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Sebastian Turner
Sebastian Turner


In the early stages of having a carcinoid tumour, you may not have any symptoms. You may also not have symptoms if the tumour is just in your digestive system, as any hormones it produces will be broken down by your liver.



Otherwise, people usually speak to their GP after they have developed symptoms. A carcinoid tumour may be diagnosed after carrying out a series of scans and tests, which may include measuring the amount of serotonin in your urine and having an endoscopy.

If the whole tumour can be removed, this may cure the cancer and symptoms altogether. But even if surgeons cannot remove the entire tumour, it usually grows slowly and can be controlled with medication.

But as the tumour grows or spreads, it will produce more and more hormones, and it may eventually be difficult to completely control symptoms with medication. You may need further surgery or other treatments.

The contribution of tumorigenic stem cells to haematopoietic cancers has been established for some time, and cells possessing stem-cell properties have been described in several solid tumours. Although chemotherapy kills most cells in a tumour, it is believed to leave tumour stem cells behind, which might be an important mechanism of resistance. For example, the ATP-binding cassette (ABC) drug transporters have been shown to protect cancer stem cells from chemotherapeutic agents. Gaining a better insight into the mechanisms of stem-cell resistance to chemotherapy might therefore lead to new therapeutic targets and better anticancer strategies.

Genomic analysis provides insights into the role of copy number variation in disease, but most methods are not designed to resolve mixed populations of cells. In tumours, where genetic heterogeneity is common, very important information may be lost that would be useful for reconstructing evolutionary history. Here we show that with flow-sorted nuclei, whole genome amplification and next generation sequencing we can accurately quantify genomic copy number within an individual nucleus. We apply single-nucleus sequencing to investigate tumour population structure and evolution in two human breast cancer cases. Analysis of 100 single cells from a polygenomic tumour revealed three distinct clonal subpopulations that probably represent sequential clonal expansions. Additional analysis of 100 single cells from a monogenomic primary tumour and its liver metastasis indicated that a single clonal expansion formed the primary tumour and seeded the metastasis. In both primary tumours, we also identified an unexpectedly abundant subpopulation of genetically diverse 'pseudodiploid' cells that do not travel to the metastatic site. In contrast to gradual models of tumour progression, our data indicate that tumours grow by punctuated clonal expansions with few persistent intermediates.

Tumour-specific CD8 T cells in solid tumours are dysfunctional, allowing tumours to progress. The epigenetic regulation of T cell dysfunction and therapeutic reprogrammability (for example, to immune checkpoint blockade) is not well understood. Here we show that T cells in mouse tumours differentiate through two discrete chromatin states: a plastic dysfunctional state from which T cells can be rescued, and a fixed dysfunctional state in which the cells are resistant to reprogramming. We identified surface markers associated with each chromatin state that distinguished reprogrammable from non-reprogrammable PD1hi dysfunctional T cells within heterogeneous T cell populations from tumours in mice; these surface markers were also expressed on human PD1hi tumour-infiltrating CD8 T cells. Our study has important implications for cancer immunotherapy as we define key transcription factors and epigenetic programs underlying T cell dysfunction and surface markers that predict therapeutic reprogrammability.

Cancer cells characteristically consume glucose through Warburg metabolism1, a process that forms the basis of tumour imaging by positron emission tomography (PET). Tumour-infiltrating immune cells also rely on glucose, and impaired immune cell metabolism in the tumour microenvironment (TME) contributes to immune evasion by tumour cells2-4. However, whether the metabolism of immune cells is dysregulated in the TME by cell-intrinsic programs or by competition with cancer cells for limited nutrients remains unclear. Here we used PET tracers to measure the access to and uptake of glucose and glutamine by specific cell subsets in the TME. Notably, myeloid cells had the greatest capacity to take up intratumoral glucose, followed by T cells and cancer cells, across a range of cancer models. By contrast, cancer cells showed the highest uptake of glutamine. This distinct nutrient partitioning was programmed in a cell-intrinsic manner through mTORC1 signalling and the expression of genes related to the metabolism of glucose and glutamine. Inhibiting glutamine uptake enhanced glucose uptake across tumour-resident cell types, showing that glutamine metabolism suppresses glucose uptake without glucose being a limiting factor in the TME. Thus, cell-intrinsic programs drive the preferential acquisition of glucose and glutamine by immune and cancer cells, respectively. Cell-selective partitioning of these nutrients could be exploited to develop therapies and imaging strategies to enhance or monitor the metabolic programs and activities of specific cell populations in the TME.

