Are Covid-19 vaccines safe for cancer patients? Here is what cancer experts say – CNN

It's a question that has been on the minds of researchers and oncologists long before the Pfizer and Moderna vaccine rollouts began. Although there is a consensus that the vaccines are safe for most cancer patients, according to the American Cancer Society and others in the medical community, research into whether they will be effective for cancer patients is still a data-free zone. The American Cancer Society recommends that cancer patients talk to their doctors before getting any type of vaccine because all patients and their courses of treatment are different.

There are several factors that may require a cancer patient to delay vaccination, including recent stem cell transplants or other recent use of therapy agents known to reduce vaccine efficacy, according to Dr. Laura Makaroff, the American Cancer Society's Senior Vice President for Prevention and Early Detection.

"As far as safety of the vaccine, every situation for every patient with cancer is a little different. And there's a spectrum of where any one patient might be in their cancer journey," Makaroff told CNN. "The Covid-19 vaccine is definitely safe for people with cancer but it's important that patients have a conversation with their healthcare provider and their cancer care team to determine when is the right time to have the vaccine."

"All the guidance that we're seeing -- the American Cancer society and other leading oncology groups -- is that Covid-19 immunization is recommended for patients in active therapy, but we really understand that there are limited safety and efficacy data on these patients," Makaroff said.

"Despite the lack of safety data specifically in patients with CLL (chronic lymphocytic leukemia), SARS-Cov-2 vaccination is anticipated to be safe."

CLL is characterized by a weakened immune system. The immunocompromization is so severe that CLL patients are advised to avoid live vaccines such as the ones for measles or yellow fever.

"The thing that people don't quite realize is that the impaired immune system in CLL patients -- due to the disease or some of the treatments for the disease -- can actually impact your response to vaccination," Ujjani told CNN.

"We recommend the Covid-19 vaccines for our patients ... but we're not really sure how effective it's going to be," she added. "Patients with blood cancers are typically excluded from the clinical trials evaluating the efficacy of the vaccine."

To remedy the lack of data, Ujjani is launching a research study involving 500 CLL patients across the country -- all of whom are already slated to receive the vaccine from their doctor or pharmacist -- to determine what kind of immune response they will have to the commercially available vaccines.

Advocacy groups for other more prevalent types of cancer are also encouraging cancer patients to get vaccinated as soon as possible. The Lung Cancer Action Network recently asked the US Advisory Committee on Immunization Practices to give lung cancer patients expedited access to the vaccines.

The scientific community agrees that more research is needed to determine the effectiveness of Covid-19 vaccines in cancer patients -- and many doctors are working around the clock to get more trials off the ground.

"We need these data so that we can better inform patients and better prioritize the allocation of the vaccines. If these vulnerable patients form an adequate immune response, we should certainly vaccinate them as early as possible," Dr. Elad Sharon, senior investigator at the National Cancer Institute, told CNN via email.

"But, if research efforts show that these patients fail to form a protective response to these vaccines, then what we will need to do will be to vaccinate everyone around these patients first, so that our medically vulnerable patients are most protected by the people living with them and caring for them."

Ujjani added, "We're all working really hard to answer this question, but it's hard because we've been working kind of against the clock as the vaccines just became available."

"A lot of our patients have suffered in isolation and fear, and they're not sure they're going to get back to a normal life," Ujjani told CNN. "So every oncologist is interested to see how their patients will respond to the vaccine."

Correction: An earlier version of this story misstated the academic journal that published a study conducted by the European Research Initiative. It was published in the journal Leukemia. It also misnamed the CLL Society by including the words of the acronym.

More here:
Are Covid-19 vaccines safe for cancer patients? Here is what cancer experts say - CNN

The race to treat a rare, fatal syndrome may help others with common disorders like diabetes – Science Magazine

Misfolded proteins (orange) in the endoplasmic reticulum may play a role in Wolfram syndromes many symptoms.

By Mitch LeslieFeb. 11, 2021 , 2:00 PM

Maureen Marshall-Doss says the first sign that her vision was deteriorating came when she misidentified the color of a dress. At a backyard get-together about 20 years ago, the Indianapolis resident pointed out an attractive yellow dress another woman was wearing. You see that as yellow? Shes wearing a pink dress, Marshall-Doss recalls her husband responding.

