Because tumour cells are more dependent than their normal neighbours on accelerated nutrient import, these up - regulated transporters could be excellent targets for selective anti-cancer therapies.
These «aggregates» can comprise hundreds of thousands of cells, be up to 2 mm in diameter and be eight times more resistant to chemotherapy drugs — firstly because hypoxic conditions are created inside the aggregates and secondly
because these tumour cells reduce growth and are therefore less sensitive.
Not exact matches
Gravekamp thinks the radioactive bacteria affected metastatic
tumours most
because cells there were still rapidly multiplying, leaving their chromosomes more open to damage than those in healthy tissues or in the original
tumour.
Because such
cells are derived from adult
cells, not pluripotent
cells — which have the potential to form a kind of
tumour called a teratoma — they might be safer than iPS
cells.
That now appears to be
because they prompt the growth of the very
tumour cells they are meant to kill.
«However, many patients do not respond
because myeloid derived suppressor
cells (MDSCs), a type of inhibitory
cell, are present in the
tumour microenvironment.»
That's
because the new technique yields
cells that have a lower, but not negligible, risk of forming
tumours once implanted.
He suggests, instead, that the team take T
cells from the site of the
tumour,
because they would already be specialized for attacking cancer.
«Pancreatic cancer is extremely hard to treat by chemotherapy, so this finding is important
because vitamin A targets the non-cancerous tissue and makes the existing chemotherapy more effective, killing the cancer
cells and shrinking
tumours.
Unlike normal
cells, however, the
tumour cells are considerably more sensitive,
because they can not repair damage well.
Most researchers assumed that this is
because a few rogue cancer
cells find ways to circumvent the drugs before the whole
tumour has been killed off.
Lead author Moustafa Abdalla writes: «Almost all genomic studies of breast cancer have focused on well - established
tumours because it is technically challenging to study the earliest mutational events occurring in human breast epithelial
cells.»
Patients with TILs do much better
because they already have cancer - fighting
cells in their
tumours.
Treatment is difficult
because pancreatic
tumours are protected by an armour of connective tissue, blood vessels and immune
cells, known collectively as the stroma.
«This is
because the stress led to poor function against the cancer by T -
cells, which are very important in the immune system's control and surveillance of
tumours and are a major target in many immunotherapy treatments.»
Other safety strategies include improving the specificity of CAR T -
cells for
tumour cells because healthy
cells also carry CD - 19 receptors.
Willet, Mills, and their colleagues believe the discovery that
cells in different organs go through the same process to become proliferative could lead to new potential targets for cancer treatment
because the factors that initiate
tumours could be the same in multiple organs.
Tumour cells are «glutamine - addicted» [1,2]
because glutamine is coupled to mechanistic target of rapamycin (mTOR) signalling, which integrates signals from growth factors, energy status and amino acid nutrition and co-ordinates these signals with
cell growth,
cell cycle progression and antioxidant machinery [3].
Targeting CTCs, the
cells responsible for spreading cancer, is important
because they carry information from the primary
tumour that can inform treatment; however, they are outnumbered by a billion - to - one by normal
cells in a patient» blood and are therefore extremely challenging to capture.
Because FeLV hijacks the
cells» replicating machinery, it is not surprising that this disease can ultimately lead to
tumour growth.