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\begin{document}

\title{Monoallelic deleterious MUTYH mutations generate colorectal cancer:a
case report}



\author[1]{Bei Zhao}%
\author[1]{Wenqi Sun}%
\author[1]{Yunrong Wang}%
\author[1]{Xinrong Wu}%
\author[1]{Yifan Li}%
\author[1]{Weiwei Wang}%
\author[1]{Muhan Ni}%
\author[1]{Peng Yan}%
\author[1]{Xiaotan Dou}%
\author[1]{Lei Wang}%
\author[1]{Min Chen}%
\affil[1]{Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University,  Nanjing, China}%


\vspace{-1em}



  
  \date{June 18, 2024}


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\textbf{Monoallelic deleterious MUTYH mutations generate colorectal
cancer:a case report}

\textbf{Abstract}

\textbf{Background:} Here we reported a particular case of
MUTYH-associated polyposis (MAP) that had only one rare heterozygous
mutation, but some particular clinical manifestations contributed to
occur in this male patient by only one defective MUTYH allele were worth
of further investigation.

\textbf{Case presentation:} We reported a case of MAP. It is about a
33-year-old man with chief complaints of hematochezia who had multiple
polyps which were found in his colon via colonoscopy. He followed his
doctor's advice and performed a genetic analysis examination. Germline
test was positive for a major heterozygous mutation: chr1:45800165 on
the MUTYH gene. MUTYH gene sequence analysis confirmed the following
heterozygous mutation: c.55CT (p.R19X) in exon 2 (ClinVar
NM\_001128425). Unfortunately, his mother and daughter have the ilk
mutation according to genetic analysis (Figure 1). However, this
mutation at the site was not detected in his father. Various types of
polyps were found on repeated colonoscopy, which tended to become latent
cancerous in the futre.

\textbf{Conclusion:} This case indicated that awareness of the risk of
carcinogenesis of polyps in carriers of monoallelic mutations might
accordingly increase and understanding of the type of genetic-related
disease will be enhanced by us.

\textbf{keywords:} MUTYH; Colorectal cancer; Hereditary colorectal
cancer; Polyposis

\textbf{Background}

Familial adenomatous polyposis (FAP), a rare autosomal dominant
inherited disease, is generally considered to be related to the APC
gene\textsuperscript{{[}1{]}}. However, there is a special type of
APC-negative but MUTYH-positive called MUTYH-associated polyposis (MAP).
MAP includes both monoallelic mutations and biallelic
mutations\textsuperscript{{[}2{]}}. Of course, biallelic mutations lead
to an increased risk of colorectal cancer. But patients with biallelic
mutations are a minority, and heterozygous variants are more common. It
is still unclear whether only one MUTYH mutation is of clinical
importance or not. Recently, more and more research has focused on the
risk of colorectal cancer caused by monoallelic
mutations\textsuperscript{{[}3{]}}. Previously, a number of studies
showed that monoallelic MUTYH had little to do with CRC. Whether
heterozygous variants increase the risk of colorectal cancer is still
under debate\textsuperscript{{[}4{]}}. Interestingly, what happens in
the gut deserves further investigation if there is another mutation
associated with colorectal polyps. In this report, we described the rare
genetic variant, which were unusual genetic mutations that improve our
awareness and understanding of the disease.

