CriterionAssessment

An assertion of whether sufficient evidence exists to satisfy some pre-defined 'variant interpretation criterion', which defines requirements for a particular type of argument relevant to the pathogenicity of a genetic variant.

SEPIO:0000191
Descended from Statement

Scope and Usage

Variant interpretation criteria are provided as part of frameworks such as the ACMG Guidelines for charaterizing the pathogenicty of genetic variants. These criteria define relevant data types and rules for interpreting this data as evidence, to make a specific type of assertion about a variant that is ultimately relevant to its pathogenicity interpretation. For example, the PM2 ACMG criterion may be met based on a study showing a variant to be absent in a particular population of healthy individuals (e.g. non-Finnish Europeans in the ExAC database). Implicit in an this criterion being 'met' is the broader assertion that the frequency of the variant is sufficiently low in healthy populations to support a meaningful argument for the pathogenicity of the variant.

In the process of generating a variant interpretation through the ACMG workflow, criterion assessments are treate as 'intermediate' assertions that establish whether a particuar criterion is met or not for the variant under review. Evidence relevant to the merit of this assertion is organized around one or more evidence lines, and the criterion assessment is itself used as evidence for the final interpretation of the variant's pathogenicity.

Attributes

Name Type Cardinality Description IRI Defined in
criterion Criterion 0..1 The rule describing how the data is being used SEPIO:0000041 CriterionAssessment
variant CanonicalAllele 1..1 Variant about which the assemssment is made SEPIO:0000275 CriterionAssessment
condition GeneticCondition 0..* Condition for which the assessment is made SEPIO:0000276 CriterionAssessment
statementOutcome @id 1..1 Result of assessing the data and criterion SEPIO:0000197 CriterionAssessment
label string 0..1 A name given to the resource. RDFS:label Entity
description string 0..1 Description may include but is not limited to: an abstract, a table of contents, a graphical representation, or a free-text account of the resource. DC:description Entity
userLabelDictionary UserLabel 0..* An optional label defined by the user. Used for custom entities or to clarify the preferred user label on existing entities with non-preferred labels. SEPIO:0000422 Statement
outcomeQualifier string 0..1 Use “NOT” as the value of this property to assert that the statement is negated. SEPIO:0000346 Statement
evidenceLine EvidenceLine 0..* supporting evidence SEPIO:0000006 Statement
contribution Contribution 0..* The contributions (agent, time and role) made to this entity SEPIO:0000159 Statement
source string 0..* A string indicating the source of a Statement DC:source Statement

Instances

ID label description userLabelDictionary outcomeQualifier evidenceLine criterion variant condition statementOutcome

CGEX:CritAssess156

Most pathogenic variants in TTN are truncating. However, a small number of missense variants in TTN are associated with ARVC (Taylor 2011 PMID:21810661 ) Because TTN is such a large gene, the statistical expectation of benign missense variants is very high.

CGEX:EvLn132

SEPIO-CG:99034

(PP2)

CAR:CA256496

SEPIO:0000224

(Not Met)

CGEX:CritAssess275

Variant is not LOF and LOF is not a known mechanism of disease associated with this gene for any condition.

CGEX:EvLn001

SEPIO-CG:99022

(PVS1)

CAR:CA090943

SEPIO:0000224

(Not Met)

CGEX:CritAssess277

This variant only occurs as LOF in an uncommon transcript (NM_133437.4). For most transcripts, the variant is intronic.

CGEX:EvLn003

CGEX:EvLn004

SEPIO-CG:99022

(PVS1)

CAR:CA238217

CGEX:GenCond047

SEPIO:0000224

(Not Met)

CGEX:CritAssess278

The assessed variant produces the same amino acid change (p.Phe285Leu) as known pathogenic variant c.853T>C

CGEX:EvLn005

SEPIO-CG:99023

(PS1)

CAR:CA261606

CGEX:GenCond003

SEPIO:0000223

(Met)

CGEX:CritAssess279

The assessed variant produces the same amino acid change (p.Met2083Ile) as known pathogenic variant c.6249G>A. But that change is pathogenic because it has been shown to disrupt splicing and create a premature stop codon. Prediction tools do not suggest c.6249G>C disrupts splicing.

CGEX:EvLn006

SEPIO-CG:99023

(PS1)

CAR:CA501220

CGEX:GenCond004

SEPIO:0000224

(Not Met)

CGEX:CritAssess280

While the two amino acid changes are not identical, they are the same amino acid change in analagous residues of HRAS and KRAS.

