ("pencil-thin stools") ^[2][11] — tumour narrows the lumen
• Tenesmus ^[2][3][11] — sensation of incomplete evacuation; particularly with rectal tumours (tumour mass is perceived as residual stool by stretch receptors in the rectal wall)
• Passage of mucus ^[2][11] — villous adenomas and mucinous carcinomas can secrete copious mucus → mucus per rectum (sometimes leading to hypokalaemia from potassium-rich mucus loss — "mucus-secreting villous adenoma causing depletion syndrome")
• Urgency/incontinence — especially with low rectal tumours that compromise anal sphincter function

• Haematochezia (fresh blood per rectum) — more common with left-sided and rectal tumours ^[2][3][11]
  • Mechanism: solid stool abrading the tumour surface → mucosal ulceration → bleeding from tumour vasculature
  • Blood is typically mixed with stool (cf. haemorrhoids where blood is on the surface or after defecation)
• Occult bleeding — more common with right-sided tumours → detected by faecal immunochemical test (FIT) or presenting as iron deficiency anaemia
• Melaena — rare, only if bleeding is brisk from a right-sided tumour and transit time is slow

• Right-sided: dull, vague, poorly localised aching pain in the right abdomen → visceral pain from distension of the caecum or tumour necrosis ^[3]
• Left-sided: colicky pain (cramping), worse before defecation → partial obstruction causing increased peristalsis against the obstructing lesion
• Rectal: deep pelvic pain, sacral pain (invasion of sacral nerve plexus) — indicates locally advanced disease

• Weight loss, anorexia, malaise/fatigue ^[2][3][11] — due to chronic illness, cancer-related cachexia (tumour-derived cytokines: TNF-α, IL-6 → muscle wasting and catabolism), and chronic blood loss
• Fever — can occur with tumour necrosis, secondary infection (abscess formation), or perforation

• Jaundice, right upper quadrant discomfort → hepatic metastases ^[2][11]
• Dyspnoea, cough → pulmonary metastases ^[2][11]
• Bone pain → skeletal metastases ^[2][11]
• Ascites → peritoneal carcinomatosis ^[2][11]
• Irritative urinary symptoms (dysuria, pneumaturia, faecaluria) → colovesical fistula from tumour invading bladder ^[2][11]
• Intractable pain (sacral nerve invasion) → locally advanced rectal cancer invading presacral plexus ^[2][11]

• Acute intestinal obstruction: colicky abdominal pain, absolute constipation (no flatus or faeces), abdominal distension, vomiting (late — faeculent vomiting in LBO) ^[11]
• Perforation: sudden severe abdominal pain, generalised peritonitis, shock → either at the tumour site or at the caecum (closed-loop obstruction if ileocaecal valve is competent → caecal distension → perforation at the weakest point, per Laplace's law)
• Massive haemorrhage: rare but can be life-threatening

• Pallor — due to iron deficiency anaemia from chronic occult blood loss (especially right-sided tumours)
• Cachexia/wasting — in advanced disease; loss of temporal fat pads, muscle wasting
• Lymphadenopathy — left supraclavicular node (Virchow's node / Troisier's sign) → indicates advanced intra-abdominal malignancy with spread via the thoracic duct ^[3]
• Jaundice — liver metastases causing biliary obstruction
• Peripheral oedema — hypoalbuminaemia from cancer cachexia or liver metastases

• Abdominal mass — particularly right-sided tumours which can grow to a large palpable mass before symptoms develop; typically firm, irregular, non-tender (unless complicated), may be fixed or mobile
• Hepatomegaly — irregular, hard, nodular liver edge → liver metastases; may have a hepatic bruit (rarely)
• Ascites — shifting dullness, fluid thrill → peritoneal carcinomatosis or liver metastases with portal hypertension
• Abdominal distension — if large bowel obstruction
• Visible peristalsis — in obstruction, with colicky pain
• Tenderness, guarding, rigidity — if perforation or local peritonitis