Today, Marshall-Doss is virtually blind. With help from custom made eyeglasses that magnify objects 500 times, I can see shapes, she says. But she can no longer drive and had to quit the job she loved as a school librarian. Along with her dimming vision, she has type 1 diabetes and has lost her sense of taste and smell.

Marshall-Doss is one of 15,000 to 30,000 people around the world with Wolfram syndrome, a genetic disease. For decades, the condition remained enigmatic, untreatable, and fatal. But in the past few years, insights into its mechanism have begun to pay off, leading to the first clinical trials of drugs that might slow the illness and sparking hopes that gene therapy and the CRISPR DNA-editing tool might rectify the underlying genetic flaws. Here is a rare disease that the basic science is telling us how to treat, says physiologist Barbara Ehrlich of the Yale School of Medicine.

The research could also aid more than the relatively few patients with Wolfram syndrome. Driving the diseases many symptoms is a malfunction of the endoplasmic reticulum (ER), the multichambered organelle that serves as a finishing school for many cellular proteins. Known as ER stress, the same problem helps propel far more common illnesses, including type 2 diabetes, amyotrophic lateral sclerosis (ALS), Parkinsons disease, and Alzheimers disease. Wolfram syndrome is the prototype of an endoplasmic reticulum disorder, says medical geneticist Fumihiko Fumi Urano of Washington University School of Medicine in St. Louis. Because Wolfram syndrome is simpler, says Scott Oakes, a cell biologist and pathologist at the University of Chicago, researchers think it could illuminate the mechanisms of other ER-disrupting diseases, which affect hundreds of millions of people worldwide.

In the late 1930s,four children with diabetes were going blind, and doctors were stumped. Like many other people in the United States struggling through the Great Depression, the siblings ate a paltry diet, subsisting on potatoes, bread, oatmeal, and a little milk. But after examining three of the children, Donald Wolfram, a physician at the Mayo Clinic in Rochester, Minnesota, and an ophthalmologist colleague ruled out malnutrition as the cause of their puzzling condition. Lead poisoning and syphilisthough common enoughwerent to blame, either. When Wolfram and his partner wrote up the cases in 1938, they concluded that the symptoms could be manifestations of an hereditary or acquired cerebral lesion.

The physicians were right that the syndrome eventually named for Wolfram is hereditary. Recessive mutations in the gene for a protein called wolframin are responsible for most cases, with glitches in a second gene causing most of the rest. However, the pair was wrong to think the defect lies only in the brain. Instead, the symptoms stem from widespread cell death. Its definitely a disease that affects the whole body, Marshall-Doss says.

The first sign of the illness, appearing when patients are children, is usually diabetes mellitus, or faulty sugar metabolism, sparked by the demise of insulin-secreting beta cells in the pancreas. Most patients also develop the unrelated condition diabetes insipidus, in which the pituitary gland doesnt dole out enough of a hormone that helps control the bodys fluid balance, causing the kidneys to produce huge amounts of urine.

Mutations in the gene for wolframin disrupt the endoplasmic reticulum and lead to cell death throughout the body, causing a range of symptoms.

DeafnessPatients usually beginto lose their hearingin their teens. Balance andcoordination difficultyThe disease attacks the cerebellum, hampering the ability to control movement. Diabetes mellitusInsulin-producing beta cells die, hindering the bodys use of sugar as energy. Difficulty breathingBy damaging thebrain stem, the diseasecan disrupt respiration. Diabetes insipidusBecause of a faultypituitary gland, the kidneys produce too much urine. Loss of visionAs cells in theoptic nerve die, patientsgradually go blind.

V. Altounian/Science

Ellie White, 19, of Centennial, Colorado, who was diagnosed with Wolfram syndrome 12 years ago, says she hasnt had a full night of sleep since she was 3 years old. She gets up again and again to use the bathroom and monitor her blood sugar.

Yet she and other patients say that as disruptive as those problems are, they are not the diseases most dismaying consequence. The biggest symptom of Wolfram syndrome that affects me the most is my vision, White says. Because neurons in the optic nerve perish, patients usually go blind within 10 years of their first visual symptoms.

Other neurons die as well. As the disease progresses, brain cells expire, and walking, breathing, and swallowing become difficult. Most people with Wolfram syndrome die before age 40, often because they can no longer breathe. At 57, Marshall-Doss is one of the oldest patients; one of her mutated genes may yield a partly functional version of wolframin, triggering a milder form of the disease, Urano says.

