Man With a Suspected Bug Bite Was Diagnosed With Leukemia

When an Ohio resident went to the doctor with what he thought was an infected bug bite that wouldn’t go away, the last thing he expected was to be admitted to the ER and scheduled an urgent appointment with an oncologist. The harmless 'bug bite' turned out to be something a lot more serious, a truly dreaded diagnosis - leukemia.
 

This man was a 46-year-old, who got a small bump on his foot that he first thought was a mosquito or spider bite when he first noticed it in August of 2018. Some time has passed, but the bump hadn't diminished at all. On the contrary, it got bigger and looked inflamed, so he went to his physician, who, like him, suspected an infected bite and prescribed an antibiotic to treat the infection.

The antibiotic didn’t help, so the puzzled doctor prescribed a stronger antibiotic, which didn’t yield the expected relief either. That's when he was admitted to the emergency room, and the blood tests revealed that the lump was actually a symptom of acute myeloid leukemia, a rare, yet very dangerous type of cancer.

This type of cancer affects the blood and bone marrow. Abnormal blood cells affected by the cancer build up in the vessels and bone marrow, interfering with normal blood circulation. Acute myeloid leukemia is characterized by rapid growth and demands urgent treatment. Typically, this type of leukemia doesn’t express itself in skin growths, the most widespread symptoms being the following:

• Increased susceptibility to infections
• Shortness of breath
• Fatigue
• Easy bruising or bleeding
• Weight loss
• Loss of appetite
• Anemia
• Bone and joint pain.

At first, he couldn’t believe the diagnosis and thought the doctors confused him for someone else, but a subsequent confirmation by an oncologist followed. Immediately, he has undergone chemotherapy, and a subsequent bone marrow transplant as well.

Cleveland Clinic, where the man was treated, reported that he is currently in remission, and today, he took upon himself to raise awareness about health, especially among men, urging everyone to undergo preventative checks on a regular basis. “The hour it takes to go get a checkup could help prevent months of health problems,” he points out.

So remember, a bug bite that lingers for more than a week or two is a concern that requires medical attention, as it’s likely not a bug bite at all. Similarly, something that looks like a minor symptom that continues for a long time or any unusual symptoms, too, may point to a greater problem.

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We hope Indian ingenuity will help make cellular therapy for cancer affordable, says Dr Siddhartha Mukherjee

Cancer physician, scientist and author of Pulitzer-winning, The Emperor of All Maladies, Dr. Mukerjee,, is setting up a cellular therapy facility in Bengaluru in the hope of developing drugs. On the sidelines of an event, he tells why personalised medicine and diet are the next frontier for cancer treatment.

At your lab in Columbia University , you and your team of scientists are researching ' living rugs' made from our own cells for cancer treatment. How does this cellular therapy work and what is its potential?
In some forms of leukemia, we could not achieve good results because drugs couldn't distinguish between cancerous and healthy cells. When we attacked the cancer cell, we also attacked the normal one. The idea we patented in my lab is to use gene editing to change the normal cells. For much of the history of cancer, we've focused on cancer cells. Here, we're inverting the logic and saying let's make the normal cells resistant to the therapy with help of gene editing, thereby making the cancer uniquely sensitive to therapy. This uses the human body, the host of cancer, as the element of change. We couldn't change the normal cells earlier because we didn't have the tools, Gene editing provides us with those tools. And all of a sudden, cancer becomes exposed.

How did you think of approaching the problems like this?
The idea occured to me while I was onvacation to Mexico city. I was making drawing with my daughter. One way to make a drawing is to make a black silhouette on white paper. And you can also make a white silhouette in black paper. And I was doing these drawings and began to realise that in cancer we've been using the cancer silhouette against the normal host as the paradign for all treatments. But what if we used the  host as the background and then attack cancer cells? We patented the idea and showed that it can eradicate this untreatable form of leukemia--- acute myeloid leukemia--- in animals and we're rapidly progressing to human studies.

What more can cells tell us about cancer?
A 2nd approach to cancer, we've taken is to ask the question whether other kinds of cells in the body, apart from T-cells, can be used for immunotherapy. One particular type of cell which has never been harnessed before is myeloid, which is a white blood cell and our body's first line of defence against infection. These can penetrate solid tumours, such as ovarian cancer and breast cancer, where Y-cells have not been very successful. A final and 3rd area that we've worked on extensively is personalising cancer medicine. The great irony of cancer is that while it grows so rapidly inside the body, it is difficult to cultivate outside in a lab. But work done by Dutch molecular geneticist, Hans Clevers in the past 10 years whose how to grow cancer cells in a dish. The cells multiply to make a 3-dimensional cluster called an organoid. So, now we take an individual's cancer cells, grow then in a dish and find out what cancer it is and what drugs does it respond to. This allows us to individuate cancer therapy. We're just about to publish a paper to show how you can find completely new cancer drugs and therapies. We're slowly moving away from the protocol-driven therapies which are sort of one-size-fits-all.

