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A study into the urgent

endoscopy referral system for

patients with suspected

gastrointestinal cancer

Christopher Jump

3rd Year Medical Student

Background information

• With the aim of improving the detection of cancers at

an early stage and therefore survival rates the 2-

week referral system was introduced in 2000 by the

Department of Health and was revised in 2005 by

NICE

• This included a referral form which specified

symptoms that needed to be present in order for the

patient to be urgently referred to a specialist

consultation or directly to endoscopy

Reasons the study was needed

• Many patient’s specimens referred as urgent to the

histopathologist are not diagnosed with malignancy.

This displaces ‘correctly’ referred urgent patients

down the waiting list, potentially causing them a

worse prognosis due to the delay of diagnosis and

subsequent treatment

Reasons the study was needed

• Each colonoscopy costs about £900



• Each oesophagogastroduodenoscopy (OGD) costs about £500-

600



• Histopathology costs are about:



o £67 per single biopsy site



o £100 for 2 biopsy sites



o £133 for 3 biopsy sites



• The PCT pays for each one they refer for, so if they are not

necessary it is a waste of their limited budget

Reasons the study was needed

• There are significant complications associated with

all types of endoscopy, which patients are being

needlessly exposed to if they are incorrectly referred



• E.g. Perforation, haemorrhage, infection, pain and

discomfort, sedation associated (cardio-pulmonary

events), etc.

Current evidence base

• Limited number of studies investigating urgent

referral for endoscopy in GI cancer patients, most of

which look into therapeutic endoscopy

• Many studies looking into the effectiveness of the

guidelines for urgent referral to a specialist in

secondary care. Have shown mixed results

regarding if the guidelines are specific enough to

detect early cancer presentation and their effect on

the outcome of patients

Main aims of the study

• To investigate:

o The number of patients that are correctly and

incorrectly referred for urgent endoscopies



o The differences in outcome between the patients

who were correctly and incorrectly referred

Method

• 50 patients included in the study, 25 who underwent an upper GI

endoscopy and 25 who had a lower GI endoscopy between the

25th February and 17th March 2009 at Southport and Formby

District General Hospital.

• Patients were identified by urgent histopathology referral forms.

• Medical records were then accessed and data collected.

• Urgent referrals were deemed to be correct or incorrect using

‘NICE referral for suspected cancer guidelines’.

• Outcomes were recorded by assessing their progress since their

endoscopy.

Results

• Mean age of 72.1 years



• 25 males and 25 females in total sample



• When divided:



o 14 females and 11 males in upper GI group



o 11 females and 14 males in lower GI group

Results- Source of referrals

• 43 (86%) of the 50 patients were referred from a GP



• 4 from hospital wards



• 1 from A&E, 1 referred by MDT, 1 surveillance

50

45

40

Number of patients









35

30

25

20

15

10

5

0

GP Hospital Ward A&E MDT Surveillance

Source of referral

Results- Number of correct and

incorrect referrals

• 18 (36%) of 50 patients were referred in accordance with NICE

guidelines

• When divided:

o Upper GI= 4 correct and 21 incorrect referrals

o Lower GI= 14 correct and 11 incorrect referrals

Figure 3. Number of patients correctly and

Figure 2. Number of patients correctly and incorrectly referred for an urgent lower GI

incorrectly referred for an urgent OGD endoscopy

25

25



Number of patients 20

20

Number of patients









15

15



10 10



5 5



0 0

Correct Incorrect Correct Incorrect

Referral type Referral type

Results- what the upper GI

referrals should have been

• Of the 21 incorrect referrals:

o 12 should have been given an urgent outpatient referral

o 5 should have been considered for an urgent outpatient referral

o 4 should have been routinely referred for an outpatient appointment

Figure 4. Amended referrals for patients incorrectly referred for

urgent OGD

14

12

Number of patients









10

8

6

4

2

0

Urgent outpatient referral Consider urgent outpatient Routine outpatient referral

referral

Type of amended referral

Results- Outcomes of correct

referrals

• Upper GI:

o 1 patient with a benign polyp, now on surveillance

o 1 patient with an oesophageal ulcer and gastritis (PPI and

discharged)

o 1 patient with duodenitis, duodenal ulcer, gastritis and 2 gastric

ulcers (PPI and discharged)

o 1 patient with gastritis and duodenitis (PPI and discharged)

• Lower GI:

o 5 cancers; 3 died, 1 is treated palliatively and 1 had surgical

excision and is now under surveillance

o 2 patients with Diverticular Disease discharged

o 2 patients with benign polyps discharged

o 5 patients normal, discharged

Results-Outcome of correct

referrals

Figure 8. Outcomes of correct urgent referrals in total sample

6







5







4

Number of patients









3







2







1







0

Normal Diverticular Disease Lower GI polyp Lower GI malignancy Upper GI polyp Oesophageal ulcer and Duodenitis, duodenal Gastritis and

gastritis ulcer, gastritis and 2 duodenitis

gastric ulcers.



