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About kaleigh’s trust
This site has been setup to highlight the battle our beautiful daughter, Kaleigh is currently fighting against a cancer known as DIPG (Diffuse Intrinsic Pontine Glioma). We wanted to use it as a platform to provide some updates when we can on Kaleigh’s progress and also share our experiences which may help others who may be going through something similar.
Please accept our apologies in advance if there is a delay responding to any questions or comments you may have, we will do our best to reply when we can.
We are so thankful to the goodwill and generosity everyone has shown to us that there aren’t enough words to express our gratitude, but thank you for your kindness and support. If you would like to donate to Kaleigh’s fund, you can do so by clicking on this donation link or by clicking on the donate button at the top of this page.
Once again, thank you and we will not give up.
Love, Scott, Yang, Kaleigh and Carson.
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Presently, there is no cure for DIPG and the only treatment available is radiotherapy, which is a palliative treatment developed over 30 years ago. Unfortunately, whereas other cancer research has improved survival rates over the years, the lack of funding for DIPG means there has been no improvement in this area. We have started an online petition (https://petition.parliament.uk/petitions/131556) in the hope the British Government will consider providing funding for research into a cure to this terrible disease and at least offer hope for future generations.
Like most girls her age, Kaleigh enjoys being a princess (especially a pink one), attending dancing lessons, singing, swimming and playing with her friends. Basically, using up the oodles of energy she has which would tire out the average adult in less than half an hour!
However, something wasn’t quite right on Thursday 14th of April 2016 as she didn’t seem her usual self. She had complained of double vision which we had put down to the cold she had been carrying, which we thought was getting heavier and had decided to keep her home from school.
To our relief, everything appeared to be okay the next day and Kaleigh was well enough to attend school and get back to being the vibrant little girl we all knew and loved.
We were eating breakfast on the morning of Saturday the 16th of April 2016 before getting ready for Chinese school, when Kaleigh laughed that she could see two of me, and we noticed her left eye turning slightly inwards.
I got in contact with a friend who is also our optician to ask for his opinion. He suggested we took Kaleigh to Moorfield eye hospital where they confirmed double vision but the eye was healthy but suggested we should get further checked out at a general hospital.
We were taken to Royal London, where they carried out a CT scan at 4.30pm, followed by a MRI scan at 9.30pm, with results close to Midnight, when we were told a lump was found in the brain area but weren’t able to elaborate on the information.
We were transferred to Great Ormond Street Hospital at 3.00AM on Sunday 17th of April 2016, where we met with other doctors and they showed us the scans and highlighted the abnormal tissue they had identified. Yang and myself were taken to a room to have a further discussion with the consultant at 11AM regarding the abnormal tissue, and advised they would provide a plan of action by Tuesday morning after their multi-disciplinary meeting.
Tuesday 19th April 2016, this was the day our world turned upside down as the consultants confirmed the diagnosis that Kaleigh had developed a condition called DIPG. At the time, we had little knowledge of what this was except we were told there is currently no known cure and this news was devastating and left us distraught. Yet, as would any parent in our position, we will do everything we can and cling on to any glimmer of hope possible.
Monday 25th April 2016 was the start of the first of 30 scheduled sessions of Radiotherapy which is due to be completed by Tuesday 7th June 2016 at University College of London Hospital. Kaleigh is currently doing very well with her radiotherapy and she has managed to go into school occasionally to see her friends even if it is only for about an hour.
We are currently travelling into hospital everyday apart from weekends and bank holidays, which has been tough of the whole family. This is where we are thankful for the support of family and friends, as this have given us the strength to keep going.
We are thankful for all your support, lots of love,
Scott, Yang, Kaleigh and Carson.
Pontine gliomas are malignant (cancerous) tumours that originate from the part of the brain known as the brain stem (pons). They develop from cells called astrocytes. Astrocytomas are the most common type of glioma. You will often hear the terms astrocytoma and glioma used interchangeably. In children, 80% of brain stem tumours are pontine gliomas.
If a biopsy is carried out they are usually found to be high grade gliomas and are classified according to the grade of aggressiveness (how quickly they grow) as either anaplastic astrocytomas (grade III) or glioblastoma multiforme (GBM). These tumours grow amongst the normal nerve cells of the brain stem making them impossible to remove surgically as the brain stem is a vital area of the brain that controls many body functions.
Who gets pontine glioma?
Less than 40 children a year develop pontine glioma in the UK. This is around 10-15% of all childhood brain tumours. They rarely occur in adults. Like most brain tumours, the cause of pontine gliomas is unknown.
Signs and symptoms
The symptoms are related to the internal pressure that the tumour applies on the brain stem. Occasionally they can cause increased pressure in the head (raised intracranial pressure). Rarely they spread into the spine. Symptoms include:
- Swallowing problems
- Slurred speech
- Facial Weakness
- Abnormal Gait (the way the child walks)
- Difficulty with tasks like handwriting
- Gradual decline in school work
- Changes in personality and behaviour
If there is increased pressure in the head:
- Nausea and Vomiting
If the tumour spreads to the spine:
- Back pain
- Difficulty walking
- Problems with bowel and bladder control
Tests / investigations
We will need to carry out some tests to find out as much as possible about the type, position and size of the tumour. This will help us to decide on the best treatment for your child. These tests include:
CT scan – it is likely a CT scan of your child’s brain was the first specific test carried out at your local hospital. Although MRI scans are usually the best way of seeing the tumour and the effects of treatment, sometimes CT scans are also useful.
MRI scan – this scan allows us to see the brain and spine in great detail and is used regularly to diagnose and follow the effect treatment is having on your child’s tumour
Diffuse Intrinsic Pontine Glioma (D.I.P.G.) is a tumor located in the pons of the brain stem. The brain stem is the bottom most portion of the brain, connecting the cerebrum with the spinal cord. The majority of brain stem tumours occur in the pons, are diffusely infiltrating (they grow amidst the nerves), and therefore are not able to be surgically removed.
Cytogenetic Characteristics of Diffuse Intrinsic Pontine Gliomas
The genomic characteristics of DIPGs appear to differ from those of most other pediatric high-grade gliomas and from those of adult high-grade gliomas. A number of chromosomal and genomic abnormalities have been reported for DIPG, including the following:
- Histone H3 genes: Approximately 80% of DIPG tumors have a mutation in a specific amino acid in the histone H3.1 (H3F3A) or H3.3 (HIST1H3B) genes. These same mutations are observed in pediatric high-grade gliomas at other midline locations but are uncommon in cortical pediatric high-grade gliomas and in adult high-grade gliomas.
- Activin A receptor, type I (ACVR1) gene: Approximately 20% of DIPG cases have activating mutations in the ACVR1 gene, with most occurring concurrently with H3.3 mutations. Germline mutations in ACVR1 cause the autosomal dominant syndrome fibrodysplasia ossificans progressiva (FOP), although there is no cancer predisposition in FOP.
- Receptor tyrosine kinase amplification: PDGFRA amplification occurs in approximately 30% of cases, with lower rates of amplification observed for some other receptor tyrosine kinases (e.g., MET and IGF1R).
- TP53 deletion: DIPG tumors commonly show deletion of the TP53 gene on chromosome 17p. Additionally, TP53 is commonly mutated in DIPG tumors, particularly those with histone H3 gene mutations. Aneuploidy is commonly observed in cases with TP53 mutations.
The gene expression profile of DIPG differs from that of non–brain stem pediatric high-grade gliomas, further supporting a distinctive biology for this subset of pediatric gliomas.