CGEX:EvLn007

CGEX:EvLn008

SEPIO-CG:99023

(PS1)

CAR:CA341206

CGEX:GenCond005

SEPIO:0000223

(Met)

CGEX:CritAssess281

IC1: Individual has condition, FH1: No family history, DNA1: variant is denovo (parentage confirmed)

CGEX:EvLn009

SEPIO-CG:99024

(PS2)

CAR:CA016441

CGEX:GenCond052

SEPIO:0000223

(Met)

CGEX:CritAssess282

De novo variant occurred on haplotype inherited from the father. Maternity no explicitly confirmed - but if variant occurred on haplotype inherited from the father, then confirmation of maternity not required.

CGEX:EvLn010

SEPIO-CG:99024

(PS2)

CAR:CA257646

CGEX:GenCond008

SEPIO:0000223

(Met)

CGEX:CritAssess286

The RASopathy group considers MEK and ERK activation assays as well validated.

CGEX:EvLn017

CGEX:EvLn018

SEPIO-CG:99025

(PS3)

CAR:CA220161

SEPIO:0000223

(Met)

CGEX:CritAssess287

statistically significant difference between affects and unaffecteds

CGEX:EvLn019

SEPIO-CG:99026

(PS4)

CAR:CA253316

CGEX:GenCond048

SEPIO:0000223

(Met)

CGEX:CritAssess288

Across publications, this variant is thought to account for 2%-10% of patients with Malignant hyperthermia. But variant is also only found in 9/66740 Europeans in ExAC (.01%). Based on these differences, groups applied PS4 to this variant classification (without a formal OR analysis).

CGEX:EvLn020

SEPIO-CG:99026

(PS4)

CAR:CA024311

CGEX:GenCond011

SEPIO:0000223

(Met)

CGEX:CritAssess290

Variant is located within the kinase domain (where multiple other pathogenic variants are located)

CGEX:EvLn022

SEPIO-CG:99027

(PM1)

CAR:CA090928

SEPIO:0000223

(Met)

CGEX:CritAssess291

Variant is located in exon 15, which the RASopathy group has decided is an established functional domain for BRAF

CGEX:EvLn023

SEPIO-CG:99027

(PM1)

CAR:CA123651

SEPIO:0000223

(Met)

CGEX:CritAssess292

The variant is near 4 other pathogenic variants

CGEX:EvLn024

SEPIO-CG:99027

(PM1)

CAR:CA352275

SEPIO:0000223

(Met)

CGEX:CritAssess293

PM2 is applicable as even though variant is not 100% absent, it is practically absent (a 95% CI for the population goes from 0.00% to 0.01%)

CGEX:EvLn025

CGEX:EvLn026

SEPIO-CG:99028

(PM2)

CAR:CA011797

SEPIO:0000223

(Met)

CGEX:CritAssess295

while the variant is absent from exac, mean coverage (11X) is insufficient to be sure that variant was fully assayed.

CGEX:EvLn028

SEPIO-CG:99028

(PM2)

CAR:CA273141

SEPIO:0000224

(Not Met)

CGEX:CritAssess298

Application of PM3 is incorrect as the variant in trans is know known to be pathogenic (it is the same variant).

CGEX:EvLn031

SEPIO-CG:99029

(PM3)

CAR:CA090904

CGEX:GenCond015

SEPIO:0000224

(Not Met)

CGEX:CritAssess299

leads to an in-frame deletion of 7 amino acids (not repeat region).

CGEX:EvLn032

SEPIO-CG:99030

(PM4)

CAR:CA090919

SEPIO:0000223

(Met)

CGEX:CritAssess300

leads to an in-frame deletion of 5 amino acids (not repeat region).

CGEX:EvLn033

SEPIO-CG:99030

(PM4)

CAR:CA090938

SEPIO:0000223

(Met)

CGEX:CritAssess301

This 15bp duplication variant results in an expansion of a 20 residue polyalanine tract to a 25 residue polyalanine tract.