Diagnosis

Results-Outcome of incorrect

referrals

• Upper GI

o 3 patients died (2 cancers, 1 unknown)

o 13 patients treated for an inflammatory condition (oesophagitis,

gastritis or duodenitis) with a PPI and discharged.

o 2 patients normal

o 2 treated for malignancy (partial gastrectomy, oesophageal stent)

o 1 patient continued on surveillance for Barrett’s oesophagus

Figure 9. Outcomes of incorrect urgent OGD referrals

14



12

Number of patients









10



8



6



4



2



0

Died Malignancy PPI, discharged Surveillance Normal,

treated OGD discharged

Outcome

Results-Outcome of incorrect

referrals

• Lower GI:

o 3 malignancies detected; 2 had successful surgical excisions,

1 treated palliatively

o 3 patients had adenomatous polyps excised, now under

surveillance

o 2 normal patients

o 1 with haemorrhoids, discharged

o 2 treated for ulcerative colitis (both medication, 1 also had a

colectomy)Figure 10. Outcomes of incorrect urgent lower GI endoscopy referrrals



4

Number of patients









3



2



1





0

Ulcerative colitis Normal, discharged Polyp excised, Haemorrhoids, Malignancy treated Malignancy,

treated surveillance discharged palliative care



Outcome

What has it shown

• Minority (36%) of urgent referrals comply with guidelines



• Majority (81%) of incorrect referrals are from GPs



• There are considerably more upper GI than lower GI incorrect

urgent referrals for endoscopy (21/25- 11/25)



• Minority of patients who are urgently referred for endoscopy

are diagnosed with cancer (24%)



• The incorrect referrals detected more cancers than the correct

referrals (7-5)

What has it shown

• Correct upper GI referrals detected no cancers, incorrect

detected 4



• Correct lower GI referrals detected 5 cancers, incorrect

detected 3



• Incorrect lower GI referrals had a higher curative treatment

rate for cancer than correct lower GI referrals (66.7%-20%)



• 3 patients out of 50 had life saving surgical resection of their

cancer over the 3 weeks this study observed



• Equates to 52 patients a year saved at an annual cost of

about £718,363 for endoscopy and histopathology only

Conclusions

• The existing guidelines are not effective as originally hoped in



detecting patients with gastrointestinal cancer



• This study suggests that for a cancer to meet the current urgent



referral guidelines it has to be at a late enough stage to exhibit



enough symptoms to fulfil the criteria, with the majority of the time



this being too late to cure the patient



• Guidelines need to be reviewed and amended with the aim of



detecting more cancers at an early stage



• Guidelines need to be made compulsory for all GPs as this is where



the main problem lies

Limitations

• Symptoms in urgent referral form not specified,

which meant many patients may have been eligible

for urgent referral but were deemed not, as form not

filled in extensively enough. E.g. ‘rectal bleeding’ but

duration not specified

• Handwriting on some referral forms illegible so

patient may have met criteria

Limitations

• Some patients had missing histology reports in their

medical files so information had to be taken from

consultants letter to GP, which contains less specific

information



• Sample size in this study is not large enough to

draw significant conclusions, so a possible future

study could expand on these findings with more

patients from a wider region

Thank you for listening

Audit of Lung Biopsies

Received at Whiston Hospital

Histopathology Department in

2009





Dr S Kelly

Dr L Forsyth

Dr S A Melmore

Aim

• To review all lung biopsies received at Whiston

in 2009.

• To assess adequacy.

• Try to further differentiate the non-small cell

carcinomas (NSCC) into adenocarcinoma

(adenoca) and squamous cell carcinoma (SCC)

– on morphology, and

– with the aid of immunohistochemistry.

Background

• Biopsy interpretation limited by

– Sampling error,

– Sample size,

– Tumour heterogeneity.

