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4. Hallmarks of Cancer (part 1)
 
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The hallmarks of cancer are a list of properties that cancerous cells all have in common. These properties are behaviours gained through mutations to genes that produce proteins that function to provide them with these abilities: They include: 1. self sufficient growth 2. insensitivity to anti-growth signals 3. tissue invasion and metastasis 4. limitless replicative potential 5. sustained angiogenesis 6. avoiding apoptosis This video covers the first 2 hallmarks. Cell division in the body is normally very tightly controlled to ensure that tissues in the body – which are made up of cells – grow in the co-ordinated fashion. Cells normally need signals from other cells to tell them when to divide. When cells break free of these controls, and start dividing even when they are not getting these signals, they begin to divide uncontrollably and neoplasms (also known as tumours) result. Tissues normally regulate their size by controlling the number of cells which are allowed to enter the cell cycle and divide. This is controlled at various points along the cycle called checkpoints. Cancerous cells are able to ignore signals that would normally stop them at these checkpoints. In addition to this, cells with DNA damage, which would include all potentially cancerous cells, are usually stopped at these checkpoints to avoid them diving and passing on their mutations. Cancerous cells are able to pass checkpoints by avoiding these mechanisms. References Hanahan and Weinberg, 2000 The hallmarks of cancer Cell, 100 (2000), pp. 57-70
6. Tumour Suppressor Genes (Retinoblastoma and the two hit hypothesis, p53)
 
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Cancers occur as a result of damage (in the form of mutations) to a cells DNA that results in the formation of malfunctioning proteins. The mutated proteins give the cancerous cells a number of specific traits, outlined in the 'hallmarks of cancer' (https://www.youtube.com/watch?v=ea-CALtn7hA). The genes that are mutated in cancers can be divided into two groups - tumour suppressor genes and proto-oncogenes. Tumour suppressor genes are genes that produce proteins that are involved in stopping mutated cells from dividing, and also act as the brakes on the cell cycle at its various checkpoints. The retinoblastoma gene is a gene that is involved in stopping cells from crossing the G1 checkpoint in the cell cycle, preventing cells from entering S phase and replicating their DNA in preparation for cell division. For the retinoblastoma gene to be rendered inactive, it needs a mutation in both of its copies (alleles). This is explained by the 'two hit hypothesis'. P53 is another example of a significant tumour suppressor gene. It is active during the cell cycle, acting by halting damaged cells at the checkpoints and then ordering the cell to destroy itself by the process of apoptosis.
2. Neoplasia part 2: Differences between benign and malignant neoplasms
 
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Part 2 of this series of videos on neoplasms - outlining: Differences between benign and malignant neoplasms Examples of instances where benign tumours can actually be harmful. Benign and malignant neoplasms differ in 4 key areas: 1. Differentiation: malignant neoplasms tend to be less well differentiated. 2. Rate of growth: Malignant neoplasms tend to be faster growing. 3. Local invasion: malignant neoplasms invade surrounding tissue - benign neoplasms do not. 4. Metastasis: malignant neoplasms have the ability to form separate tumours in other parts of the body by spreading through the bloodstream, lymphatics or body cavities. Benign tumours never metastasise. Even though benign tumours are usually not harmful, there are some instances when they can cause problems. Examples include an adenoma- a benign tumour of glandular tissues that releases hormones; polyps - which can undergo transformation and become malignant; and brain tumours - which can compress structures around them and stop them from functioning (even though they are not actually invading the tissue). References Kumar, V., & Robbins, S. L. 1. (2007). Robbins basic pathology (8th ed.). Philadelphia, PA: Saunders/Elsevier
Staging cancers: TNM and I-IV systems
 
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Staging cancers is important to determine the prognosis of a patient and what treatment they might best benefit from. It is also vital to structuring research and developing guidelines for cancer treatment. The most widely used system is the TNM system. T stands for tumour, and gives an impression of how large, or how locally invasive the primary tumour is. N stands for node. This refers to the number of lymph nodes close to the tumour that are affected. M stands for Metastases. If a tumour has spread and begins to form secondary tumours in other parts of the body it is said to have metastasised. The number system (Stage I-IV) integrates information from the TNM system to come up with a simplified score. References http://cancerstaging.org/references-tools/Pages/What-is-Cancer-Staging.aspx
1. Neoplasia part 1: definition, how it relates to cancer
 
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1. Neoplasia: what is neoplasia? How does it relate to cancer? The successful function of multicellular organisms relies on the co-ordination and co-operation of all of the cells in the body. As part of this deal, division of cells is very tightly controlled, and only occurs when cells are permitted to. Unfortunately, this process is prone to error. This video shows that Neoplasms, or 'new growths' (also known as tumours) when a cell begins to divide at a faster rate, and not co-ordinated with it's surrounding tissue, and continues to grow even when the stimulus that brought about that change has gone. These neoplasms (new growths, AKA tumours) do not support the function of the organism as a whole and can often be detrimental. Neoplasms are divided into two camps: benign and malignant, according to how they behave. The main difference is that malignant neoplasms invade their surrounding tissue, and can spread and form tumours in other parts of the body (metastasis). Cancer is a more commonly used term to describe malignant neoplasms. Part 2 of the series outlines in more detail the difference between benign and malignant neoplasms: https://youtu.be/ZcVSHYl_THE References: Kumar, V., & Robbins, S. L. 1. (2007). Robbins basic pathology (8th ed.). Philadelphia, PA: Saunders/Elsevier
Lung Cancer: An Overview
 
