Assignment: Biology Diagnosis and Treatment of Craniopharyngioma Article Summary

Assignment: Biology Diagnosis and Treatment of Craniopharyngioma Article Summary

Question Description
I’m working on a biology writing question and need an explanation and answer to help me learn.

find a primary research article on Suprasellar craniopharyngioma- Their impact on vision and the endocrine system then write the summary. the summary should include Author and Title of article (published in 2016 or later)

Craniopharyngioma (CP) is a rare embryonic malformation of
the sellar/parasellar region with a low histological grade.
Clinical manifestations are related to hypothalamic/pituitary
deficiencies, visual impairment, and increased intracranial
pressure. Recent insight into the molecular pathogenesis of
CP opens new perspectives on targeted therapy in papillary
CP harboring BRAF-V600E mutations. Further research to elucidate pathogenic mechanisms and hopefully prevent hypothalamic involvement of CP is warranted. If the tumor is favorably localized, the therapy of choice is complete resection,
with care taken to preserve the optical and hypothalamic
functions. In patients with unfavorable tumor localization
(i.e., hypothalamic involvement), the recommended therapy
is a limited hypothalamus-sparing surgical strategy followed
by local irradiation. Surgical treatment strategies should be
based on a multidisciplinary approach involving experienced
teams. Centralizing the treatment of CP in experienced “centers of excellence” and multicenter-based networks for reference assessments should be considered to assure a high
standard of treatment quality. CP recurrence and progression
are frequent. Irradiation has proven effective in reducing recurrences and progression. Proton beam therapy, available
in a wider range in the near future, will help to avoid radiooncological side effects. Anatomical involvement and/or surgical lesions of posterior hypothalamic areas can result in serious sequelae that compromise quality of life (QoL), such as
hypothalamic obesity and psychopathological symptoms.
Novel insights into neuropsychological sequelae after CP occurrence should be the basis for the development of therapeutic neuropsychological interventions. CP should be managed as a frequently chronic disease, providing ongoing care
of pediatric and adult patients’ clinical and QoL consequences by experienced multidisciplinary teams.
© 2019 S. Karger AG, Basel
Introduction
Craniopharyngioma (CP) is a rare embryonic malformation with a low histological grade (WHO Io) originating from the remnants of the craniopharyngeal duct in the
sellar and parasellar area. Overall survival rates at 20 years
after childhood-onset CP are high (87–95%). However,
long-term quality of life (QoL) is frequently impaired due
754 Neuroendocrinology 2020;110:753–766 Müller
DOI: 10.1159/000504512

Assignment: Biology Diagnosis and Treatment of Craniopharyngioma Article Summary

to the sequelae caused by the anatomical proximity of the
tumor to the hypothalamic-pituitary axis and optic nerve/
chiasm [1–4]. Initial hypothalamic involvement of CP
and/or treatment-related lesions to the hypothalamic-pituitary axis result in hypothalamic obesity (HO). Unfortunately, no generally accepted lifestyle interventions or
pharmacological and bariatric therapy for hypothalamic
obesity in CP have been proven effective in randomized
controlled trials. Currently, the prevention of hypothalamic sequelae is recommended including hypothalamussparing therapeutic approaches that respect the integrity
of nuclei located in posterior hypothalamic areas.
Pathology and Molecular Genetics
Adamantinomatous CP (ACP) and papillary CP (PCP)
are the 2 CP subtypes. ACP is driven by somatic mutations in CTNNB1 (encoding β-catenin), mostly point mutations within exon 3 affecting regulatory residues involved in β-catenin protein stability [5–7]. The consequence of these mutations is that β-catenin cannot be
efficiently degraded, accumulates within the cell, and
overactivates the WNT/β-catenin pathway [8, 9].
PCP, like ACP, also has a low mutational rate (15 mutations/MB), but instead of CTNNB1 mutations, it harbors somatic BRAF-V600E mutations.

So far, no other
recurrent mutations or genomic aberrations have been
identified [7, 10]. The expression of oncogenic BRAFV600E is observed in the vast majority of the tumor cells
[7, 11]. However, the activation of the MAPK pathway is
not observed in all tumor cells, as would be expected, but
is rather restricted to a few tumor cells (i.e., the basal cells
surrounding the fibrovascular cores) [12]. Based on these
novel findings in molecular genetics, targeted therapy has
provided new promising perspectives for treating PCP
haboring BRAF-V600E mutations, exclusively detected in
adult-onset PCP [13–16].
Clinical Manifestations
The diagnosis of childhood-onset CP is often made
late, frequently years after the initial manifestation of
symptoms [17–19], with a clinical picture characterized
by symptoms of increased intracranial pressure (e.g.,
nausea and headache) at the time of diagnosis (Fig. 1).
Further primary manifestations are endocrine deficits
(52–87%) and visual impairments (62–84%). Endocrine
deficiencies are frequently caused by tumor- and/or treatment-related lesions to the hypothalamic-pituitary axis
that affect the secretion of growth hormone (GH, 75%),
gonadotropins (LH/FSH, 40%), thyroid-stimulating hormone (TSH, 25%), and adrenocorticotropic hormone
(ACTH, 25%). At the time of CP diagnosis, 40–87% of
patients present with at least 1 endocrine deficit [20–22].
Other hormonal symptoms such as neurohormonal diabetes insipidus are observed preoperatively in 17–27% of
all CP patients [21–23]. An analysis of anthropometric
data obtained in routine checkups before CP diagnosis in
90 children [18] revealed reduced growth velocity in infants as young as 12 months. Weight gain, predictive of
hypothalamic obesity, occurred as a later manifestation,
shortly before CP was diagnosed. Hoffmann et al. [17]

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Important information on Writing a Discussion Question

• Your response needs to be a minimum of 150 words (not including your list of references)
• There needs to be at least TWO references with ONE being a peer reviewed professional journal article.
• Include in-text citations in your response
• Do not include quotes—instead summarize and paraphrase the information
• Follow APA-7th edition
• Points will be deducted if the above is not followed

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• Follow APA 7th edition
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• Remember to use and follow APA-7th edition for all weekly assignments, discussion questions, and participation points.
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