• BTS guidelines (2001)recommend 90%

adequacy with 5+ biopsies in cases of

suspected malignancy.

• Small cell carcinoma (SMCC) → chemotherapy.

• NSCC → surgery.



• New medical treatments for adenoca

– without squamous differentiation (folate

antimetabolite chemotherapy drugs under

assessment by NICE), and

– with EGFR-TK mutations (EGFR-TK

inhibitors).

• Immunohistochemistry (IHC) may aid further

differentiation.

• Limitations include;

– inadequate sample size,

– crush artefact,

– positive staining of normal lung constituents,

– overlapping immunophenotypes, and

– previous studies conducted on resection

specimens and cytology but not biopsies.

Immunohistochemistry

• Squamous cell carcinoma; CK5, p63 and

34βE12.

• Adenocarcinoma; CK7, CK20 and TTF1.

• P63

– Nuclear, SCC 78-100%, adenoca 1-33%, SMCC

77%.

• CK 5/6

– SCC 100%.

• TTF1

– Nuclear, adenoca 68-85%, SMCC 84%, 5-21%

SCC.

– Poorly differentiated more likely to be negative.

SCC





H&E



TTF -ve









P63 +ve

Adenoca







TTF +ve





H&E









P63 -ve

Method

• Telepath search for all lung biopsies in 2009.

• All cases reviewed by 2 consultants and 1 SpR.

• Number of biopsy fragments counted.

• Morphological diagnosis given.

• All carcinoma NOS, 6 adenoca and 6 SCC →

– TTF-1 and p63.

• TTF1 and p63 - ve →

– CK5/6

– Case notes and reports from RLBUHT

reviewed.

Results

• Pieces 1 2 3 4 5 6



• Negative (9) 2 4 2 0 1 0

• Suspicious (1) 0 0 1 0 0 0

• Malignant (49) 4 12 17 7 5 4



• Total (64) 6 16 20 7 6 4

• % of total 9.4 25 31.3 11 9.4 6.3

Number of adequate = 15.7 %

• Total 64



• Inadequate 5

• Negative 9

• Low grade dysplasia, 1

• Adenocarcinoma 9

• Squamous cell carcinoma, 17

• Carcinoma (NOS) 11

• Small cell carcinoma 8

• Metastatic or other 4

Not TTF1+ TTF1+ TTF1 – TTF1- TTF1 +

satisfactory p63+ p63- p63 + p63 - p63 +/-





Adenoc 0 1 5 0 0 0

(17%) (83%)





sqcc 2 0 0 4 0 0

(100%)





Carcinoma 2 0 4 0 4 1 (11%)

NOS (44%) (44%)

• 83% of adenocarcinoma TTF1 + (75-85% in

studies).

• 1 adenocarcinoma TTF1 + p63 + (1-33%

literature).

• 100% of satisfactory biopsies of sqcc p63 +.

• 4 cases of carcinoma NOS TTF1 +, p63 -

probably adenocarcinoma.

• 1 case p63 +/- , showed a positive internal

control. (Patient with cerebral metastases so no

resection performed).

H&E TTF +ve









CK 5/6 -ve P63 +/-ve

• 4 cases TTF1 - ve, p63 – ve,

– all internal controls for p63 + ve, and

– all CK5/6 – ve.

– 1 was small cell marker - ve on biopsy,

• resection showed a squamous cell carcinoma.

– 3 showed possible squamous morphology,

• no resection due to the patient’s co-morbidities,

metastases or locally advanced disease.

Conclusion

• We diagnosed 5/64 cases as inadequate on

H&E.

• Only 10/64 (15.7%) of the remaining cases

contained 5+ fragments of tissue.( vs. 90%).

• We made a morphological diagnosis of

malignancy on 49/64 cases, (9/49 had 5+

biopsies), and

• Differentiated type on H&E in 38/49 cases (6/38

had 5+ biopsies).

• 4/23 cases sent for IHC were inadequate.

– diagnosed on H&E as 2 x SCC, 2 x carcinoma NOS

• Our cases are comparable with the literature for

these robust IHC stains.

• For morphologically classic adenocarcinoma

TTF1 and p63 can be used in combination to

confirm the absence/presence of squamous

differentiation.

• For poorly differentiated NSCC cells the use of

TTF1 and p63 may aid further differentiation.

• Immunohistochemistry should be interpreted

together with morphology and clinical history.

• Sub classification should be avoided if uncertain.