CGEX:EvLn034

SEPIO-CG:99030

(PM4)

CAR:CA501224

SEPIO:0000224

(Not Met)

CGEX:CritAssess302

From CLINVAR: Doolan et al. (2005) (PMID:15698845) reported mutations at the same residue (R162P) in patients with HCM, supporting the functional importance of this residue in the protein. This rare R162P variant observed multiple times in is Likely Pathogenic in ClinVar with 1 star assertion. Other variants in the same residue R162W has conflicting evidence of pathogenicity(Path by GeneDx : SCV000209174.2 and VUS by LMM:SCV000203864.2). Considered these two only as they have provided assertion criteria.

CGEX:EvLn035

CGEX:EvLn036

CGEX:EvLn037

SEPIO-CG:99031

(PM5)

CAR:CA021744

CGEX:GenCond016

SEPIO:0000223

(Met)

CGEX:CritAssess303

Other pathogenic variants at the same residue per ClinVar : NM_000531.5(OTC):c.119G>A (p.Arg40His) However no assertion criteria is provided for these variants. So pathogenicity needs to be determined by literature search. So PM5 is applicable when assessing p.Leu1764Il

CGEX:EvLn038

SEPIO-CG:99031

(PM5)

CAR:CA090910

CGEX:GenCond017

SEPIO:0000224

(Not Met)

CGEX:CritAssess304

Another variant at this position, but different AA change, has been observed and called pathogenic for breast ovarian cancer by ENIGMA expert panel:

CGEX:EvLn039

SEPIO-CG:99031

(PM5)

CAR:CA501227

CGEX:GenCond050

SEPIO:0000223

(Met)

CGEX:CritAssess305

while the variant is absent from exac, however 1) very low coverage across this region (~5X) and usually 20X is used as a cut-off to say “absent” 2) variant is 21 nt deletion - databases may not be able to call a variant of that size (I rarely see an indel of this size in ExAC).

CGEX:EvLn040

SEPIO-CG:99028

(PM2)

CAR:CA090919

SEPIO:0000224

(Not Met)

CGEX:CritAssess306

Two sporadic cases of BHD contain this allele

CGEX:EvLn041

CGEX:EvLn042

SEPIO-CG:99032

(PM6)

CAR:CA090951

CGEX:GenCond018

SEPIO:0000223

(Met)

CGEX:CritAssess307

affected child with CFC was found to carry c.158T>C. Both parents are unaffected and from Sanger seq neither parent was found to carry c.158T>C variant - so authors conclude variant occurred de novo. Since there was no mention of parental confirmation, PS2 cannot be used but PM6 is applicable

CGEX:EvLn043

SEPIO-CG:99032

(PM6)

CAR:CA279966

CGEX:GenCond019

SEPIO:0000223

(Met)

CGEX:CritAssess308

3 unrelated probands with CFC were found to carry c.1741A>G variant. There is no family history of CFC in any family and all three sets of parents were confirmed to not have the variant. Since there was no mention of parental confirmation, PS2 cannot be used but PM6 is applicable. However, since there are 3 de novo observations, many groups (including Noonan and MYH7) would allow PM6 to be upgraded to Strong (PM6_S)

CGEX:EvLn044

CGEX:EvLn045

CGEX:EvLn046

SEPIO-CG:99032

(PM6)

CAR:CA279976

CGEX:GenCond068

SEPIO:0000223

(Met)

CGEX:CritAssess309

In total, 4 segs from 2 families

CGEX:EvLn047

SEPIO-CG:99033

(PP1)

CAR:CA010136

CGEX:GenCond020

SEPIO:0000223

(Met)

CGEX:CritAssess310

In total, 8 segs from 2 families (can combine hom segs and compound het segs). Most groups would allow this to be shifted up the Moderate (PP1_M)

CGEX:EvLn048

SEPIO-CG:99033

(PP1)

CAR:CA143213

CGEX:GenCond021

SEPIO:0000223

(Met)

CGEX:CritAssess311

PP1 is for “Co-segregation with disease in multiple affected family members” PP1 is not applicable for this variant because it’s only a single segregation.

CGEX:EvLn049

SEPIO-CG:99033

(PP1)

CAR:CA501226

CGEX:GenCond051

SEPIO:0000224

(Not Met)

CGEX:CritAssess316

even though the computational tools for AA changes are NOT predicting an impact, splicing tools are predicting an impact - so PP3 is applicable

CGEX:EvLn054

SEPIO-CG:99035

(PP3)

CAR:CA022019

SEPIO:0000223

(Met)

CGEX:CritAssess321

OMIM is not considered an expert or reputable source for variant interpretations. Further, OMIM’s evidence for this pathogenic call is available (the publication link - PMID:21620354 - and free text summary) so people should use the evidence from OMIM in their assessment NOT OMIM’s interpretation. This is marked as Insufficient Evidence rather than refuted because the OMIM entry does not rule out a later application of PP5 based on eg. an expert panel.

