Glossary of Terms

Descriptions of all the cell model annotations found within the Cancer Dependency Map at Sanger.

Model Terms


Model: Identifiers

Passport Identifiers

The core identifiers used by the passport represent each point in the Patient, Sample, Model hierarchy. See model relationships for additional information.

  • Sanger IDentifier Patient (SIDP)
  • Sanger IDentifier Sample (SIDS)
  • Sanger IDentifier Model (SIDM)
External Resource Identifiers

Additional commonly used identifiers and database links to support cross referencing and integration of data sets. Currently these comprise of:

  • COSMIC
  • Cellosaurus (RRID)
  • Broad (CCLE)
Supplier & Catalogue Identifiers

Repositories and cell banks where the cell model can be obtained with their associated catalogue ID's.

Model: Descriptors & Derivation Information

Model Name

The name of the model as used by the Sanger Dependency Map. Synonyms are also been provided where applicable.

Tissue

Describes the site of the tumour from which the sample was taken. Where a model was derived from a metastatic tissue lists the site of the primary tumour.

Cancer Type

A broad disease classification describing the sample tumour. Cancer type also highlights samples obtained from non-cancerous tissue. All cancer types are NCIT terms.

Cancer Type Detail & NCIT ID

The most detailed description of the tumour available on the passport using NCI Thesaurus terms. Definitions of these terms are available via the NCIT ID links.

Tissue Status

Defines the sample as originating from:

  • Tumour
  • Metastasis
  • Normal
  • Transformed (e.g. lymphoblastoid cells transformed using Epstein Barr virus)
  • Precancerous (e.g. Adenoma or Barrett's Esophagus)
Sample Site

The location in the body or tissue from which the sample was taken.

Growth Properties

Models have been grouped into three categories, Adherent, Semi-Adherent and Suspension.For detailed information on the cell type and morphology refer to the repository documentation. Only applies to cell line models.

Relationship Details

A description of the relationship between models linked to the same patient and the source of the data to support this relationship.

Model Treatment

Model treatments occur during or following model derivation. Drug resistant subclones are the most frequent example.

GDSC Growth Estimate

See the detailed growth rate documentation.

Publication

The original (or earliest available) publication outlining how the cell model was established.

Date Generated

The date that the model was generated, sourced from repositories or publications.

Clinical Information

  • Cell Lines: Clinical information for the cell lines has been obtained from the model providers and publications.
  • Organoids: Clinical data for the organoid models is provided directly by the clinical sites alongside the tissue used for model derivation. This enables the Cell Model Passports to provide extensive patient, treatment and disease specific data for these models.
Species, Gender & Ethnicity

Basic patient information. Ethnicity has been divided into six broad classifications based on the data available, for more specific data refer to the cell model supplier.

Age

The age of the patient at the time sample tissue was obtained for model derivation. All ages are presented in years.

Smoking Status

Describes the patient’s smoking history:

  • Current Smoker
  • Ex-Smoker
  • Non-Smoker
  • Never Smoked
Sample Treatment (Prior Treatment) & Treatment Details

Treatment data has been annotated both at the sample and model level. Sample treatment refers to any therapy the patient received prior to sampling and has been broadly classified into groups such as chemotherapy and radiotherapy. Treatment Details provides specific information on the drugs or treatment undertaken.

Prior Therapy Outcome

Describes the clinical response of the tumour to the treatment indicated in 'Sample Treatment'.

  • Complete Response
  • Partial Response
  • Stable Disease
  • Progressive Disease
TNM Status

A set of clinical descriptions used to describe tumours. These are determined using tissue obtained at the time of sampling (pTNM).

  • Tumour (T) describes the size of the tumour.
  • Node (N) details if the cancer has spread to the lymph nodes.
  • Metastasis (M) describes if the cancer has spread to other areas on the body.

TNM staging uses the UICCv7 standards, definitions of which for each cancer type can be found on the SEER*RSA website.

Tumour Stage

Describes the size of the tumour and and it’s spread from the location in which it originated. Stage descriptions within the passports associated with organoids use established NHS standards found here.

Tumour Grade

Provides information on the cell types and aggressiveness of a tumour. Grade descriptions within the passports associated with organoids use established NHS standards here.

Family History of Cancer

Indicates if a first-degree relative of the patient has been diagnosed with a cancer of the same or a different type.

Prior Malignancies

Indicates if the patient has a history of a prior malignancy. Identifies if the malignancy was of the same or different cancer type from that of the model.

Sampling Procedure

The clinical procedure used to obtain the sample from which the model was derived.

Prior Diagnosis of Reflux Disease

Indicates if the patient has a history of reflux disease.

Reflux Disease Treatment

Where the patient was clinically diagnosed with reflux disease a description of the treatment received.

H. pylori Infection Status

Indicates whether the patient was at the time of sampling, or previously, diagnosed with a Helicobacter pylori infection.

Barrett's Esophagus Status

Indicates whether the patient was at the time of sampling, or previously, diagnosed with Barrett's Esophagus.

Goblet Cell Status

Where Barrett's Esophagus has been diagnosed were goblet cells present.

Disease Metastasis Status

Was there evidence of metastasis.

Disease Metastasis Sites

Indicate the site(s) of metastasis.

Colorectal Cancer Risk Factors

Were additional colorectal cancer risk factors are documented in the patient's medical record. These include:

  • A diet that is high in red meats and processed meats
  • Diagnosis of familial adenomatous polyposis in patient or family member
  • Obesity - weight > 20% ideal body weight
  • Previous colorectal polyps
  • Diagnosis of Lynch syndrome in patient
  • Type II diabetes
  • Other (specified by clinician).
Prior Diagnosis of Gastrointestinal Disorder

Had the patient previously been diagnosed with a Gastrointestinal Disorder, includes:

  • Adenomatous polyposis coli
  • Hereditary non-polyposis colon cancer
  • Peutz-Jeghers disease
  • Ulcerative colitis
  • Crohn disease
  • Celiac disease

Where diagnosed the corresponding disorder will be shown.

