Pallano

IN THE SUPERIOR COURT OF THE STATE OF DELAWARE

IN AND FOR NEW CASTLE COUNTY

ANAJAI CALCAÑO PALLANO, et al., )
)
Plaintiffs, )
)
v. ) C.A. No. N09C-11-021 JRJ
)
THE AES CORPORTATION, et al., )
)
Defendants. )

ORDER

AND NOW TO WIT, this 11th day of December, 2015, the Court having

heard and duly considered Plaintiffs’ Motion to Exclude the Testimony of

Defendants’ Expert Samuel Moore, M.D.; 1 AES’s Opposition; 2 and Plaintiffs’

Reply; 3 IT APPEARS THAT:

1. It is undisputed that Minor Plaintiff Isael Altagracia Andujar suffers from

Hirschsprungs disease, a congenitally acquired condition arising from the

1
Plaintiffs’ Motion to Exclude the Testimony of Defendants’ Expert Samuel Moore, M.D.
(“Pls.’ Mot. Exclude Dr. Moore”) (Trans. ID. 57346390). This Motion is one of nineteen
Daubert Motions filed by the parties. Defendants have challenged seven of Plaintiffs’ causation
experts and four of Plaintiffs’ exposure experts. Plaintiffs have challenged six of Defendants’
causation experts and two of Defendants’ exposure experts. The parties submitted twenty-six
Joint Daubert Exhibits, which include each expert’s report, deposition, and curriculum vitae (“J.
Ex.”) (Trans. ID. 57342400). See J.Ex. 20.A Dr. Samuel Moore Expert Report on Isael
Altagracia Andujar (“Dr. Moore Expert Report”).
2
AES’s Opposition to Plaintiffs’ Motion to Exclude the Testimony of Dr. Samuel Moore at 12
(“Defs.’ Opp’n.”) (Trans. ID. 57536580).
3
Plaintiffs’ Reply in Further Support of its Motion to Preclude the Testimony of Defendants’
Expert Samuel Moore, M.D. (“Pls.’ Reply”) (Trans. ID. 57627760).
abnormal development of the nerves of the gastrointestinal system. 4 For over

thirty years, Defendants’ expert Samuel Moore, M.D. (“Dr. Moore”) has focused

his research and clinical practice on Hirschsprungs disease. In addition to treating

over 500 Hirschsprungs patients, Dr. Moore has researched, published, and

presented extensively on the genetic causes of Hirschsprungs disease, including a

peer-reviewed publication identifying the RET gene as a primary contributor to

Hirschsprungs disease. 5

2. According to Dr. Moore, “the widely accepted [ ] opinion on the etiology

of Hirschsprungs disease [is] that it results chiefly from genetic changes resulting

in the enteric nervous system maldevelopment and not environmental factors,”6

and, “[a]lthough there is no specific single genetic site attributed to Hirschsprungs

disease etiology, Hirschsprungs disease is widely recognised as resulting primarily

from variations in the RET proto-oncogene (with some autosomal dominant

4
See Pallano, et al. v. AES Corp., et al., 2015 WL 7776612 (Del. Super. Nov. 24, 2015)
(Opinion Denying Defendants’ Daubert Motion to Exclude the Testimony of William P.
Konicki). The Court incorporates by reference the facts, background, and the discussion of
Delaware Rule of Evidence 702 and Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579 (1993),
set forth in that opinion.
5
Dr. Moore received his medical degree in 1971 from the University of Cape Town. Dr. Moore
Expert Report at 1. He has published 134 publications, thirty-one abstracts, twenty textbook
chapters, and authored two student books about paediatric surgery. Id. Fifty of Dr. Moore’s
publications directly address aspects of Hirschsprungs disease, and twenty-eight publications
address the development of the enteric nervous system and related dysfunctional syndromes. Id.
at 2. Dr. Moore has presented at 195 scientific meetings, fifty-one relating to Hirschsprungs
disease and allied conditions. Id. In 2014, Dr. Moore received the Denis Browne Medal for an
outstanding contribution to paediatric surgery from the British Association of Paediatric
Surgeons. Id. at 1.
6
Id. at 5.
2
inheritance).”7 Dr. Moore also explains that there are also reports of susceptibility

mutations in at least eleven other genes. 8 In describing the complex genetic

etiology of Hirschsprungs disease, Dr. Moore explains that Hirschsprungs disease

follows a “multigenetic” model—i.e. that Hirschsprungs disease usually results

from the interaction of variants in several genes, rather than from a variant in a

single gene. 9

3. Dr. Moore opines that Plaintiff Isael’s Hirschsprungs disease is most

likely caused by a genetic variation, and not environmental factors.10 Plaintiffs

seek to exclude Dr. Moore’s opinion under D.R.E 702 and Daubert arguing that:

(1) he lacks the requisite qualifications to offer a causation opinion about genetics

because he is a surgeon not a geneticist; (2) his opinion is not peer-reviewed, it is

untestable, and was developed only for litigation; and (3) he did not rule out

alternative causes such as the individual constituents of Coal Ash waste.