Two advanceshave made it possible to begin to tackle those symptoms. The first was Uranos discovery nearly 20 years ago that linked Wolfram syndrome to ER stress. The ER is where about one-third of a cells newly made proteins fold into the correct shapes and undergo fine-tuning. Cells can develop ER stress whenever they are under duress, such as when they dont have enough oxygen or when misfolded proteins begin to pile up inside the organelle.

In test tube experiments, Urano and his colleagues were measuring the activity of genes to pinpoint which ones help alleviate ER stress. One gene that popped up encodes wolframin, which scientists had shown in 1998 was mutated in patients with Wolfram syndrome. Following up on that finding, Urano and his team determined that wolframin takes part in whats known as the unfolded protein response, which is a mechanism for coping with ER stress in which cells take steps including dialing back protein production.

Scientists think wolframin plays a key role in the unfolded protein response, though they havent nailed down exactly how. When wolframin is impaired, cells become vulnerable to ER stress. And if they cant relieve that stress, they often self-destruct, which could explain why so many neurons and beta cells die in the disease.

Defective wolframin may harm cells in other ways. The ER tends the cells supply of calcium, continually releasing and absorbing the ion to control the amount in the cytoplasm. Changes in calcium levels promote certain cellular activities, including the contraction of heart muscle cells and the release of neurotransmitters by neurons. And wolframin affects calcium regulation.

Beta cells genetically engineered to lack functional wolframin brim with calcium, Ehrlich and colleagues reported in July 2020 in theProceedings of the National Academy of Sciences. When exposed to lots of sugar, the altered cells release less insulin and are more likely to die than healthy beta cells, the team found. The cells share that vulnerability with beta cells from patients with Wolfram syndrome. We think that excess calcium is leading to excess cell death, Ehrlich says.

ER malfunctions could hamstring other organelles as well. The ER donates calcium to the mitochondria, the cells power plants, helping them generate energy. In 2018, a team led by molecular biologist Ccile Delettre and molecular and cellular biologist Benjamin Delprat, both of the French biomedical research agency INSERM, discovered that in cells from patients with Wolfram syndrome, mitochondria receive less calcium from the ER and produce less energy. Those underpowered mitochondria could spur the death of optic nerve cells, the researchers speculate.

Fumihiko Urano holds dantrolene, a muscle relaxant drug he helped test as a treatment for Wolfram syndrome.

The link between ER stress and Wolfram syndrome has been crucial for identifying potential treatments because otherwise we would have nothing to target, Urano says. But a second development was also key, he says: the advocacy and support of patient organizations, such as the Snow Foundation and the Ellie White Foundation, headed by its namesakes mother. The foundations have stepped up with money for lab research and clinical trials when other sources, including government agencies, didnt come through.

Scientists, patients, and their advocates say Urano also deserves much of the credit. Besides treating patients, he heads the international registry of cases and has taken the lead in organizing clinical trials, screening compounds for possible use as treatments, and devising potential therapies. Fumi is clearly the driving force, says Stephanie Snow Gebel, co-founder of the Snow Foundation, who about 10 years ago helped persuade him to forgo a plum job as department chair at a Japanese university and take over the Wolfram program at Washington University.

Patients could soonstart to reap the benefits. In 2016, Urano and colleagues started the worlds first clinical trial for the disease: a phase 1/2 study of dantrolene, an approved muscle relaxant. The molecule was a top performer when they screened 73 potential treatments for their ability to save cells with terminal ER stress. Dantrolene didnt improve vision in the 22 participants, including White, the scientists reported in an October 2020 preprint. But in some patients, beta cells appeared to be working better and releasing more insulin. The drug is safe, but Urano says it will need to be chemically tweaked to target its effects before future trials are warranted.

Researchers are pursuing other possible treatments targeting ER stress or calcium levels. In 2018, U.K. scientists launched a trial that will include 70 patients to evaluate sodium valproate, a therapy for bipolar disorder and epilepsy that, in the lab, prevents cells with faulty wolframin from dying. Last year, another compound that emerged from Uranos screens, the diabetes drug liraglutide, entered a clinical trial. Also last year, an experimental drug developed by Amylyx Pharmaceuticals for Alzheimers disease and ALS received orphan drug designation from the U.S. Food and Drug Administration for Wolfram syndrome because it curbs ER stress. That designation offers tax breaks and other incentives, and it will get trials started sooner, Urano says.