CGEX:EvLn058

SEPIO-CG:99037

(PP5)

CAR:CA128479

CGEX:GenCond024

SEPIO:0000224

(Not Met)

CGEX:CritAssess324

Globally, this variant has a MAF of 0.0454 (4.5%) which would put it under the 5% rule and thus BA1 would not be applicable. However, variant is enriched in East Asian population - 29% MAF - so way over the 5% cut-off. So now BA1 is applicable

CGEX:EvLn061

CGEX:EvLn062

SEPIO-CG:99038

(BA1)

CAR:CA134997

SEPIO:0000223

(Met)

CGEX:CritAssess325

Although this variant has been seen in the general population, its frequency is low enough to be consistent with a recessive carrier frequency.

CGEX:EvLn063

SEPIO-CG:99028

(PM2)

CAR:CA501229

CGEX:GenCond045

SEPIO:0000223

(Met)

CGEX:CritAssess328

Perrault syndrome may be underreported due to misdiagnosis. If the prevalence estimates rise, this assessment may need to be revisited

CGEX:EvLn066

SEPIO-CG:99039

(BS1)

CAR:CA501230

CGEX:GenCond028

SEPIO:0000224

(Not Met)

CGEX:CritAssess329

According to Baylor internal data on this variant, it has been observed multiple times in asymptomatic parents internally and in controls and observed once as a homozygotes internally in unaffected. Although the evidence for full penetrance is weak, the fact that there are multiple asymptomatic occurrences helps the case.

CGEX:EvLn067

CGEX:EvLn068

SEPIO-CG:99040

(BS2)

CAR:CA090918

CGEX:GenCond029

SEPIO:0000223

(Met)

CGEX:CritAssess330

This variant was observed in unaffected healthy control chromosomes. PMIDs: 15122587, 18199528, 22703879, 24728327

CGEX:EvLn069

CGEX:EvLn070

CGEX:EvLn071

CGEX:EvLn072

SEPIO-CG:99040

(BS2)

CAR:CA008351

CGEX:GenCond030

SEPIO:0000223

(Met)

CGEX:CritAssess331

Although this variant was found in 5 individuals with Marfan Syndrome, it was identified in 2 unaffected relatives from two separate families. PMID:12402346

CGEX:EvLn073

CGEX:EvLn074

SEPIO-CG:99040

(BS2)

CAR:CA013604

CGEX:GenCond072

SEPIO:0000223

(Met)

CGEX:CritAssess336

The inconsistent segregation data is reasonably explainable as a phenocopy, and therefore does not provide evidence for the benignity of this allele.

CGEX:EvLn080

SEPIO-CG:99042

(BS4)

CAR:CA010777

CGEX:GenCond065

SEPIO:0000224

(Not Met)

CGEX:CritAssess337

In a family tested by the LMM, the c.1484C>T variant was identified in a proband with clinical diagnosis of HCM. This proband has two relatives that also have clinical diagnosis of HCM however never relative carries the c.1484C>T variant.

CGEX:EvLn104

SEPIO-CG:99042

(BS4)

CAR:CA133141

CGEX:GenCond066

SEPIO:0000223

(Met)

CGEX:CritAssess340

Homozygous truncating variants in LOXHD1 are associated with autosomal recessive hearing loss. This was demonstrated by both identification in human patients and a mouse model. (I used the OMIM entry as a source, but you could also directly use the papers.)

CGEX:EvLn083

SEPIO-CG:99043

(BP1)

CAR:CA090950

CGEX:GenCond059

SEPIO:0000223

(Met)

CGEX:CritAssess341

While truncations are usually the cause of TTN related DCM, missense variants in certain regions can also cause disease.

CGEX:EvLn084

SEPIO-CG:99043

(BP1)

CAR:CA256496

CGEX:GenCond053

SEPIO:0000224

(Not Met)

CGEX:CritAssess344

although this variant was found in trans with another variant in the same gene, that variant is VUS and not an established pathogenic variant and cardiomyopathies can be variable in penetrance.