• Limitations include;

– small sample size,

– difficult morphology,

– variable immunohistochemical staining and

interpretation,

– tumour heterogeneity,

– previous studies done on resection

specimens.

The future

• As the prospect of mutational analysis on

more/all of these tumours draws closer, and

• The use of IHC is used increasingly to choose

the tumours that will benefit from treatment,

• Clinicians will need to be aware of

– The need for an adequate sample, and

– The impact on turnaround times will mean

• waiting for a delayed report, or

• receiving preliminary and supplementory reports.

Recommendations

• Use TTF1 and p63;

– to confirm squamous differentiation in

morphologically diagnosed adenocarcinoma,

– in poorly differentiated NSCC but be aware of the

limitations.

• Cut spare sections on all levels for IHC.

• Check results of subsequent resections.

• Comment on BTS adequacy in reports.

• Disseminate this information to all

histopathologists and relevant clinicians.

Take Home Message

• For clinicians

– An adequate sample is required for accurate

diagnosis, and

– extensive IHC and mutational testing is time

consuming.

• For pathologists

– Immunohistochemistry should ALWAYS be

interpreted together with morphology and

clinical history.

Thank you

Any questions?

Cancer Data for Outcomes



Desperately Seeking NHS North West

Supplier Data

Your Support Report 2010/11









Data Supply

‘We can only be sure to improve

Data Quality

what we can actually measure’

– Lord Darzi

Poor Survival

Key Questions?

• Stage at Presentation

– Does my population have a problem with late stage

presentation? (not amenable to healthcare)

– Do I know where and with whom there are delays in

presentation/delays in diagnosis?

– Am I able to make informed investment/disinvestment

decisions?

• Access to Diagnosis and Treatment

– Does the population and sub-populations of my PCT

access the right services at the right time?

March 2011 – Electronic Path

Pipe delimited txt files

PROVIDER Pathology Comment



AINTREE UNIVERSITY HOSPITALS NHS

FOUNDATION TRUST GREEN

ALDER HEY CHILDREN'S NHS FOUNDATION 04/10/2010 First electronic send. Received

TRUST

a file from Jan 2009 to June 2010.

GREEN Receiving monthly sends thereafter

COUNTESS OF CHESTER HOSPITAL NHS

FOUNDATION TRUST GREEN

ROYAL LIVERPOOL AND BROADGREEN Receipt re-established

UNIVERSITY HOSPITALS NHS TRUST GREEN

SOUTHPORT AND ORMSKIRK HOSPITAL NHS Still sending paper

TRUST RED

ST HELENS AND KNOWSLEY HOSPITALS NHS

TRUST GREEN

WALTON CENTRE FOR NEUROLOGY AND Still sending paper

NEUROSURGERY NHS TRUST RED

WARRINGTON AND HALTON HOSPITALS NHS

FOUNDATION TRUST

GREEN

WIRRAL UNIVERSITY TEACHING HOSPITAL NO DATA RECEIVED SINCE MARCH 2010

NHS FOUNDATION TRUST

RED

Pathology Mark Up



Breast





Size





Laterality









Grade









No of Nodes

Timeliness

• Timeliness of Data Supply

• Timeliness of Data Quality Feedback

– Don’t want to study history

• Timeliness of commentary on services as

they are currently configured and delivered

Summary

• Outcomes Framework a key driver for

regular, high quality, timely cancer data

• Informed service planning depends upon

high quality data – across patient pathway

• Need to achieve full electronic data

supply by March 2011

• Leverage vital for a step change in data

capture and reporting

Emerging technologies and

targeting treatments: EGFR



JR Gosney

Consultant Thoracic Pathologist

Royal Liverpool University Hospital

Epidermal growth factor

receptor (EGFR)

• EGFR (HER-1;

ErbB1)

• HER-2 (neu;

ErbB2)

• HER-3 (ErbB3)

• HER-4 (ErbB4)