Ehrlich and her team have a candidate of their own that they have begun to test in rodents: the drug ibudilast, which is approved in Japan to treat asthma. The researchers found it reduces calcium levels in beta cells lacking wolframin and boosts their survival and insulin output. New screening projects may reveal still more candidates.

But Urano knows that even if a treatment receives approval, it would be only a Band-Aid for Wolfram syndrome. Hoping to develop a genetic cure, he and colleagues are introducing replacement genes into cells from patients and from mice engineered to replicate the disease. The researchers are endowing the cells with healthy copies of the gene for wolframin or the gene for a protein that reduces ER stress to determine whether they restore cellular function and reduce cell death. At INSERM, Delettre and colleagues are also evaluating whether directing a working gene into optic nerve cells can curtail vision loss in mice with faulty wolframin. The scientists are still gathering data, but early results suggest the treatment can halt the deterioration.

Urano and his collaborators have also turned to the genome editor CRISPR, deploying it to correct the gene defect in patients stem cells and then growing them into beta cells. When the researchers transplanted the revamped cells into mice with diabetes, the animals blood sugar returned to healthy levels, the team reported in April 2020 inScience Translational Medicine.

Stem cell biologist Catherine Verfaillie of KU Leuven is collaborating on the CRISPR research. But she notes that because the faulty wolframin gene affects so many tissues, researchers will have to figure out how to deliver the CRISPR components to most cells in large organs such as the brain and livera prospect she calls pretty daunting. Urano agrees, predicting that CRISPR-based Wolfram therapies might take 10 to 20 years to develop. The alternative approach, gene therapy, could reach clinical trials more quickly, in 3 to 10 years, he says, because researchers have more experience with gene therapy and have created several treatments that have already been approved for other illnesses.

Because it stems from a single genetic glitch, Wolfram syndrome could also help scientists tease out the role of the ER in more complex diseases, including neurological conditions, type 2 diabetes, and cancer. The ER also falters in those diseases, causing cells to die, but the mechanism is harder to discern because they stem from myriad genetic and environmental factors. In Alzheimers disease, for instance, neurons develop ER stress as misfolded proteins accumulate inside and outside the cells.

Besides deepening researchers understanding of other conditions, the research on Wolfram syndrome might even deliver candidate treatments. Everyone would be very excited if we can make advances in targeting ER stress in Wolfram syndrome, Oakes says. It would open up the whole field to doing this in other degenerative diseases.

Here is the original post:
The race to treat a rare, fatal syndrome may help others with common disorders like diabetes - Science Magazine

Arlo’s Army needs stem cell donor as mum begs for help to save three-year-old’s life – Glasgow Live

Gorgeous little Arlo McArthur looks the picture of health and happiness.

Loved and adored by his family this little lively three-year-old from Milngavie is spoiled rotten by his three big sisters and his ultimate day out is playing golf with his daddy.

But behind the cheeky grin lies a devastating truth - he's a "ticking-timebomb" and needs a stem cell transplant to save his life.

So today, we've joined with Arlo's mum Nicole, dad Ian and his three doting sisters Carys, Brooke and Holly in asking Glasgow Live readers to step up and help this brave little boy.

They need young men, between 16 and 30 to volunteer to be tested to see if they are a match for the toddler. There's not much to it, a simple swab test carried out at home is enough for the experts to determine if you're a match.

The more people who register to be tested the better chance there is of finding the ideal candidate willing to donate the bone marrow little Arlo desperately needs.

For this family your help could mean the difference between life and death.

They've lived with the knowledge since he was 10 weeks old that a rare genetic condition could rob their precious little boy of his future.

Diagnosed with Wiskott-Aldrich Syndrome, it means Arlo's immune system doesn't function properly and it's difficult for his bone marrow to produce platelets, making him prone to bleeding.

Its estimated there are between 1 and 10 cases per million males worldwide. Arlo was only the third case at Queen Elizabeth University Hospital.

Doctors say they cant take the risk with an older donor as he was lucky to survive a previous transplant which failed when he was a baby.

His back-up is his dad Ian, 31, but he's only a half-match.

Sadly little Arlo's story isn't unique, across the country 2,300 people a year need a stem cell transplant and charity Anthony Nolan coordinates the search and raises money to support their vital work.

Nicole, 37, dreams of seeing her little boy attend his first day at school next August and believes someone out there can help that dream come true.

She pleaded: "Were asking as many people as possible to register and help give Arlo the life he deserves.

"We want to love and enjoy having our little boy around for a long time. He should be able to live out his life of dreams.