CGEX:EvLn088

SEPIO-CG:99044

(BP2)

CAR:CA501235

CGEX:GenCond007

SEPIO:0000224

(Not Met)

CGEX:CritAssess346

BP3 does not apply for this variant because it is not an in-frame deletion (it's a deletion of 10 bp) and, although the I Band is a repetitive region that contains tandem arrays of immunoglobulin domains, these folds may be an important component for TTN's elasticity.

CGEX:EvLn090

SEPIO-CG:99045

(BP3)

CAR:CA273551

SEPIO:0000224

(Not Met)

CGEX:CritAssess350

While AI111 is considered probably damaging by at least one in silico predictor, the transcript for AI111 ( NM_133379.3 ) is not clinically relevant. In clinically relevant transcripts, thisthis canonical allele is intronic.

CGEX:EvLn105

SEPIO-CG:99046

(BP4)

CAR:CA501237

SEPIO:0000224

(Not Met)

CGEX:CritAssess351

The evidence here only explicitly describes a single individual with a likely pathogenic variant in TNNT2, but there are numerous other examples that have been observed in internal LMM data.

CGEX:EvLn093

SEPIO-CG:99047

(BP5)

CAR:CA012381

CGEX:GenCond067

SEPIO:0000223

(Met)

CGEX:CritAssess354

Variants in COL2A1 are associated with dominant spondyloepiphyseal dysplasia congenita (a primary bone dysplasia). CA112 was identified in a proband with CA113, which is pathogenic for another primary bone dysplasia, dominant Pseudoachondroplasia. However, this does not provide supporting evidence for CA112 being benign because the combination of a COL2A1 and COMP variant are known to produce a more severe phenotype, Pseudoachondroplastic spondyloepiphyseal dysplasia syndrome, which is the phenotype of the proband. Because the combination of alleles may produce a qualitatively different phenotype, the bone dysplasia caused by the COMP variant does not provide evidence that the COL2A1 variant is benign for any bone dysplasias in general.

CGEX:EvLn096

SEPIO-CG:99047

(BP5)

CAR:CA204551

CGEX:GenCond040

SEPIO:0000224

(Not Met)

CGEX:CritAssess348

Seven of the nine predictions found this variant to be benign, which we consider sufficient to support.

CGEX:EvLn092

SEPIO-CG:99046

(BP4)

CAR:CA020822

SEPIO:0000223

(Met)

CGEX:CritAssess360

This variant is a silent variant that does not result in an amino acid change. It is not very conserved and splicing tools suggest no change. However, BP7 does not apply because the variant is located in the first base of exon 4 of RAF1, which is part of the 3’ splice region of the exon. For that reason, we can’t fully trust computational tools. Functional assays would have to confirm that this variant truly does not alter splicing.

CGEX:EvLn102

SEPIO-CG:99049

(BP7)

CAR:CA177682

SEPIO:0000224

(Not Met)

CGEX:CritAssess361

This variant occurs in the invariant region (+/- 1,2) of the splice consensus sequence and in vitro studies confirmed that it leads to aberrant splicing and reduced DSC2 protein levels (Heuser 2006 PMID:17186466). Splice and other loss-of-function variants in DSC2 have been reported in individuals with ARVC (http://arvcdatabase.info/).

CGEX:EvLn103

SEPIO-CG:99022

(PVS1)

CAR:CA022880

CGEX:GenCond046

SEPIO:0000223

(Met)

CGEX:CritAssess363

This variant was identified in one individual with pathogenic variants in another gene. Internal LMM data: The proband had one pathogenic and one likely pathogenic variant in (in trans) in SLC26A4. This proband had mild to profound hearing loss with EVA, which is characteristic of Pendred Syndrome. SLC26A4 is the only gene associated with Pendred Syndrome

CGEX:EvLn106

SEPIO-CG:99047

(BP5)

CAR:CA090950

CGEX:GenCond058

SEPIO:0000223

(Met)

CGEX:CritAssess369

This variant has been reported in 1/66564 European chromosomes by the Exome Aggregation Consortium (ExAC, http://exac.broadinstitute.org; dbSNP rs397514042).

CGEX:EvLn107

SEPIO-CG:99028

(PM2)

CAR:CA022880

SEPIO:0000223

(Met)

CGEX:CritAssess371

This variant is present in 0.2% (31/16512) of South Asian Chromosomes in ExAC.

CGEX:EvLn108

SEPIO-CG:99039

(BS1)

CAR:CA013536

SEPIO:0000223

(Met)

CGEX:CritAssess372

This variant is present in 2% (27/1384) of African American Chromosomes in ESP.