EGFR gene mutations

and gefitinib

Sensitising mutations of

EGFR gene

• Classically in

peripheral, well

differentiated, acinar,

non-mucinous

adenocarcinomas with

a bronchioloalveolar

component

• About 60% of non-

smoking, Eastern Asian

women with

adenocarcinoma

• About 10% of Western

subjects with NSCLC

EGFR protein expression



• Immunochemical

detection of EGFR

protein is not

currently a reliable

indicator of

sensitising

mutations nor of

sensitivity to TKIs

EGFR gene amplification

• High EGFR gene

copy number is an

imprecise reflection

of mutational status

and sensitivity to

TKIs and its

detection by in situ

hybridization is time

consuming and

technically

demanding

Detecting mutations

• Mutations are detectable by

screening or targeted detection

– Trials of gefitinib employed an

amplification-refractory mutation

system (ARMS)-based kit that targets

29 mutations in the EGFR gene

– This technique is sensitive and

robust and does not require a high

level of technical expertise

EGFR mutational analysis

In the Merseyside & North

Cheshire Network

• About 750 new cases of NSCLC diagnosed by histo-

or cytopathology per annum

• Paraffin wax block with accompanying report and

H&E-stained section sent by referring pathologist to

Department of Pathology at RLUH

• Histological assessment with possible

microdissection followed by DNA extraction and

mutational analysis

• Return of report of analysis to managing oncologist

and to referring histopathology laboratory for

integration with histopathology report

• Correlation of histopathology with mutational status

for quality control, audit and development of service

December 2009-

November 2010

• Phillipe Tanière, University of

Birmingham

• Funded by AstraZeneca

• Non-small cell lung cancer

• Any stage

• 200 cases sent for analysis

December 2009-

November 2010

• 96 male

• 190 adenocarcinoma, 9 squamous, 1 LCNEC

• 170 tissue biopsies, 15 cytology (10 FNAs (8

EBUS), 4 pleural fluid, 1 washing), 15 from

resections

• 11 sensitizing mutations (5%)

• 2 mutations conferring resistance (1%)

• Mean turnaround time 15 days (8-34)

Eleven sensitizing

mutations

• Six male, five female

• Two of Chinese, one of Pakistani origin

• Eight new diagnoses: three needle cores, two

bronchial biopsies, one lymph node, one bronchial

washings, one from wedge resection

• Three recurrent disease: one original needle biopsy,

one vertebral metastasis, one from previous

resection

• Six point mutations (one 719 exon 18; one 861 exon

21, four 858 exon 21), five deletions (all exon 19)

• Nine adenocarcinoma, two non-small cell carcinoma

not otherwise specified

From December 2010

• Mutational analysis at Royal Liverpool

University Hospital

• Budget for analysis (and gefitinib) held

at Clatterbridge Centre for Oncology

• Locally advanced or metastatic disease

(according to license and NICE

guidance)

• Non-squamous tumours only

Pooja Jain

Consultant Clinical Oncologist

Clatterbridge Centre for Oncology

• EGFR in NSCLC

• Targeting EGFR

– Tyrosine Kinase Inhibitors







• John Gosney

• Key drivers in the

process of

– Cell growth

– Proliferation



• EGFR activating

mutation

– promotion of tumour cell

growth

– blocking of apoptosis

– increasing the production

of angiogenic factors

– facilitating the processes

of metastasis

Tyrosine kinase inhibition

• Initially developed as second line therapy

– BR 21

– Increase in the objective response rate (9%

90% of mutations in mCRC found in codons 12 and 13

~5% of mutations found in codon 61

detection of KRAS mutations at

LWH

• Why Pyrosequencing?

• Unambiguous detection of ALL possible

mutations in codons 12, 13 and 61

• Sensitive

• Detects 5%-10% mutant depending on the

mutation

• Results obtainable from DNA isolated from

PETs

• DNA of poor quality

• DNA of low quantity

• Proven technology

Example KRAS Pyrosequencing

results

Non-mutated patient (normal

sequence)

Visible light









Gene sequence (codons 12 and 13)

KRAS mutation +ve and –ve

results

c.34G>T,

p.Gly12Cys









No mutation









c.38G>A, p.Gly13Asp

KRAS testing 6th

May 2010 to 2nd



Dec 2010

• 28 referrals (cut sections or tissue blocks)

from 5 pathology laboratories:

• Arrowe Park 6

• Chester 7

• Royal Liverpool 3

• Southport 8

• Whiston 4





• KRAS results obtained for 28/28 referrals

KRAS testing 6th May 2010 to 2nd

Dec 2010

• Reporting times of 28 referrals

• Mean reporting time 5.5 working days

• 18 (64%) reported within 5 working days

KRAS reporting times

Number of referrals









8



6



4



2



0

2 3 4 5 6 7 9 10

Working days taken to report results

KRAS testing 6th May 2010 to 2nd

Dec 2010

• 16/28 - no detectable KRAS mutation

• 12/28 (43%) - detectable KRAS mutation

34G>T

• 10 in codon 12 (Gly12Cys), 2



• 2 in codon 13

35G>T

• 0 in codon 61 (Gly12Val), 6









Normal, 16

35G>A

(Gly12Asp), 2



38G>A

(Gly13Asp) , 2

Proportion of KRAS mutations

detected

Sensitivity / UKNEQAS (quality

assessment scheme)