\textbf{Case description}

A 33-year-old man was taken for counseling after discovering genetic
mutations. Firstly, on March 21st, 2022, the patient went to Anhui
Provincial Hospital for treatment with chief complaint of hematochezia
for several months. He then underwent a colonoscopy which was showed
that a 3.5 cm long pedunculated polyp could be seen in the descending
colon at a distance of 55 cm from the edge of the anus. And then a 0.8
cm size polyp was detected near to it. In addition, another larger
polyp, about 6 cm in size, was found at the junction of the sigmoid and
descending colon. It was worth noting that this distinct sessile polyp
with a lobulated surface and varicose veins of the surrounding mucosa
almost blocked the intestinal lumen. Several polyps ranging in size from
0.5 cm to 1 cm also were found in the rest of the colon. Pathologic
findings after biopsy confirmed that the maximal polyp is a
tubulovillous adenoma with moderate dysplasia. A computed tomography of
the abdomen, performed half a month later, documented multiple lesions
in the splenic flexion of the colon and in the sigmoid, considering the
larger one, which is local with intussusception proximal to the sigmoid.
Genetic analysis revealed a deleterious single allele heterozygous
germline mutation. MUTYH gene sequence analysis confirmed the following
heterozygous mutation: c.55CT (p.R19X) in exon 2 (ClinVar
NM\_001128425). In addition, the LHX4 mutation: c.256G\textgreater{}A
(p.G86S) in exon 3 (ClinVar NM\_033343) also was notable. The
electrophoretic sequence of MUTYH exon 2 revealing mutations is shown in
Figure 2. This genetic analysis confirmed that the MUTYH mutation was a
single allele heterozygous mutation. A diagnosis of MAP was then
confirmed. His mother and daughter have the same MUTYH gene mutation,
however, while no particular genetic variations occurred in his father.
Interestingly, this MUTYH mutation carrier had a family history
consistent with dominant inheritance. When he was admitted to another
Class A tertiary hospital on May 2nd, 2022, he underwent endoscopic
mucosal resection surgery. Pathological analysis showed that cystic
fibrosis located 25 cm from the margin of anus was a microvillous
tubular adenoma with high grade intraepithelial neoplasia and local
carcinogenesis. Specifically, cancerous tissue at the site has
infiltrated into the 3mm submucosal layer, but the vertical and lateral
margins were both negative. The surgeon recommended abdominal surgery
for the patient, but failed. Almost about 22 days later, the patient
sought further endoscopic treatment and came to our hospital. An
abdominal enhancement CT was later performed, documenting multiple mass
lesions of the colonic splenic curvature and sigmoid colon. The next day
the patient underwent colorectal EMR and ESD (Figure 3). Lesions between
5 mm and 6 cm are found during surgery. The largest tissue sample with
dissociative tissue pieces was a villous tubular adenoma consisting of
large low-grade and rarely high-grade intraepithelial neoplasia. In
addition, a lesion grows nearby, the pathology of which was a villous
tubular adenoma with low-grade intraepithelial neoplasia. The splenic
flexure and sigmoid also have several similar polyps. Some hyperplastic
polyps were detected in the rectum. All pathologically confirmed lesion
strains were negative. Immunohistochemistry analysis was added showing
that the junction of the descending colon with the sigmoid, sigmoid and
splenic flexure showed similar results: all polyps were sent for
investigation manifested as Desmin (mucosal muscle +), CEA (+), P53 (+),
including wild-type and partially mutant and various grades of Ki67(+).

Three months ago, he came to our hospital for colonoscopy surveillance.
And the positron emission tomography (PET-CT) scan was unremarkably
normal. When he was hospitalized this time, his bowel preparation was
not fairly satisfactory as a large amount of feces remained in the
bowel(Figure 4). Many polyps were found again after the colonoscopy.
Tubular adenomas and hyperplastic polyps were removed with the technique
of a cold snare. Considering the poor bowel preparation, he was
instructed to repeat the colonoscopy after 3 months. At present, he went
to our hospital again for a colonoscopy. During this process, several
newly emerged polyps were found in the colon and were removed via
conventional EMR. These polyps remain concentrated in the distal colon,
including the descending colon, sigmoid colon, and rectum(Figure 5). In
order to avoid unnecessary risks, we also arranged an additional CT
examination for him, and this time there were no signs of
intussusception and other potential malignant changes.

\textbf{Discussion}

According to relevant research, the particular genetic mutation has been
reported only in Asian regions, in contrast to MUTYH-related common gene
mutations in Caucasians \textsuperscript{{[}5-8{]}}. MUTYH-associated
familial intestinal polyposis caused by this gene also is attenuated
compared to regular MAP. MAP occurred mainly in the proximal colon, and
polyps are mainly tubular adenomas, some tubular villous adenomas, and
occasionally hyperplastic polyps \textsuperscript{{[}9{]}}.
Interestingly, the vast majority of polyps in this patient were located
in the left colon, in contrast to MAP, which occurred in the right
colon. However, recent literature has shown that patients associated
with MYH deficiency resulting in hyperplastic polyps are not uncommon
and present in a condition where hyperplastic polyps coexisted with
adenomatous polyps\textsuperscript{{[}9-10{]}}.This is consistent with
the pathologic features of polyps in this patient, with proliferative
polyps, tubular adenomas, and choriotubular adenomas growing together.

He has a heterozygous mutation in the MUTYH gene, which is a monoallelic
mutation. The clinical severity is low, however, caused by this
monoallelic heterozygous mutation was not yet reported in any relevant
case. Unlike biallelic mutations, which could accelerate the development
of adenomas in subsequent years, according to previous literature and
ESGE guidelines, patients with uniallelic mutations rarely developed
adenomatous polyposis or had only a slightly increased risk of
developing CRC\begin{CJK}{UTF8}{gbsn}\textsuperscript{{[}4、11{]}}\end{CJK}\selectlanguage{english}. As mild as the description
in the literature is, his immunohistochemical results predicted that the
tumor had a strong invasive and metastatic capacity. This might indicate
the need for closer follow-up care. As understanding increases, there
also is a growing body of literature showing that even patients with
single allelic mutations have a higher risk of cancer than other normal
people \begin{CJK}{UTF8}{gbsn}\textsuperscript{{[}12、13、15{]}}\end{CJK}\selectlanguage{english}. Tumorigenesis by a mechanism
of functional heterozygous somatic deletion of the MUTYH allele in
tumors due to monoallelic pathogenic MUTYH germline variants. And the
carriers of the monoallelic pathogenic germline variant MUTYH have a
higher risk of developing tumors, particularly those with frequent
events of loss of heterozygosity \textsuperscript{{[}13{]}}.