"Put yourself in the shoes of a parent whose child is ill, or someone else who is about to lose a loved one. Youve just been told in a room that they wont make it without stem cells. How does it feel?

"Its not just our Arlo, there are plenty of Arlos out there who need your help."

"People don't realise how easy it is to do. It's not this big operation, just a few injections and a day at an out-patient clinic to save someone's life. I wish it was opt-out, like organ donation.

"We dont have much time but I know in my heart the right match is out there."

To find out how you can can join the register and help the fight to save little Arlo and others just like visit Anthony Nolan's website here.

See more here:
Arlo's Army needs stem cell donor as mum begs for help to save three-year-old's life - Glasgow Live

Arlo’s Army: mum opens up on heartbreaking decision to make 3-year-old sick to save his life – Glasgow Live

Little Arlo McArthur has spent his short life fighting.

No one knows better than his mum Nicole just how tough this little warrior is.

Diagnosed with a deadly blood disorder at just 10 weeks old, the three-year-old desperately needs a stem cell transplant to save his life.

And as the campaign to encourage males between 16 and 30 to volunteer to be tested to see if they are a match gathers pace, Nicole has opened up in heartbreaking detail about the harrowing battle to save Arlo.

She told Glasgow Live: "This is every parents worst nightmare. I cannot lose my son. We have such a fight ahead of us.

"He's doing really well at the moment but it's really scary looking at him, knowing he is so vulnerable. It hurts us so much."

It was only two weeks after bringing their baby boy home in 2017 that Nicole and husband Ian discovered something was wrong with him.

"We rushed him to A&E after he vomited a blood clot." Nicole recalls. "Doctors initially diagnosed a severe cows milk allergy and sent us home. Later he vomited again, and we found blood in his poo so we returned.

"It was suggested that it may be leukaemia as his platelets were so low. When they said that, I knew there was something deeply wrong. After that was ruled out, we waited ten more weeks for answers.

This was the point that I realised that doctors were only human, they are not God. They dont know everything: Its about eliminating all of these possibilities until they get to what it is. It was tough.

The Milngavie family spent weeks agonising in the dark and were offered leaflets on living without a diagnosis but kept in touch with medics.

One doctor mentioned that she thought his symptoms matched up with a rare condition, but did not want to define it to Nicole until the test results were confirmed.

After asking another member of staff, the sickened mum discovered they were testing her baby for Wiskott Aldrich Syndrome.

She said: "I Googled it when I got home and I was utterly traumatised to learn that the life expectancy for a child with this condition was five. I was beside myself.

"My friends and family were saying dont be silly and stay positive. I was praying and hoping it wasnt, but I knew in my gut it was what Arlo had."

Nicola steeled herself for the worst, but nothing could have prepared her for the moment she was given the bad news at the hospital. She broke down before the doctor had finished delivering the diagnosis.

Worse still, she was alone as her husband was unable to take any more time off work.

I was complete mess I was in full crazy mode, crying. I had to deliver the news to my husband over the phone. I never imagined it would be like this," she said.

The doctor tried to calm me down and said we could get him a bone marrow transplant. I didnt even know what that was before then.

Wiskott Aldrich Syndrome is a rare genetic immunodeficiency disease that keeps a child's immune system from functioning properly. It also makes it difficult for a child's bone marrow to produce platelets, making them prone to bleeding.

Its estimated there are between 1 and 10 cases per million males worldwide. Arlo was only the third case at Queen Elizabeth University Hospital.

A 10/10 donor match was found for him on December 22 the best Christmas present ever and shipped over from the US. The family battled to have it transported to Scotland from Heathrow in an Uber after flights were grounded during a snow storm.

The baby's transplant was successful, and the cells were engrafting. But that started to change, and his engraftment started to drop with each check in.

He also contracted severe sepsis and began suffering from seizures and it emerged entophilitis, a form of meningitis, had entered his brain. His neck lolled and his eyes danced around. He was taken into intensive care after being discharged.

We thought he might have had brain damage. It sounds terrible but we were accepting of that. Well take anything as long as hes with us. Well deal with what we have to. We just wanted him to live. Thankfully the symptoms resolved themselves.

If he didnt have that within six months, he wouldnt have made it to his first birthday. He was very, very sick.

Arlo urgently needs to find a young, male, donor aged 16-30. His back-up is his dad, who is a half-match.