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Lung cancer is one of the most common types of cancer, behind breast and prostate, and the most common cause of cancer death. The vast majority of cases are related to cigarette smoking. They can be divided in to two broad types: non-small cell and small cell lung cancer. They most often present with a prolonged cough, or haemoptysis (coughing up blood). They are diagnosed with imaging that will include a chest x-ray, CT scan, and Tissue diagnosis is usually with bronchoscopy and biopsy. Treatment includes surgery, radiotherapy and chemotherapy and choice varies with the histological type and stage of the tumour. Please subscribe to the channel for more videos!
Neutropenic Sepsis
 
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Neutropenic sepsis is a medical emergency and complication of cancer treatment, usually chemotherapy. It is thought to be brought about through a combination of the effect of chemotherapy in supressing the bone marrow, and in turn the production of white blood cells, as well as the breakdown of the lining of the gastrointestinal tract, allowing for bacteria to enter the blood stream. It is a medical emergency, and patients with suspected neutropenic sepsis should receive broad spectrum, empirical antibiotics no later than 1 hour after arriving at hospital.
Tumour Lysis Syndrome
 
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Tumour Lysis syndrome is an oncological emergency whereby the lysis (or breakdown) of vast numbers of cells leads to the release of their contents, which can have catastrophic consequences for the function of the kidneys, heart and central nervous system. This video describes the pathophysiology of TLS, risk factors, clinical definition and diagnosis, prevention and management. References Larson, R., & Piu, C. (2016). Tumor lysis syndrome: Definition, pathogenesis, clinical manifestations, etiology and risk factors. In D. Savarese (Ed.), UpToDate. Retrieved December 10, 2017, from https://www.uptodate.com/contents/tumor-lysis-syndrome-definition-pathogenesis-clinical-manifestations-etiology-and-risk-factors Larson, R., & Piu, C. (2016). Tumor lysis syndrome: Prevention and treatment. In D. Savarese (Ed.), UpToDate. Retrieved December 10, 2017, from https://www.uptodate.com/contents/tumor-lysis-syndrome-prevention-and-treatment
5. Hallmarks of cancer (part 2)
 
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The hallmarks of cancer are the 6 key traits that cancer cells share in common; they are the properties that make them cancerous. In the previous video we learned about the first two - self sustained growth and insensitivity to anti-growth signals. In this video we cover the last 4: Tissue invasion and metastasis: cancerous cell need to be able to break free of the extracellular matrix in tissues, enter the bloodstream or lymphatics, leave the blood stream and seed in another tissue/organ. Limitless replicative potential: most cells have a limit to the number of times they can divide. This is decided by the length or telomeres - portions of non coding DNA at the end of chromosomes that act as a protective cap, and get shorter with each division. Cancers must be able to activate enzymes that maintain the length of telomeres. To learn more about telomeres and the 'end replication problem' have a look at this video: https://www.youtube.com/watch?v=AJNoTmWsE0s Sustained angiogenesis: as cancers grow, they need to keep a steady supply of nutrients. This means stimulating processes that lead to the growth of new blood vessels that are able to supply them with their nutritional needs. Avoiding apoptosis: cells which have damaged DNA are normally detected and mechanisms lead them to self destruct in order to avoid passing on mutations to their daughter cells. Mutations in genes coding for proteins involved in this process can allow cancerous cells to ignore these signals. A more recent version of the hallmarks of cancer have added a further 4 hallmarks (making 10 in total) - these will be covered in a later video. References Hanahan and Weinberg, 2000 The hallmarks of cancer Cell, 100 (2000), pp. 57-70
7. Proto-oncogenes and Oncogenes
 
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Proto-oncogenes are genes that produce proteins that are involved in encouraging cells to move through the cell cycle and divide. If they become mutated in such a way that they are permanently active they will encourage the growth of tumours. Mutated counterparts of proto-oncogenes are called oncogenes. This video explains the role of oncogenes in the development of cancer, using the example of the RAS oncogene.
Superior vena cava syndrome
 
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Superior vena cava syndrome occurs when the superior vena cava becomes blocked. This is most commonly due to tumours that either compress the vessel from the outside, or invade the vessel itself.
3: Molecular basis of cancer part 1: changes in DNA underlie cancer
 