Prior Synchronous Tumours

Indicates whether synchronous colon or rectal tumours were present when the sample was collected.

Colon Polyp History

Indicates the presence of colon polyps in the patient's history.

Colon Polyp Status

Indicates if polyps were present in the colon when the sample was collected.

Alcohol Status

Describes the alcohol intake of the patient, self reported.

Alcohol Frequency

The average number of days per week on which the patient consumes alcohol, self reported.

Diabetic

Has the patient been diagnosed with Diabetes.

Diabetes Treatment

Describes the Diabetes treatment the patient was receiving at the time of sampling.

  • Injected Insulin
  • Biguanide
  • Sulfonylurea
  • Thiazolidinedione
  • Alpha Glucosidase Inhibitor
Prior Diagnosis of Chronic Panreatitis

Indicates whether the patient had a history of clinical Chronic Pancreatitis.

Clinical Staging (Pre-Sampling)

The tumour stage prior to sampling. This information is based on the clinical data obtained prior to the sampling of the tumour (cTNM).

TNM staging uses the UICCv7 standards, definitions of which for each cancer type can be found on the SEER*RSA website.

Tumour Regression Score

Currently only available for Esophageal organoids:

  • TRG1 Complete regression. Absence of residual cancer and fibrosis extending through the different layers of the oesophageal wall.
  • TRG2 Presence of rare residual cancer.
  • TRG3 An increase in the number of residual cancer cells, but predominantly fibrosis.
  • TRG4 Residual cancer outgrowing fibrosisTRG5TRG5 Absence of regressive changes.
Venous Invasion

Indicates if there was evidence of venous invasion of the tumour.

Venous Invasion Type

Record if the venous invasion was extramural or intramural.

Lymphatic Invasion

Indicates if there was evidence of lymphatic invasion.

Perineural Invasion

Indicates if there was evidence of perineural invasion.

Tumour Crosses GEJ

Indicates whether the tumour is located across the gastro-esophageal junction (GEJ).

Esophageal Columnar Metaplasia

Indicates the presence of Esophageal Columnar Metaplasia ( Esophageal Intestinal Metaplasia).

ECM Goblet Cells

Indicates if goblet cells are present within the esophageal columnar mucosa (ECM).

Dysplasia Of Non-cancerous ECM

Displays the degree of dysplasia within the non-cancerous esophageal columnar mucosa (ECM).

  • Negative / No dysplasia
  • Low grade dysplasia
  • High grade dysplasia
  • Indefinite dysplasia
Peripancreatic Lymph Nodes Tested

Displays the number of peripancreatic lymph nodes tested at surgery.

Peripancreatic Lymph Nodes Positive

Indicates the number of positive peripancreatic lymph nodes.

Preoperative CEA Level

Indicates the preoperative CEA level in ng/mL.


The following fields, prefixed with 'Clinical' describe the outcome of the clinical profiling for the patient's tumour. This is distinct from the profiling and genomic characterisation of the established cell model.

Clinical MSI Status

Describes the mismatch repair status and the methodology used.

  • Evidence of MMR mutation by sequencing.
  • Evidence of MMR protein loss by IHC.
  • MMR loss evidence hypermutation phenotype (>10 mutations/Mb).
  • No evidence of MMR alteration.
Clinical Gene Expression

Displays the outcome of gene expression testing where performed for the following genes*:

  • MLH1
  • MSH2
  • PMS2
  • MSH6
  • BRAF
  • PTEN

*Individual fields for each gene.

Clinical Gene Mutation Status

Displays the outcome of mutational status tests for the following genes*:

  • BRAF
  • PIK3CA
  • PTEN
  • KRAS

*Individual fields for each gene.

Clinical MLH1 Promoter Methylation Status

Indicates the promoter methylation status of MLH1.

Model Genomics

MSI Status

Displays the microsatellite instability status of a cell model. See here for further details

  • MSI: Microsatellite Instable
  • MSS: Microsatellite Stable
Ploidy

Refers to the ploidy status of the cell model determined by using mean copy-number obtained from PICNIC using the Affymetrix SNP6 data. See here for further details

Mutations per Mb

Shows the mutation rate per Mb estimated from Whole Exome Sequencing. See here for further details

Project Score & CRISPR KO

Core Fitness Gene

Genes which are required for the fitness of the majority of cell lines from a given cancer type or across multiple cancer types.

Fitness Score

Quantitative measure of the reduction of cell viability elicited by a gene inactivation, via CRISPR-Cas9 targeting. This is based on Bayes Factor value computed using BAGEL starting from CRISPRcleanR corrected gene depletion fold changes, and scaled to a 5% false discovery rate threshold (from classifying reference essential/non-essential genes based on BF rankings)

Corrected Fold Change

CRISPRcleanR corrected gene depletion fold change, computed between average representation of targeting sgRNAs at the end of screening versus the plasmid library.

BAGEL

A supervised learning method for analysing gene knockout screens and inferring gene fitness effects, starting from the observation of those elicited by two reference sets of essential/non-essential genes. Further details can be found in the corresponding article.

CRISPRcleanR

An unsupervised method for identifying and correcting gene-independent responses to CRISPR-Cas9 targeting; based on segmentation of sgRNA fold change values across the genomes. Further details can be found in the corresponding article.