CGEX:EvLn109

SEPIO-CG:99039

(BS1)

CAR:CA090950

CGEX:GenCond057

SEPIO:0000223

(Met)

CGEX:CritAssess373

This is a synonymous variant with little conservation and no predicted impact on splicing. AllConservation and splicing algorithm values are listed below.

CGEX:EvLn117

SEPIO-CG:99046

(BP4)

CAR:CA013536

SEPIO:0000223

(Met)

CGEX:CritAssess374

Flag-tagged construct with the variant was transfected into HEK cells. As per the RASopathy working group’s approved assays (see example 3 above), Smith et al. showed that the Y337C mutation increased levels of pERK in starved HEK cells via western blotting.

CGEX:EvLn116

SEPIO-CG:99025

(PS3)

CAR:CA090930

SEPIO:0000223

(Met)

CGEX:CritAssess375

A personal communication to our lab informed us of an individual and his son who both harbored the variant but with clinical workup did not appear to have Noonan Syndrome or symptoms indicative of Noonan Syndrome.

CGEX:EvLn123

SEPIO-CG:99042

(BS4)

CAR:CA090930

CGEX:GenCond056

SEPIO:0000223

(Met)

CGEX:CritAssess377

Parental testing in our lab confirmed this variant was present de novo in 1 proband with clinical features of CFC. (LMM internal Data)

CGEX:EvLn128

SEPIO-CG:99032

(PM6)

CAR:CA280055

CGEX:GenCond069

SEPIO:0000223

(Met)

CGEX:CritAssess378

Another variant at the same residue (Lys483Asn) was identified as a de novo variant in an individual with features of a Noonan spectrum disorder (LMM unpublished data). The other variant: NM_004333.4(BRAF):c.1449A>C (p.Lys483Asn) is classified as likely pathogenic by LMM for Rasopathy.

CGEX:EvLn130

SEPIO-CG:99031

(PM5)

CAR:CA280055

CGEX:GenCond049

SEPIO:0000223

(Met)

CGEX:CritAssess276

CGEX:EvLn002

SEPIO-CG:99022

(PVS1)

CAR:CA090898

CGEX:GenCond001

SEPIO:0000223

(Met)

CGEX:CritAssess283

SEPIO-CG:99024

(PS2)

CAR:CA354186

CGEX:GenCond009

SEPIO:0000223

(Met)

CGEX:CritAssess284

CGEX:EvLn012

CGEX:EvLn013

CGEX:EvLn014

CGEX:EvLn015

SEPIO-CG:99025

(PS3)

CAR:CA090410

SEPIO:0000223

(Met)

CGEX:CritAssess285

CGEX:EvLn016

SEPIO-CG:99025

(PS3)

CAR:CA090884

SEPIO:0000223

(Met)

CGEX:CritAssess289

CGEX:EvLn021

SEPIO-CG:99026

(PS4)

CAR:CA123287

CGEX:GenCond012

SEPIO:0000224

(Not Met)

CGEX:CritAssess294

CGEX:EvLn027

SEPIO-CG:99028

(PM2)

CAR:CA011797

SEPIO:0000224

(Not Met)

CGEX:CritAssess296

CGEX:EvLn029

SEPIO-CG:99029

(PM3)

CAR:CA090919

CGEX:GenCond062

SEPIO:0000223

(Met)

CGEX:CritAssess297

CGEX:EvLn030

SEPIO-CG:99029

(PM3)

CAR:CA176145

CGEX:GenCond010

SEPIO:0000223

(Met)

CGEX:CritAssess312

CGEX:EvLn050

SEPIO-CG:99033

(PP1)

CAR:CA006429

CGEX:GenCond002

SEPIO:0000223

(Met)

CGEX:CritAssess313

CGEX:EvLn051

SEPIO-CG:99034

(PP2)

CAR:CA016087

SEPIO:0000223

(Met)

CGEX:CritAssess314

CGEX:EvLn052

SEPIO-CG:99035

(PP3)

CAR:CA090928

SEPIO:0000223

(Met)

CGEX:CritAssess315

CGEX:EvLn053

SEPIO-CG:99035

(PP3)

CAR:CA090884

SEPIO:0000223

(Met)

CGEX:CritAssess318

CGEX:EvLn055

SEPIO-CG:99036

(PP4)