• Mutations can be present at low level

• Tumour heterogeneity

• Accompanying normal tissue

• Pyrosequencing detects mutations down

to 5-10% depending on mutation

• Current mutation detection rate is 43%

• Agrees with published data

• Suggests we have not missed any mutations

• Full marks in recent UKNEQAS scheme

• Not all participating labs received full marks

• ? include % neoplastic cells on KRAS reports

12, 13 and 61 have the same effect

on anti-EGFR therapy?









De Roock et al., JAMA. 2010;304(16):1812-1820

BRAF V600E ?

• A proportion of tumours with no KRAS

mutation will not respond to anti-EGFR therapy

• Other biomarkers?

• BRAF V600E detected in 5-12% of mCRC

• Same pathway as KRAS

• V600E increases BRAF activity ~10 fold

• Predicts resistance to anti-EGFR therapy

34G>T

(Gly12Cys), 2





35G>T

(Gly12Val), 6









Normal, 16

35G>A

(Gly12Asp), 2



38G>A

(Gly13Asp) , 2

Colorectal Cancer

Place of K-ras testing

Colorectal Cancer

Stage Incidence 5yr survival

Dukes A 10% 90+%

Dukes B 22% 60-80%

Dukes C 39% 30-60%

Metastatic 29% 1 76%

– Gd 3/4 12%

– maximal at wk3 then improves

– ? Rash associated with improved survival

CRYSTAL – Ph III Ist line

• 1198 pts

• FOLFIRI +/- cetuximab



Pfs 8.9m 8m

RR 47% 39%

OS 23.5m 20m ns

COIN – first line 3 arm trial

• FOLFOX/XELOX + cet continuous

• FOLFOX/XELOX continuous

• FOLFOX/XELOX + cet intermittent



• 1630pts randomised

• No difference in OS or PFS

EGFR expression



• Not a useful predictive factor

– Heterogeneity of EGFR expression

– Variable affinity of EGFR for cetuximab

– Inconsistency in measurement

K-ras oncogene

• Encode proteins downstream from EGFR

• Essential component of EGFR signalling

• Can acquire activating mutations in exon 2

• Does mutation status of K-ras affect

response to anti-EGFR monoclonals?

CO.17

394/572 samples available for K-ras

analysis



K-ras mutation detected in 40%

CO.17

Cetuximab BSC



Mutated ms 4.5m 4.6m

1yr 13% 19%

RR 1% 0%



Wild Type ms 9.5m 4.8m

1yr 28% 20%

RR 12% 0%

CO.17 - Survival

EGFR signaling









Baselga. Eur J Cancer 2001;37 Suppl 4:S16-S22.

CRYSTAL K-ras WT pts

• Post hoc analysis for NICE (TA176)

• 348pts FOLFIRI + cetuximab



WT Mutant

PFS 9.9 8.7m p=0.0167

MS 24.9m 21 m ns

RR 66% 43% p=0.0028

Surgery 7% 3.7%

COIN – WT analysis

• 729 WT pts OXFp +/- cetuximab



• PFS ns

• OS ns

• RR 64% vs 57% p=0.049

OPUS – first line Ph II

• 336pts 134 K-ras WT

• FOLFOX +/- cetuximab



WT Mutant

PFS 7.7 m 7.2 m p=0.01

RR 60% 37% p = 0.011

Surgery 11% 4.1% sig not reported

CELIM – first line

• Randomised ph II

• 114 pts

• Initially unresectable liver metastases

• folfiri + cetuximab vs folfox + cetuximab

• RR 68% vs 57%

• Subsequent resection 43 vs 40%

1st line cetuximab + Ctx

• Variable effect on survival

• ? Consistently higher response rates

Liver metastases - down sizing









Inoperable Operable

liver metastasis liver metastasis

Chemotherapy



5yr survival< 5% 5yr survival 30-40%





• Systemic therapy may render tumours operable

• 95/701 (13.5%) rendered resectable

– Reason unresectable

• 60% (too large),

• 49% (ill located),

• 34% (multinodular),

• 18% (extrahepatic) Adam Ann Surg Oncol 2001

Survival after chemotherapy-facilitated

resection of metastases is the same as

that for initially resectable metastases

Proportion surviving

1.0





0.8

54%

0.6



50% 34%

0.4 27%



34%

0.2 29%

19%



0.0

 Resectable (n = 425)

0 1 2 3 4 5 6 7 8 9 10

Survival time (years)  Initially unresectable (n = 95)







Adam R. Ann Oncol 2003;14:ii13-ii16.