The food-is-medicine approach is a grey area in modern science. But your lab is researching the impact of diet on cancers. What have you found so far?
 
We. as a community, have neglected diet for long. Diet is part of the micro-environment of cancer cells, which sustains them. We- and many more labs- have started studying the role of diet in a highly systematic and scientific manner. Certain chemotherapies lead to a rise in blood sugar and hence insulin, which controls sugar. It's a side-effect. And insulin allows cancer cells to become resistant to a particular form of chemotherapy. By reducing the amount of insulin, for instance, through manipulation of the diet ( consuming lots of protein, little fat and no carbs) you can make cancers sensitive to chemotherapy. It's important to note that it's a combination of diet and drugs. The diet on its own won\t help. Human trials for this study are about to start. We\re testing it for lymphoma and endometrial cancers.

You've set up a cellular therapy facility in Bengaluru. Why did you choose India?
 
This is a collaboration with Kiran Majumdar Shaw. We hopefully will be able to deliver T-cell therapy and other cell therapies which have previously been unavailable in India. While the facility has already started we're not producing cells yet because you require incredible infrastructure to make these living drugs. Why India? Because we hope it will bring down the cost of these therapies. In India, the combination of engineering and scientific ingenuity has been able to bring the costs down in IT and tech industries. We are hoping to use the same innovative capacity of local scientists and doctors to be able to reduce the cost five to ten fold and make cellular therapies accessible to more people.


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Scientists discover a drug that could target acute myeloid leukemia

Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterised by the rapid growth of abnormal white blood cells that build up in the bone marrow and interfere with the production of normal blood cells.

AML is the most common acute leukemia affecting adults, and its incidence increases with age. Mainstream AML treatments have remained unchanged for decades and fewer than one in three people survive the cancer.

But, now a study has found an unexpected new  drug target for acute myeloid leukemia (AML) that could open new avenues to develop effective treatments against this potentially lethal disease. The scientists used CRISPR-Cas9 gene-editing technology to screen cancer cells for vulnerable points.
They created mouse leukemia cells with mutations in the genes that may be targetted in human AML cells and systematically tested each gene, finding which were essential for AML survival.

The researchers ended up with 46 likely candidate genes, many of which produce proteins that could modify RNA. Amongst these, METTL3 was one of the genes with the strongest effect. They found that whilst it was essential for the survival of AML cells, it was not required for healthy blood cells, making it a good potential drug target.

Talking about the research, a  Professor said, "New treatments for AML are desperately needed and we have been looking for genes that would be good drug targets. We identified the methyl transferase enzyme METTL3 as a highly viable target against AML. Our study will inspire pharmaceutical efforts to find drugs that specifically inhibit METTL3 to treat AML."

For proteins to be produced in a cell, the DNA is transcribed into messenger RNA, which is then translated into the proteins that the cell needs. However, modifications to the RNA can control if a protein is produced.

This is a recently-discovered type of gene regulation called RNA editing. Having found a potential target in METTL3, the researchers investigated how it worked. They discovered that the protein produced by METTL3 bound to the beginning of 126 different genes, including several required for AML cell survival.

Then, as RNAs were produced, the METTL3 protein added methyl groups to their middle section, something which had not been previously observed.

The scientists found that these middle methyl groups increased the ability of the RNAs to be translated into proteins. They then showed that when METTL3 was inhibited, no methyl groups were added to the RNA. This prevented the production of their essential proteins so the AML cells started dying.

One of the first authors on the study noted, "This study uncovered an entirely new mechanism of gene regulation in AML that operates through modifications of RNA. We discovered that inhibiting the methyl transferase activity of METTL3 would stop the translation of a whole set of proteins that the leukemia needs. This mechanism shows that a drug to inhibit methylation could be effective against AML without affecting normal cells."

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New drug may provide hopes for blood cancer patients

Scientists have developed a new drug that has the potential to strip cancer cells of their “immortality”, a finding that could help in treating patients suffering from one of the most aggressive forms of leukaemia. Acute myeloid leukemia (AML) is a type of cancer of the blood and bone marrow with excess immature white blood cells and is responsible for 265,000 worldwide cases each year. The drug candidate, called HXR9, works by preventing the cancer cells from sidestepping the natural process that causes unhealthy and damaged cells to die — known as apoptosis.

“Acute myeloid leukaemia is a pretty intractable disease and doesn’t respond to many treatments. This is a novel therapeutic target that hasn’t been shown before to be effective against this form of leukaemia,” said a Professor. The drug targets a particular family of genes, called HOX genes, which helps to give cancer cells the ability to continuously grow and divide.  HXR9 was found to strip the cancer cells of this ability by turning off the HOX genes,the Prof. said.