CAR:CA090915

CGEX:GenCond022

SEPIO:0000223

(Met)

CGEX:CritAssess319

CGEX:EvLn056

SEPIO-CG:99036

(PP4)

CAR:CA501234

CGEX:GenCond064

SEPIO:0000224

(Not Met)

CGEX:CritAssess320

CGEX:EvLn057

SEPIO-CG:99037

(PP5)

CAR:CA019369

CGEX:GenCond023

SEPIO:0000223

(Met)

CGEX:CritAssess322

CGEX:EvLn059

SEPIO-CG:99037

(PP5)

CAR:CA276116

CGEX:GenCond025

SEPIO:0000223

(Met)

CGEX:CritAssess323

CGEX:EvLn060

SEPIO-CG:99038

(BA1)

CAR:CA090891

SEPIO:0000223

(Met)

CGEX:CritAssess326

CGEX:EvLn064

SEPIO-CG:99039

(BS1)

CAR:CA017597

CGEX:GenCond026

SEPIO:0000223

(Met)

CGEX:CritAssess327

CGEX:EvLn065

SEPIO-CG:99039

(BS1)

CAR:CA090926

CGEX:GenCond027

SEPIO:0000223

(Met)

CGEX:CritAssess333

CGEX:EvLn075

CGEX:EvLn076

SEPIO-CG:99041

(BS3)

CAR:CA132727

SEPIO:0000223

(Met)

CGEX:CritAssess334

CGEX:EvLn077

CGEX:EvLn078

SEPIO-CG:99041

(BS3)

CAR:CA501231

SEPIO:0000223

(Met)

CGEX:CritAssess335

CGEX:EvLn079

SEPIO-CG:99042

(BS4)

CAR:CA023690

CGEX:GenCond035

SEPIO:0000223

(Met)

CGEX:CritAssess338

CGEX:EvLn081

SEPIO-CG:99043

(BP1)

CAR:CA020822

CGEX:GenCond036

SEPIO:0000223

(Met)

CGEX:CritAssess339

CGEX:EvLn082

SEPIO-CG:99043

(BP1)

CAR:CA020822

CGEX:GenCond037

SEPIO:0000223

(Met)

CGEX:CritAssess342

CGEX:EvLn085

CGEX:EvLn086

SEPIO-CG:99044

(BP2)

CAR:CA143572

CGEX:GenCond038

SEPIO:0000223

(Met)

CGEX:CritAssess343

CGEX:EvLn087

SEPIO-CG:99044

(BP2)

CAR:CA182840

CGEX:GenCond039

SEPIO:0000223

(Met)

CGEX:CritAssess345

CGEX:EvLn089

SEPIO-CG:99045

(BP3)

CAR:CA148212

SEPIO:0000223

(Met)

CGEX:CritAssess347

CGEX:EvLn091

SEPIO-CG:99045

(BP3)

CAR:CA184168

SEPIO:0000223

(Met)

CGEX:CritAssess352

CGEX:EvLn094

SEPIO-CG:99047

(BP5)

CAR:CA137502

CGEX:GenCond060

SEPIO:0000223

(Met)

CGEX:CritAssess353

CGEX:EvLn095

SEPIO-CG:99047

(BP5)

CAR:CA137502

CGEX:GenCond071

SEPIO:0000223

(Met)

CGEX:CritAssess355

CGEX:EvLn097

SEPIO-CG:99048

(BP6)

CAR:CA276195

CGEX:GenCond073

SEPIO:0000223

(Met)

CGEX:CritAssess356

CGEX:EvLn098

SEPIO-CG:99048

(BP6)

CAR:CA016113

CGEX:GenCond043

SEPIO:0000223

(Met)

CGEX:CritAssess357

CGEX:EvLn099

SEPIO-CG:99048

(BP6)

CAR:CA113946

CGEX:GenCond044

SEPIO:0000224

(Not Met)

CGEX:CritAssess358

CGEX:EvLn100

SEPIO-CG:99049

(BP7)

CAR:CA501232

SEPIO:0000223

(Met)

CGEX:CritAssess359

CGEX:EvLn101

SEPIO-CG:99049

(BP7)

CAR:CA013536

SEPIO:0000223

(Met)

CGEX:CritAssess376

CGEX:EvLn126

SEPIO-CG:99028

(PM2)

CAR:CA280055

SEPIO:0000223

(Met)