Resection rate correlates with tumor response rate in both

selected and non-selected patients





Resection rate Studies including selected

patients

0.6

(liver metastases only,

0.5 no extrahepatic disease)

(r=0.96, p=0.002)

0.4

Studies including all

0.3

patients with mCRC

0.2 (solid line)

(r=0.74, p<0.001)

0.1



0.0 Phase III studies including

0.3 0.4 0.5 0.6 0.7 0.8 0.9 all patients in mCRC

Response rate (dashed line)

(r=0.67, p=0.024)





Folprecht et al. Ann Oncol 2005;16:1311-1319.

NICE guidance TA176



• Recommended Cetuximab + Chemotherapy for patients



– With inoperable CRC metastases confined to the liver

– Who were fit for surgery

– Who might be downsized to surgery following systemic therapy

CCO – Survival from I-CET



44pts

MS 10m (6 – 13)

CCO – Survival from 1st line

CTX



44pts

MS 36m (32 – 39)

Nov 08









Xelox x 12 weeks

Feb 09

May 09









Irinotecan x 12 wks

Oct 09

Jan 10









I-Cetux

Adjuvant Cetuximab

• FOLFOX +/- cetuximab

• NCCTG Intergroup phase III trial NO147

• 1760pts st III colon cancer wild type K-ras



Folfox Fotfox + cet

3yr dfs 74% 73%

3yr os 87% 82%

Cetuximab 2010

• Downsizing liver metastases to resection

 In combination with oxaliplatin/5FU/Irinotecan





• Third line treatment in pts previously

responding to chemotherapy

 In combination with Irinotecan





 Adjuvant cetuximab not of value

The National Cancer Dataset

Project

- especially pathology!

Di Riley

Director for Clinical Outcomes

CRS, December 2007





.....Better information on cancer services and

outcomes will enhance patient choice, drive up

service quality and underpin stronger commissioning;



.....Collection of defined datasets on all cancer

patients will be mandated through the national model

contract. PCTs will be responsible for ensuring that

this information is collected by MDTs and sent to

cancer registries

CRS, December 2007





.....We particularly need to collect and

use high quality data on:





.....Clinical outcomes, including survival,

with adjustments for co-morbidity and

stage of disease.

60

50

Risk-adjusted APE rate









40

30

20

10









0 100 200 300 400 500

Number of surgically treated rectal cancer patients

Five-year relative survival for colorectal cancer patients (diagnosed 1996-

2002) by stage at diagnosis, England

Number of cases (1996-2006) and five-year relative survival of colorectal

cancer patients (diagnosed 1996-2002) by stage at diagnosis, England

Project Purpose



• To redevelop the National Cancer Dataset for

use as a full operational standard in England



• To review the current business needs for the

collections and make sure that the output is fit

for purpose

NCIN ‘Data Views’



Patient Pathway

Refer- Diag Stage Rx Rec/Mets Rx Pall. Death

ral Care

Diagnostics

Datasets/Sources









CWT



MDT



RTDS



HES

NCASP



Ca. Reg

SSCRG progress

• Approved mandated datasets

– Cancer registration – additional review

– GFoCW

– Radiotherapy

– CDS

• 12 SSCRGs identified ‘site specific’ items

– Link to ‘output’ requirements

– Based on existing datasets e.g. NCASP, BAUS

– Period of definitional testing



• Mandated for NHS from October 2012

Challenges....

• Clinical data from MDTs?