Nicole explains that the success rate is higher for children under five in a healthier condition. When they find the match, the toddler will have to undergo high-dose chemotherapy to break down his immune system to allow the transplant to take place. He last had this when he was six months old.

One nurse described it to me as taking the body as close to death as they possibly can and rebuilding it. Its really harsh on the body its basically a poison," she said.

He really wasnt well the first time and he ended up on morphine for the pain. He had mucositis all the way from his throat to his gut and had to be fed through a tube to bypass his stomach. It was horrible.

"But if he doesnt do this as soon as he can, his immune system wont be able to withstand it. He could be at risk of leukaemia. I know hes a ticking time-bomb.

While doctors are hopeful that the next transplant will help Arlo, they warned the family to brace themselves for it not working out again. The mortality rate for a transplant is also around 20 per cent but Nicole said its a risk the family is willing to take to give their boy his best chance.

She said: The doctors do speak to you and say You do know if we dont get the result youre looking for things can go wrong. You have to sign paperwork to confirm that you know this could result in death.

So much can happen. You could undergo a transplant to fix one thing, and come out with another.

Once I played devils advocate and asked the doctor what Arlos life would be like if we chose not to take the transplant.

"He told me that Arlo would have a poor quality of life and they could possibly get him to his teenage years, maybe even his late teens. But it 'wouldnt be a nice way to live.' I said thats not an alternative. "

She added: To make him sick and risk his life to make him better all at the same time is heartbreaking. But theres that chance he could live a better life and thats what we are fighting for.

If we lose Arlo in the process, we know that we have done everything in our power to give him a normal life that we possibly can. That's in God's hands. It is our only option.

To find out how you can can join the register and help the fight to save little Arlo and others just like visit Anthony Nolan's website here.

Follow this link:
Arlo's Army: mum opens up on heartbreaking decision to make 3-year-old sick to save his life - Glasgow Live

Bone marrow transplant shows signs of curing brave little boy with one in a million condition – Shields Gazette

One-year-old Max Gardner was diagnosed with aplastic anaemia, in October 2020, a serious condition in which the bone marrow and stem cells do not produce enough blood cells.

After Max developed significant bruises and a rash over his body, parents, Connor Gardner and Rachel Nicholson, from Hebburn, were referred to South Tyneside District Hospital, where their brave little boy underwent tests.

Doctors initially believed that Max had an immune disorder but after he was admitted to the Royal Victoria Infirmary (RVI) further tests helped to diagnose him with aplastic anaemia.

Read More

The family was told that the condition could be fatal if not treated properly.

Doctors said Max needed to have a bone marrow transplant, which has the potential to cure him.

Dad Connor, 29, and mum Rachel, 27, were both tested to see if they would be a bone marrow match and the pair were overjoyed when Rachel was found to be a 9/10 match.

Max started chemotherapy on January 7 at the RVI and mum Rachel donated stem cells on January 13 at Newcastles Freeman Hospital.

The following day, January 14, Max underwent the transplant at the RVI.

The family is now waiting for the results of a Chimerism Test which will tell them for definite whether the stem cells have worked but signs are already looking positive.

Delighted dad, Connor, said: "His neutrophils [a type of white blood cell that protect us from infections] have been more than 0.50 for three days in a row, which means that he is essentially engrafted, which means that his body is accepting the transplant.

"So it is working, but we still have to wait for the test results."

Doctors say there is no doubt that it has worked with the way the numbers have gone up but they have to officially do it like that to make sure, Connor continued.

"But there is no reason why it shouldnt have [doctors] say.

"He has done really well to get to this stage, he has absolutely sailed through it, everyone is surprised with how well he has done.

This the best outcome we could have hoped for.

But it hasnt been plain sailing for the family, who have also had to face additional challenges during the treatment.

Parents Connor and Rachael initially were not allowed to visit Max at the same time due to Covid rules, however the hospital has now eased the restriction in their case.

The family also became sick with Norovirus in the run-up to the transplant, causing concern over whether it would have to be pushed back.

Thankfully, the transplant went ahead as planned and the family made a good recovery, although Max still needs help with his eating.

Max will now have to remain in hospital for a while longer as he recovers from the transplant.

Connor added: We can feel that we are nearly at the end of it.

"His neutrophils are the highest they have ever been since he became poorly so we feel like we are coming to the end.

See original here:
Bone marrow transplant shows signs of curing brave little boy with one in a million condition - Shields Gazette