Cell-free circulating tumour DNA (ctDNA) in plasma has been shown to be informative of the genomic alterations present in tumours and has been used to monitor tumour progression and response to treatments. However, patients with brain tumours do not present with or present with low amounts of ctDNA in plasma precluding the genomic characterization of brain cancer through plasma ctDNA. Here we show that ctDNA derived from central nervous system tumours is more abundantly present in the cerebrospinal fluid (CSF) than in plasma. Massively parallel sequencing of CSF ctDNA more comprehensively characterizes the genomic alterations of brain tumours than plasma, allowing the identification of actionable brain tumour somatic mutations. We show that CSF ctDNA levels longitudinally fluctuate in time and follow the changes in brain tumour burden providing biomarkers to monitor brain malignancies. Moreover, CSF ctDNA is shown to facilitate and complement the diagnosis of leptomeningeal carcinomatosis.

TP53 gene A gene that provides instructions for making a protein called tumour protein p53. Some people inherit an altered TP53 gene, which can result in a rare inherited cancer syndrome called Li-Fraumeni syndrome. This can increase the risk of getting breast cancer.

A brain tumour can cause headaches but it is unusual for this to be the only symptom. Other common symptoms include feeling sick and seizures. Symptoms depend on where the tumour is in the brain and how slowly or quickly it grows. They may develop suddenly, or slowly over months or even years.

If your GP thinks you may have a brain tumour, they may arrange for you to have a brain scan. Or they may refer you directly to a doctor who specialises in brain disorders (neurologist) for a diagnosis. People with brain tumours are treated in specialist hospitals. You may have to travel further to your nearest one.

A lumbar puncture is when a doctor removes some cells from the cerebrospinal fluid (CSF) to check for tumour cells. Not everyone needs this test. Your doctor will explain if it is likely to be useful.

After your treatment has finished, you usually have regular check-ups and scans. This will depend on your situation and the type of tumour. Your doctor or nurse can tell you more about this and how often you need to go to the clinic.

Brain cancers include primary brain tumours, which start in the brain and almost never spread to other parts of the body, and secondary tumours (or metastases), which are caused by cancers that began in another part of the body.

Headaches are often the first symptom of a brain tumour. The headaches can be mild, severe, persistent, or come and go. A headache isn't always a brain tumour but if you're worried, be sure to see your GP.

If a brain tumour is suspected, the doctor may check how different parts of the brain are functioning by checking your reflexes, muscle strength, balance and coordination, ability to feel pin-pricks and to distinguish between hot and cold. An ophthalmoscope is used to view the optic nerve, which may bulge if the pressure in the skull is raised, for example by a tumour.

Some tumours can be removed completely by surgery (craniotomy). Post-operative radiotherapy improves local control and survival. For glioblastomas, temozolomide may be added during or after radiotherapy to further improve outcomes.

If a tumour cannot be removed, the aim of treatment is to slow growth and relieve symptoms by shrinking the tumour and any swelling around it. Treatment options include radiation therapy with or without temozolomide.

Brain tumours are usually graded on a scale of 1 to 4, based on how quickly they are growing and their ability to invade nearby tissue: grades 1 and 2 are the slowest growing and are called low-grade tumours; grade 4 is the fastest growing.

We publish a monthly e-News with items of interest to the international brain tumour community. We also publish a major annual magazine called Brain Tumour which is sent for free to recipients in 110 countries. Subscribe to Brain Tumour magazine and IBTA e-News

During a TURBT operation, your surgeon removes any abnormal growths (tumours) in your bladder. The tumour or tumours will be sent to a laboratory to find out if they are cancerous and if they have grown into the bladder wall.

Your surgeon will then pass surgical instruments through the cystoscope to remove the tumour. These instruments use heat from electricity or a laser to remove the tumours. The heat also stops any bleeding from where the tumours are removed.

A brain tumour is a lump of abnormal cells growing in your brain. Your brain controls all the parts of your body and its functions and produces your thoughts. Depending on where it is, a tumour in your brain can affect these functions. 041b061a72


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