Patients receiving the drug will not require any chemotherapy

A new Cancer drug that curred 97% of blood tumors in mice is set to be tested on humans this year on low-grade lymphomas. 

Patients receiving the drug will not require any chemotherapy as the jab’s side effects expected to just a fever and a slight soreness following the injection.

If the new drug is approved, researchers say the treatment will be expected to reach the public within a year.

Researchers claim the drug acts by activating the immune system to attack tumors. If low-grade lymphoma responds with desired results tot he treatment, the drugs could be widely used amongst cancer patients.

The DailyMail reports: Lead author Dr Ronald Levy, from Stanford University, said: ‘We have a huge problem in cancer and we will never be satisfied until we find solutions for everyone.’

What the study will involve

The vaccine will be tested across two studies.

A total of 35 lymphoma patients will take part in the trials overall.

Each participant will receive a low dose of radiation alongside two rounds of the vaccine over six weeks.

Further details, such as the time between vaccines, are unclear.

‘Tip of the iceberg’ of cancer treatment

A similar immune-system targeting approach is already approved for types of leukemia and lymphoma.

This involves removing immune cells from patients’ bodies and genetically engineering them to attack tumors before they are reintroduced.

Yet such a treatment, known as CAR-T, costs around half a million dollars per patient and can cause fever, confusion, organ failure, and immune-system dysfunction.

Cancer specialist Dr. Michelle Hermiston, from the University of California, San Fransisco, said: ‘It’s not a trivial therapy.’

She adds research should be carried out to determine if tumors can be manipulated to make them respond better to the immune system.

Dr. Hermiston said: ‘Can we make the tumor more visible to the immune system? We are at the tip of the iceberg right now.’

Cured cancer in mice

The researchers implanted two identical tumors in separate sites in mice’s bodies.

One of these tumors was injected with the vaccine, which triggered the activation of T cells. Such cells launch an immune response against invading substances, such as viruses, in animals’ bodies.

The degree of response was measured by the jab’s effect on the untreated tumor.

Results suggest the vaccine cures multiple types of cancer and prevents the disease from occurring.

The findings were published in the journal Science Translational Medicine.

Cancer drug hijacks tumours’ ‘survival mechanisms’

This comes after research released in January this year suggested a cancer drug is in development that could stop the disease in its tracks.

The unnamed medication targets a specific enzyme that fuels the spread of tumours.

It does this by binding to the membrane of rapidly multiplying cells, a study found.

This hijacks cancer’s ‘survival mechanism’ and prevents tumours from attaching to the protein they need to thrive.

It is unclear when the drug could be available.

The anti-cancer drug binds to cancerous cells’ membrane protein, known as dehydroorotate dehydrogenase (DHODH).

The researchers analysed how fats, which are the building blocks of cell membranes, and drugs bind to DHODH.

Study author Dr Erik Marklund, from Uppsala University, said: ‘Our simulations show the enzyme uses a few lipids as anchors in the membrane.

‘When binding to these lipids, a small part of the enzyme folds into an adapter that allows the enzyme to lift its natural substrate [the substance an enzyme acts on] out of the membrane.

‘It seems the drug, since it binds in the same place, takes advantage of the same mechanism.’

Study author Sir David Lane, from the Karolinska Institute, in Sweden, added: ‘The study helps to explain why some drugs bind differently to isolated proteins and proteins that are inside cells.

‘By studying the native structures and mechanisms for cancer targets, it may become possible to exploit their most distinct features to design new, more selective therapeutics.’

The findings were published in the journal Cell Chemical Biology.