• Transport via standard NHS data flows

– SUS, Open Exeter (Cancer Waits)

– Direct Cancer Registries & Nat. Repository

– Direct to NCASP

• Linking activity and ‘care record’ data

– OPCDS + radiotherapy

– CWT + ‘registration’

– NHS number linked data views

• Coded data from path/radiology/etc

Pathology Data

• Patient care & management

– MDT

– Staging

– Ongoing care



• Cancer Outcomes/Registration

– Staging

– Morphology, topography, grade

– Risk adjusted analysis

NCRD – pathology

items -1

Diagnosis

DIAGNOSIS DATE (CANCER)

PRIMARY DIAGNOSIS (ICD)

TUMOUR LATERALITY

BASIS OF DIAGNOSIS (CANCER)

HISTOLOGY (SNOMED)

GRADE OF DIFFERENTIATION (AT DIAGNOSIS)



Staging

T CATEGORY (FINAL PRETREATMENT)



STAGING CERTAINTY FACTOR (T CATEGORY)



N CATEGORY (FINAL PRETREATMENT)



STAGING CERTAINTY FACTOR (N CATEGORY)



M CATEGORY (FINAL PRETREATMENT)



STAGING CERTAINTY FACTOR (M CATEGORY)



TNM CATEGORY (FINAL PRETREATMENT)



STAGING CERTAINTY FACTOR (TNM CATEGORY)



SITE SPECIFIC STAGING CLASSIFICATION

TNM CATEGORY (INTEGRATED)

T CATEGORY (INTEGRATED STAGE)

N CATEGORY (INTEGRATED STAGE)

M CATEGORY (INTEGRATED STAGE)

NCRD – pathology

items -2

Pathology Details

PATHOLOGY INVESTIGATION TYPE

SAMPLE RECEIPT DATE

INVESTIGATION RESULT DATE

CONSULTANT CODE (PATHOLOGIST)

ORGANISATION CODE (OF REPORTING PATHOLOGY)

PRIMARY DIAGNOSIS (ICD)

TUMOUR LATERALITY

INVASIVE LESION SIZE

SYNCHRONOUS TUMOUR INDICATOR

HISTOLOGY (SNOMED)

GRADE OF DIFFERENTIATION

CANCER VASCULAR OR LYMPHATIC INVASION

EXCISION MARGIN

NODES EXAMINED NUMBER

NODES POSITIVE NUMBER

T CATEGORY (PATHOLOGICAL)

N CATEGORY (PATHOLOGICAL)

M CATEGORY (PATHOLOGICAL)

TNM CATEGORY (PATHOLOGICAL)

SERVICE REPORT IDENTIFIER

SERVICE REPORT STATUS

SPECIMEN NATURE

ORGANISATION CODE (REQUESTED BY)

CARE PROFESSIONAL CODE (REQUESTED BY)

T CATEGORY EXTENDED (PATHOLOGICAL)

M CATEGORY EXTENDED (PATHOLOGICAL)

RCPath Datasets

• Guidelines for good clinical reporting

– Specific for different cancer sites

• What proportion of pathologists use

proforma-based reporting tools?

• How to or should we progress to encoded

data?

• Cancer registration & outcomes analysis

would benefit from it?

• Would MDTs also benefit - MDT dataset?

NCIN/RCPath Pathology

Project

• Structured or proforma reporting

• Codify & mandate ‘Core’ items

• Direction of travel too great

– Systems not available

– Change in clinical practice

– Patient management v outcomes analysis



• What is the solution?

– Professional & Clinical Record Standards

Professional Standard -

Stage 1

• Clarification of content to be provided within

free text reports (RCPAth Core Items)

• Or the use of the RC Path proforma.

• Communication to Pathologists of content

specification and mechanism for

transmission to Registries.

• Both of these aspects covered by RC Path

guidance

Standards - Stage 2



• Professional Standard version 2

– stipulation of proforma to be used for

reporting

– introduction of structured/coded items





• Patient Record Standard version 1

– identification of items which can be

structured and have SNOMED CT codes

Standards - Stage 3



• Professional Standard version 3

– structured data items



• Patient Record Standard version 2

– all items structured with SNOMED CT

coding

– identification of the linkage standards to

allow record to Registry transmission and

use.

Timescales & Process

• Working Group

– RCPath / NCIN / CfH /DH

– National Clinical Content & Requirements Board

(NCCRB)

– Role of RCPath for governance key

– Align with other related initiatives

• Estimated time – 5 years (2015)

– Content Proposal – approved November 2010

– Requirements Statement

– Assurance Statement

– Then the Information Standards Board

60

50

Risk-adjusted APE rate









40

30

20

10









0 100 200 300 400 500

Number of surgically treated rectal cancer patients


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