In the study, the team analysed gene expression data from 269 AML patients and found an association between the activity of a group of HOX genes and the patient survival rate. When HXR9 was tested on cancerous cells, they underwent a process known as necroptosis. Necroptosis causes the cells to explode and spew their contents into the bloodstream rather than simply digesting themselves as normally occurs in apoptosis. This increases the likelihood that there will be a subsequent immune reaction against the cancer cells, Morgan noted. In addition, HXR9 “could well be used in combination treatments but the initial trials will be as a single therapy”, the Prof. said.

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New targets found for treating bone marrow disorders

Scientists have found a new mechanism that controls blood cell function and several possible molecular targets for treating a group of pre-malignant disorders in which bone marrow does not produce enough healthy blood cells.

Myelodysplasia syndromes (MDS) can lead to acute myeloid leukaemia (AML), a fast-spreading blood cancer that can be deadly if not treated promptly.

Researchers from Cincinnati Children's Hospital Medical Centre in the US led by cancer biologist Daniel Starczynowski, found that overexpression of a protein called TRAF6 in hematopoietic (blood) cells drives the onset of MDS.

TRAF6 normally functions as an immune sensor of pathogens, researchers said.

"We found that TRAF6 over-expression in mouse hematopoietic stem cells results in impaired blood cell formation and bone marrow failure," said Starczynowski, from the Cincinnati Children's Hospital Medical Centre.

"Based on our paper, a number of therapeutic approaches can be tested and directed against TRAF6 and other related proteins responsible for MDS," said Starczynowski.

In testing on laboratory mouse models and human MDS/AML samples, the researchers identified a novel substrate of TRAF6 called hnRNPA1, an RNA binding protein.

They also found molecular interactions with Cdc42, a protein that helps regulate cells also implicated in cancer.

All of these could be potential treatment targets for cases of MDS triggered by over-expression of TRAF6, according to Starczynowski, who said future studies will test their therapeutic potential in mouse models of MDS.

The researchers were able to identify the new molecular targets by conducting a global proteomic analysis of human leukemia cells.

This allowed them to the see entire complement of proteins regulated by TRAF6 in leukemia cells.

Beyond the potential for new therapeutic approaches in treating MDS or AML, the research showed a new and critical immune-related function for TRAF6, scientists said.

In response to various pathogens, the protein also regulates RNA isoform expression, an important step in the translation of genetic code into protein and cell formation.

In the context of the current study, TRAF6's regulation of RNA isoform expression is important to the function of hematopoietic cells and reveals another dimension to how cells respond to infection, Starczynkowski said.

The research was published in the journal Nature Immunology.

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'Fasting may kill cancer cells of common childhood leukaemia'

Intermittent fasting may inhibit the development and progression of the most common type of childhood leukemia, a new study has claimed.

The strategy is not effective, however, in another type of blood cancer that commonly strikes adults, researchers said.

"This study using mouse models indicates that the effects of fasting on blood cancers are type-dependent and provides a platform for identifying new targets for leukemia treatments," said Chengcheng Zhang, associate professor at University of Texas Southwestern Medical Centre in the US.

"We also identified a mechanism responsible for the differing response to the fasting treatment," he added.

Researchers found that fasting inhibits the initiation and reverses the progression of two subtypes of acute lymphoblastic leukemia, or ALL - B-cell ALL and T-cell ALL.

The same method did not work with acute myeloid leukemia (AML), the type that is more common in adults.

ALL, the most common type of leukemia found in children, can occur at any age. Current ALL treatments are effective about 90 per cent of the time in children, but far less often in adults, said Zhang.

The two types of leukemia arise from different bone marrow-derived blood cells, he said.

ALL affects B cells and T cells, two types of the immune system's disease-fighting white blood cells. AML targets other types of white blood cells such as macrophages and granulocytes, among other cells.

In both ALL and AML, the cancerous cells remain immature yet proliferate uncontrollably.

Those cells fail to work well and displace healthy blood cells, leading to anemia and infection. They may also infiltrate into tissues and thus cause problems.

Researchers created several mouse models of acute leukaemia and tried various dietary restriction plans.

They used green or yellow florescent proteins to mark the cancer cells so they could trace them and determine if their levels rose or fell in response to the fasting treatment.

"We found that in models of ALL, a regimen consisting of six cycles of one day of fasting followed by one day of feeding completely inhibited cancer development," he said.

At the end of seven weeks, the fasted mice had virtually no detectible cancerous cells compared to an average of nearly 68 per cent of cells found to be cancerous in the test areas of the non-fasted mice.

Compared to mice that ate normally, the rodents on alternate-day fasting had dramatic reductions in the percentage of cancerous cells in the bone marrow and spleen as well as reduced numbers of white blood cells, he said.

"In addition, following the fasting treatment, the spleens and lymph nodes in the fasted ALL model mice were similar in size to those in normal mice," he said.

"Mice in the ALL model group that ate normally died within 59 days, while 75 per cent of the fasted mice survived more than 120 days without signs of leukemia," he said.

The study was published in the journal Nature Medicine.

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