• Palpable rectal mass: hard, irregular, friable (bleeds on palpation), may be ulcerated
• Fixed vs mobile: a fixed mass suggests invasion into perirectal tissues or presacral structures
• Blumer's shelf — palpable hard nodule in the pouch of Douglas (peritoneal metastasis)
• Blood/mucus on glove — occult or gross bleeding
• Sphincter tone assessment — low rectal tumours may compromise the external sphincter

• Obstruction: abdominal distension, tympanic percussion, high-pitched tinkling bowel sounds with rushes (early) → absent bowel sounds (late)
• Perforation: peritonism (board-like rigidity, rebound tenderness, absent bowel sounds), tachycardia, hypotension, fever
• Fistula: pneumaturia, faecaluria (colovesical fistula), faeculent vaginal discharge (colovaginal fistula)

• Koilonychia (spoon-shaped nails)
• Angular cheilitis (cracking at corners of mouth)
• Glossitis (smooth, painful tongue)
• Pallor of conjunctivae, palms, nail beds

• Acanthosis nigricans — velvety, dark, thickened skin in axillae and neck folds; associated with GI malignancies
• Dermatomyositis — heliotrope rash, Gottron's papules, proximal muscle weakness; strong association with underlying malignancy (especially in older patients)
• Thrombophilia / Trousseau syndrome — migratory thrombophlebitis; malignancy-associated hypercoagulability (tumour produces tissue factor and mucin → activates coagulation cascade) → DVT, PE ^[12]

"Colonoscopy" = "colon" + "-oscopy" (Greek skopein = to look at) — literally, looking at the colon.

Colonoscopy is the most accurate and versatile diagnostic tool for CRC ^[2]. It is both diagnostic (visualisation + biopsy) and therapeutic (polypectomy, stenting).

Indications for colonoscopy (in the CRC context) ^[20]:

• Lower GI symptoms: altered bowel habit, PR bleeding, chronic diarrhoea, abdominal pain
• Positive faecal occult blood (FIT/FOBT)
• Iron deficiency anaemia
• Abnormal imaging (CT finding of colonic wall thickening or mass)
• Screening/surveillance purposes (FAP, Lynch, IBD, post-polypectomy, post-CRC resection)
• Palliative stenting for malignant obstruction

What to look for — Endoscopic appearance ^[2]:

• Majority are endoluminal masses — exophytic or polypoid — but occasionally can be flat ^[2]
• May have bleeding (oozing/frank bleeding) in friable, necrotic, or ulcerative masses ^[2]
• May be circumferential → may obstruct distal scoping ^[2] (i.e. you cannot pass the scope beyond a tight annular tumour)
• Right-sided: more likely fungating/polypoid
• Left-sided: more likely annular/constricting ("apple-core" morphology)

Biopsy ^[2][3]:

• Biopsies, brushings, or polypectomy ^[2]
• Important to tattoo location at polypectomy for future surgical resection if proven to be invasive carcinoma ^[2] — because after polypectomy, the site heals and becomes indistinguishable from surrounding mucosa; the tattoo (India ink/SPOT) allows the surgeon to localise the site intraoperatively
• Especially important in distal rectal CA as anorectal squamous cell carcinoma (SCC) is treated by upfront chemoradiotherapy instead of surgery ^[2] — the histological distinction between adenocarcinoma (from rectal mucosa) and SCC (from anal squamous epithelium) fundamentally changes the treatment approach

Histological patterns with prognostic significance ^[2]:

• Mucinous carcinoma and poorly differentiated carcinoma are associated with poorer prognosis ^[2]
• Well, moderately, and poorly differentiated adenocarcinoma
• Signet-ring cell component (very aggressive)

Performance ^[2]:

• Missed CRC rate: only 2-6% ^[2] — these "missed" cancers are usually flat/sessile lesions (serrated pathway) or in difficult-to-visualise areas (behind folds, at flexures)
• Important to scope the ENTIRE colon ^[2]
• Incomplete colonoscopy occurs in 11-12% of cases ^[2] (due to tight stricture, poor bowel preparation, patient intolerance, or tortuous sigmoid)

Complications of colonoscopy:

• Perforation (~1/1,000 diagnostic; ~1/500 with polypectomy)
• Post-polypectomy bleeding (~1-2%)
• Sedation-related complications
• Incomplete procedure

Used when the caecum cannot be reached by colonoscopy, or in patients unfit for colonoscopy.