4. Dr. Moore’s opinion is based on the causal links between Plaintiff Isael’s

individual genetic variations and Hirschsprungs disease, and the absence of any

known study showing an association between Hirschsprungs disease and

teratogenic exposure. Dr. Moore relies on genetic testing showing that Plaintiff

Isael has at least three genetic variations: (1) a variation on the RET gene (exon
7
Id.
8
Id.
9
Id. at 3.
10
Id. at 3–5. (“[T]he evidence for a predominant genetic etiology (cause) for Isael’s
Hirschsprungs disease is overwhelming . . .”).
3
20); (2) copy loss at chromosome 21; and (3) copy loss at chromosome 22. 11

According to Dr. Moore, each of these variations is located in a highly sensitive

area close to critical genes involved in the development of the enteric nervous

system. 12 Consistent with the multigenetic nature of Hirschsprungs disease, the

identification of multiple genetic variations in Isael’s genetic testing (each

associated with chromosomal and/or congenital abnormalities) also strengthens the

strong likelihood of a genetic cause. 13

5. Plaintiffs argue that Dr. Moore’s theory with respect to Plaintiff Isael’s

RET variation is not peer-reviewed and is untestable because a RET gene variation

at the identical sub-genetic location (exon 20) has never been described in

literature linking the variant with Hirschsprungs disease.14 Isael’s exon 20

variation is located in the last region (“tail”) of the RET gene, the particular area of

the RET gene where Dr. Moore has extensively focused his research.15 Dr. Moore

explains that this critical intracellular tyrosine kinase tail of the RET gene plays a

critical role in the development of the enteric nervous system and it is common for

Hirschsprungs patients with variations in the RET gene to have them in this

11
Dr. Moore Expert Report at 2–3.
12
Id. at 3.
13
Id.
14
Pls.’ Mot. Exclude Dr. Moore at 14–15.
15
Dr. Moore Expert Report at 2. Dr. Moore has focused his research on the “under researched”
intracellular receptor tyrosine tail of the intracellular tyrosine kinase portion of the gene, which
includes exon 20. Id.
4
specific area.16 Accordingly, based on the position of the variation at the very tail

of the RET gene, Dr. Moore concludes that Plaintiff Isael’s “alteration in exon 20

must be considered as highly likely to play a part in the etiology of Isael’s

Hirschsprungs disease in conjunction with other contributing genetic defects” such

as the multigenetic nature of Hirschsprungs disease. 17 Dr. Moore also cites three

pieces of literature finding exon 20 variations in Hirschsprungs patients. 18 Finally,

Dr. Moore notes that Isael’s genome scan showed that he inherited the variation in

exon 20 from his unaffected mother.19 Relying on literature relating to familial

transmission of Hirschsprungs disease, Dr. Moore states that, “[o]ne of the

strongest arguments for the genetic origin of Hirschsprungs disease is the

consistent recurrence in families,”20 and “[t]he consistency of familial transmission

of Hirschsprungs disease strongly supports the current genetic etiology for Isael’s

condition.”21

6. With respect to Isael’s copy number variations, Dr. Moore explains that

the clinical association between Hirschsprungs disease and chromosome 21 and

chromosome 22 has long been established.22 For example, Down syndrome, which

16
Id. at 3–4.
17
Id. at 4.
18
Defs.’ Opp’n at 12–13; Dr. Moore Export Report at 9, 24–32.
19
Dr. Moore Export Report at 9, 15.
20
Id. at 15. Dr. Moore cited an article finding “180 times higher familial risk than the estimated
0.26% expected in the general population.” Id.
21
Id.
22
Id. 9–12.
5
is caused by having an extra copy of chromosome 21, is the most common

chromosomal anomaly associated with Hirschsprungs disease.23 In support of this

opinion, Dr. Moore cites several studies explaining the clinical association between

these missing chromosomes and Hirschsprungs disease, including the importance

of the location of chromosome 21 and chromosome 22 in connection with

Hirschsprungs disease. 24

8. Dr. Moore’s opinion passes muster under D.R.E. 702 and Daubert.

Based on Dr. Moore’s research, experience, and extensive expertise related to

Hirschsprungs disease, the Court finds Dr. Moore is qualified to opine about the

genetic causes of Hirschsprungs disease. Dr. Moore’s report thoroughly discusses

the complex genetic etiology of Hirschsprungs disease, the functional significance

of Isael’s specific gene variations, and notes the absence of any known study

showing an association between Hirschsprungs disease and teratogenic exposure

(specifically any of the substances found in Coal Ash Waste). Dr. Moore’s

proffered testimony is based upon sufficient facts and data, is the product of

reliable principles and methods, and he has applied the principles and methods

reliably to the facts of this case. Dr. Moore articulates his thought process,

evaluation methods, and conclusions.

WHEREFORE, because the Court finds that the opinions set forth in Dr.

23
Id. at 9–11.
24
Id. at 9–12.
6
Moore’s Expert Report are both relevant and reliable, the Plaintiffs’ Motion to

Exclude is DENIED.

IT IS SO ORDERED.

_____________________________
Jan R. Jurden, President Judge

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