According to the family study, just like the patient in our report, the
Clinvar database categorizes his gene as causative, and his mother and
daughter have the same gene mutation site, and their colorectal cancer
risk was more than approximately
three-fold\begin{CJK}{UTF8}{gbsn}\textsuperscript{{[}14-15、16{]}}\end{CJK}\selectlanguage{english}. And depending on the
genetic make-up of mother and daughter, it is more like an autosomal
dominant inheritance. In addition, family genealogy analyzes can be used
to better evaluate the common mutations in Asian populations in order to
better assess and intervene in colorectal cancer hazard in monoallelic
carriers \textsuperscript{{[}15{]}}.

It was worth mentioning that he has an another mutation in LHX4, but the
genetic report does not explicitly mention the association with
colorectal cancer. At present, the expression pattern of LHX gene in
colorectal cancer is still unclear. The literature posits that LHX4
upregulates \selectlanguage{greek}β-\selectlanguage{english}catenin levels in colorectal cancer cell lines, and LHX4
associated mutations or deletion disrupted the direct LHX4-\selectlanguage{greek}β-\selectlanguage{english}catenin
interaction , as well as significantly reduced the capability of LHX4 to
both combine and trans-increase target gene promoters. Importantly,
deletion or mutation of LHX4 also abolished its tumor-promoting
function, suggesting that its mediated LHX4-catenin interaction was
crucial for LHX4's tumor suppressor functions\textsuperscript{{[}17{]}}.
It is unknown whether the progression of colon polyps is balanced when
the two genetic mutations are present at the same time. In clinical
work, we must pay more attention to the results of patients' genetic
examinations to prevent rare reported gene mutations from being
overlooked, and carry out individual follow-up protocols to study in
detail the clinical manifestations caused by polygenic mutations.

Malignant tumors accounted for up to 90\% of adult intussusception, so
if adult intussusception is present, the possibility of tumorigenesis
cannot be overlooked and endoscopy should be considered for surveillance
screening and regular follow-up \textsuperscript{{[}18{]}}.

In our case report, patients should appropriately lengthen and shorten
the endoscopic follow-up time according to the bowel preparation and
whether the pathology is prone to cancer, and individualize the
endoscopic polypectomy plan so that the patient's lesions do not develop
as much as possible.

\textbf{Conclusions}

At present, colon cancer triggered by homozygous mutations in the MUTYH
gene was no longer surprising, and serious lesions caused by
heterozygous variants have rarely been reported. Our results underscored
the need for closer follow-up when patients with this gene mutation are
present, and we recommended that family members of patients should be
included in the follow-up population.

\textbf{Ethics}

Written informed consent was obtained from the patient for inclusion in
this case report. The case was approved by the institutional review
board of the affiliated Drum Tower Hospital of Nanjing University,
Medical School (2023-CR002-01).

\textbf{Statement}

No funding was obtained for this study.

\textbf{Competing interests}

All the authors declared that they had no conflicts of interest or
financial ties to disclose.

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\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Figure 1. Family tree of patient The proband's age at onset of the
polyposis (33 years). The patient's father was unaffected, but his
mother and daughter had a heterozygous mutation(without colonoscopy).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 2.Partial chromatogram of the junction sequencing MUTYH gene
sequence analysis confirmed the following heterozygous mutation: c.55CT
(p.R19X) in exon 2 (ClinVar NM\_001128425). Only the patient's father
does not have the mutation in this gene.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Figure 3. First colonoscopy in our hospital A:A huge mass can be seen at
the junction of the descending colon and the sigmoid colon.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

B:This is the specimen of the lesion that was removed. The pathology
indicates that it is a villous tubular adenoma, most of which are
accompanied by low-grade intraepithelial neoplasia, and a small number
of high-grade intraepithelial neoplasia on the surface of the adenoma.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

Figure 4. Second colonoscopy in our hospital The intestinal mucosa was
not completely exposed because the intestinal preparation was not good
and only a few polyps were seen this time. As shown in the image, there
are polyp-like growths in the descending colon.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image6/image6}

\end{center}
\end{figure}

Figure 5. Third colonoscopy in our hospital This time colonoscopy found
many flat (0-IIa and 0- IIb)polyps. It is worth noting that larger lesions
missed at the last colonoscopy were also seen in the rectum and at the
sigmoid junction. Not surprisingly, Polyps remain concentrated in the
left colon.

\selectlanguage{english}
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