• Spiral CT with IV contrast, air insufflation, and intraluminal contrast (enema) ^[2]
• Non-invasive; allows virtual "fly-through" like a colonoscopy ^[2]
• Requires mechanical bowel preparation (stools can simulate polyps) ^[2]
• Performance: may be similarly sensitive as colonoscopy for tumours > 1 cm ^[2][3], but cannot detect polyps < 5 mm and sessile/flat polyps ^[3]
• Not therapeutic — still requires colonoscopy for biopsy ^[2][3]
• Provides extraluminal information ^[3] — can incidentally detect other intra-abdominal pathology (liver metastases, lymphadenopathy, aortic aneurysm)
• Preferred over barium enema where access to colonoscopy is limited ^[2]

• Examines rectum, sigmoid, descending colon (up to splenic flexure)
• No sedation required — an office procedure ^[2]
• Considered inadequate for diagnosis due to the gradual worldwide shift towards proximal (right-sided) tumours ^[2]
• Bowel prep is not required (or minimal) ^[3]
• If positive, requires full colonoscopy to assess the rest of the colon ^[3]
• Right-sided cancer missed in ~25% ^[3]
• Its use followed by barium enema may be considered for patients with major comorbidities ^[2]

• Largely superseded by CT colonography ^[3]
• Barium + air ^[3] — barium coats the mucosa, air distends the lumen, creating a "double contrast" effect on X-ray
• Classical finding: "apple-core" lesion — near-circumferential involvement of bowel walls ^[3] with shouldering (abrupt transition from normal to abnormal mucosa)
• Risk of barium peritonitis if perforation occurs ^[3] — this is why it has fallen out of favour
• Limited diagnostic value ^[2]

CEA = "carcino" (cancer) + "embryonic" (found in foetal tissue) + "antigen" — a glycoprotein normally produced during foetal development, but re-expressed by certain cancers.

CEA is an epithelial tumour marker — but NOT a screening or diagnostic test ^[3].

• Cut-off: < 4.7 ng/mL (some sources use < 5) ^[3]
• Low diagnostic ability: low sensitivity + low specificity for CRC ^[3]:
  • Elevated in only ~50% of CRC ^[3] — because CEA may be first-pass metabolised by the liver (i.e. tumours draining via the portal system may have their CEA cleared by hepatic metabolism before it reaches systemic blood; this is why liver metastases often have high CEA — the CEA bypasses hepatic clearance or the liver is too diseased to metabolise it) ^[3]
  • False positives: pregnancy, smoking, TB, IBD, other carcinomas (GI, pancreas, breast) ^[3]
• Post-operatively: takes 4-6 weeks to return to normal ^[3]

This is the workhorse staging investigation for all CRC. It assesses:

Key CT findings in CRC:

• "Apple-core" lesion: irregular annular constriction with shouldering (abrupt edges) — classic for left-sided CRC
• Asymmetric bowel wall thickening with mucosal irregularity
• Pericolonic fat stranding (if tumour extends beyond muscularis propria — T3+)
• "Dirty fat" sign — haziness of pericolic fat indicating extramural tumour spread

MRI provides superior soft tissue resolution compared to CT, making it the modality of choice for local staging of rectal cancer.

MRI pelvis assesses:

• T stage with precision: invasion depth through the rectal wall
• Circumferential resection margin (CRM): the distance from the tumour to the mesorectal fascia. A threatened CRM (tumour ≤ 1 mm from mesorectal fascia) predicts local recurrence and indicates the need for neoadjuvant chemoradiotherapy before surgery ^[19]
• Extramural venous invasion (EMVI): tumour cells within veins beyond the bowel wall — an independent adverse prognostic factor
• Relationship to sphincter complex: critical for determining whether a sphincter-preserving low anterior resection is feasible, or whether abdominoperineal resection (permanent stoma) is required
• Lymph node assessment: morphological criteria (irregular border, mixed signal intensity) rather than size alone

All patients with rectal cancer should have MRI pelvis for local staging prior to treatment planning ^[19]

• Alternative to MRI for local T staging of early rectal cancer
• Excellent for distinguishing T1 from T2 lesions (important because T1 tumours may be amenable to local excision / transanal endoscopic microsurgery without radical surgery)
• Operator-dependent; limited by inability to pass the probe beyond obstructing tumours
• Less accurate than MRI for CRM assessment — MRI is preferred in most centres

• 18F-FDG (fluorodeoxyglucose) PET: cancer cells have increased glucose metabolism → increased FDG uptake → "light up" on PET ^[19]
• Not routinely used for initial staging of CRC ^[2]
• Indications:
  • Evaluating for resectability of isolated liver or lung metastases — to confirm there is no additional occult metastatic disease elsewhere that would make curative metastasectomy futile
  • Equivocal findings on CT (e.g. indeterminate pulmonary nodule or liver lesion)
  • Rising CEA without identifiable lesion on conventional imaging
• Limitations:
  • False positives: inflammation, infection
  • False negatives: mucinous tumours (low cellularity, low metabolic activity), small lesions < 1 cm
  • Brain metastases are difficult to detect due to high background glucose metabolism ^[19]

• Quick, cheap baseline assessment for pulmonary metastases
• Low sensitivity compared to CT thorax — largely replaced by CT thorax as part of staging CT

Anti-VEGF contraindications ^[24] (understand these by thinking about what VEGF does — it promotes angiogenesis, wound healing, and vascular integrity):

• Haemorrhage — VEGF inhibition impairs vascular integrity → bleeding risk
• Impaired wound healing — must stop bevacizumab ≥ 4-6 weeks before surgery and not restart until wound healed
• Arterial thromboembolic diseases — paradoxically, anti-VEGF increases thrombotic risk (endothelial dysfunction, loss of PGI2/NO production)
• Other: hypertension, proteinuria, GI perforation (especially if tumour is in situ)

ONLY indicated in Stage IV (metastatic) disease. There is NO evidence to support use of targeted therapy in the adjuvant setting ^[24]

Why does RAS mutation status matter? ^[4][5][24]:

• EGFR sits at the top of the RAS-RAF-MEK-ERK signalling cascade
• If RAS (KRAS or NRAS) is mutated → the pathway is constitutively active regardless of whether EGFR is blocked → anti-EGFR has no effect
• KRAS mutation results in constitutive activation of the RAS-RAF-ERK pathway leading to resistance to anti-EGFR therapy ^[24]
• RAS-mutant disease does not benefit from anti-EGFR monotherapy or its routine addition to chemotherapy; KRAS G12C inhibitor–anti-EGFR combinations are a specific later-line exception
• KRAS and BRAF V600E mutations are usually mutually exclusive; interpret the actual molecular report
• BRAF V600E requires combined pathway targeting: cetuximab is an essential partner of encorafenib, not a contraindicated drug in that combination

Anti-EGFR side effects: cutaneous reactions (acneiform rash, pruritus, nail changes — the rash actually correlates with efficacy!), headache, diarrhoea, infection, hypomagnesaemia, infusion reactions ^[24]

Tumour sidedness and anti-EGFR ^[4][5]:

• Anti-EGFR works better in LEFT-sided tumours than right-sided, even if RAS wild-type
• This is because right-sided tumours more frequently harbour alternative oncogenic drivers (BRAF, MSI-H, serrated pathway) that bypass EGFR dependence
• Current practice: anti-EGFR (cetuximab/panitumumab) preferred for left-sided RAS WT mCRC; anti-VEGF (bevacizumab) preferred for right-sided or RAS mutant mCRC ^[4][5]

Why do checkpoint inhibitors work in MSI-H tumours? ^[4][5]:

• MSI-H tumours have defective DNA mismatch repair → accumulate thousands of somatic mutations → generate abundant neoantigens (abnormal proteins displayed on cell surface by MHC)
• These neoantigens are "seen" by T cells → strong anti-tumour immune response
• BUT the tumour upregulates PD-L1 to evade this immune attack (PD-L1 binds PD-1 on T cells → "turns off" the T cell)
• PD-1 inhibitors (pembrolizumab, nivolumab) block PD-1 → "release the brakes" on T cells → restore anti-tumour immunity
• MSS tumours have low mutation burden → few neoantigens → checkpoint inhibitors are ineffective

• Encorafenib + cetuximab + fluorouracil-based chemotherapy is a first-line option for BRAF V600E-mutant mCRC; encorafenib + cetuximab also has established use after prior therapy (BEACON). See the BREAKWATER update above.
• Rationale: BRAF V600E constitutively activates the RAF-MEK-ERK pathway. But in CRC (unlike melanoma), single-agent BRAF inhibitor causes feedback activation of EGFR → combination with anti-EGFR is needed to block this escape route

• For previously treated KRAS G12C-mutant mCRC, combine a KRAS G12C inhibitor + anti-EGFR therapy:
  • Sotorasib + panitumumab
  • Adagrasib + cetuximab
• This is a later-line, biomarker-directed exception to the usual rule that RAS-mutant CRC does not benefit from anti-EGFR therapy. The anti-EGFR antibody is not used alone; it suppresses feedback EGFR reactivation during KRAS G12C inhibition.

High tie vs low tie of IMA ^[3]: High tie (at IMA origin) provides better lymph node clearance and reduces anastomotic tension, but low tie (distal to left colic artery origin) avoids damage to the hypogastric nerve and carries a lower risk of autonomic dysfunction ^[3]

Low anterior resection (LAR) syndrome is a highly clinically relevant late complication of rectal cancer surgery ^[3][29]:

• Symptoms: change in bowel movement persisting ≥ 1 month after surgery, ranging from constipation to faecal urgency, faecal incontinence, clustering of bowel openings, and evacuation dysfunction ^[3]
• Pathophysiology: multifactorial ^[3]:
  • Colonic dysmotility: loss of the rectal reservoir and colonic denervation alter transit
  • Neorectal reservoir dysfunction: the surgically created "neorectum" has reduced capacity and compliance compared to the native rectum
  • Anal sphincter dysfunction: stretch injury from the circular stapler, radiation damage, autonomic nerve injury
• Prevention: post-operative pelvic floor muscle exercises, antegrade colonic irrigation via stoma or enema, fecal diversion ^[3]
• Management: antidiarrhoeal agents (loperamide), transanal irrigation, pelvic floor rehabilitation, sacral nerve stimulation ^[3]

If a stoma (colostomy or ileostomy) is created during surgery, it carries its own set of complications ^[3][29]:

Early (< 30 days) ^[29]:

• Stomal bleeding: usually minor, from mucocutaneous junction
• Stomal necrosis: ischaemia of the exteriorised bowel segment (compromised mesenteric blood supply during stoma creation). The stoma appears dusky, dark, or black. May require revision if necrosis extends below fascial level
• Stomal retraction: the stoma sinks below skin level → difficulty with appliance adherence → leakage and skin irritation. Due to tension on the mesentery or inadequate bowel mobilisation
• Mucocutaneous separation: dehiscence at the junction of stoma and skin. Usually heals by secondary intention
• Skin irritation and dermatitis: Most common in end and loop ileostomy due to high-output and high alkaline enzymatic effluent ^[29] — the proteolytic enzymes in ileal output (which have not yet been neutralised by colonic bacteria) are very caustic to skin

Late (> 30 days) ^[29]:

• Parastomal hernia: most common late stoma complication. Herniation of bowel through the fascial defect around the stoma. May cause obstruction or incarceration. Often requires surgical repair with mesh
• Stomal prolapse: the bowel telescopes outward through the stoma. More common with loop colostomy
• Stomal stenosis: narrowing of the stoma at skin or fascial level → difficulty passing stool, thin ribbon-like output. May require revision