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proteins. This video, the first in a series on the molecular basis of cancer, seeks to explain that changes in DNA, and more specifically genes, underlie cancer. Cells in a single tumour originate from a single cell that has undergone malignant transformation. The changes occur in the formation of a mutation to the cells DNA. Mutations cause permanent changes in genes - the sequences of DNA that provide a code for making proteins. Proteins are important because the proteins a cell makes determines what kind of cell it is and what it does (how it behaves). Mutations cause permanent changes in the function of proteins produced. Because DNA is passed on from one cell to the next, these changes are inherited by the cell's progeny (the cells it produces when it divides). This is why cancer is considered to be a genetic disease. It doesn't necessarily mean all cancers are inherited - rather that the damage that underlies cancer is, by and large, to genes. The next video in the series will look at the specific abilities cells need to gain, through mutations, to become cancerous. References Kumar, V., & Robbins, S. L. 1. (2007). Robbins basic pathology (8th ed.). Philadelphia, PA: Saunders/Elsevier
Colorectal Cancer Surgery: principles and types
 
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The main principles of colorectal cancer surgery and the most common options for surgery based on anatomical location of the cancer. The majority of colorectal cancer surgeries are performed with curative intent. They aim to remove the tumour, with margins free from disease, as well as local tissues including lymph nodes. Consideration is also made to how bowel function can be preserved as close to normal post surgery. Surgery may be used before or after chemo or radiotherapy. Many operations are now laparoscopic (keyhole) but occasionally an open operation is required. The aim in the majority of cases is to join the ends of bowel after the excision in what is called a primary anastomosis. Occasionally a defunctioning loop stoma is required to allow the join to heal. Operations include - right hemicolectomy, left hemicolectomy, sigmoidectomy, high and low anterior resections, and abdominal perineal excision of the rectum and anus (APER). The choice depends on where the tumour is. The majority are performed with a primary anastomosis, with the exception of APER where the rectum is completely removed, meaning an end colostomy is required (a permanent stoma). Other surgeries include transanal endoscopic microsurgery (TEMS) for superficial rectal tumours, and total/subtotal colectomy for polyposis. For a basic overview of colorectal cancers please have a look at our last video: https://youtu.be/7BHMb9uBhr4
8. Clonal Selection
 
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The chances of any individual cell randomly gaining the combination of mutations needed to make it malignant is very small, infact nearly impossible. So why are cancers so common, and how do they gain these mutations? On prominent theory is clonal selection. Tumours are clones - that is they are all the offspring of a single mutated cell. But they also mutate quickly and as a result they are genetically diverse. Some cells gain mutations which make them better at competing for space and resources. These cells will outcompete their neighbours. These cells will form a tumour with the new mutation. This sequence repeats over and over until the cell has enough of the mutations to make it cancerous. One well described example of this is colon cancer. Colon cancers often develop from benign tumours - adenomas. As cells within the adenomas gain more mutations, they form new clones with an enhanced ability to grow. When they gain the ability to invade the surrounding tissue, they become cancerous.
Introduction to Oncological Emergencies
 
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Oncological emergencies are complications of either the disease process of a cancer itself, or side effects of the treatment that have potentially serious or life threatening consequences. There are many complications that can be included under the banner of oncological emergencies and often people like to arrange them into these three categories, which are – mass effects of the tumour (or tumours), metabolic or hormonal effects, and treatment related effects. In the following videos in this series, I'll introduce the most important oncological emergencies - namely superior vena cava syndrome, spinal cord compression, hypercalcaemia, tumour lysis syndrome and neutropenic sepsis.
Principles of Cancer Treatment
 
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This video outlines the basic principles of cancer treatment - what the main treatment types are, who is involved in deciding and providing the treatments, how those treatments are used in combination and other factors in choosing cancer treatments. The main three types of treatment described are surgery, radiotherapy, and medical therapies. Decisions are made by a multi-disciplinary team, made up of oncologists, surgeons, physicians, radiologists, histopathologists and specialist nurses. Broadly speaking, the aims of treatment are either to cure (curative, or radical treatment) or palliative - aimed at controlling symptoms and extending life. There are also a number of terms that refer to how that treatment is given, particularly in reference to the main, or primary, treatment. Neo-adjuvant treatments are given before the primary treatment to maximise the benefits of the main intervention, whereas adjuvant treatments are given afterward to reduce the risk of the cancer recurring. A number of different factors come in to play when deciding which treatments to use and in which order. These are tumour factors: i.e. what kind of cancer is it and what stage is it? Treatment factors refer to whether a treatment is actually available, how likely it is to work and whether it is likely to produce significant side effects. Patient factors concern whether the patient is fit enough to have a treatment, and their personal preferences as to whether they want a treatment or not.
Metastatic spinal cord compression
 
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Metastatic spinal cord compression (MSCC) is an oncological emergency that describes when tumours (usually having spread from another part of the body) grow in the spinal column and compress the spinal cord. This video describes the effects in terms of symptoms and signs of MSCC, which cancers it is most commonly associated with, diagnosis and management.
Introduction to Cancer Epidemiology
 
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A short overview looking at what exactly cancer epidemiology is, the history behind its development a brief section what epidemiology has told us so far about the causes of cancer. This video covers the aims of cancer epidemiology - i.e. the who what and where's. Despite cancer having been around for as long as we know, the knowledge of the causes is relatively new, and are the result of the development of epidemiological study and statistics. Epidemiology looks at the link between factors called exposures, and their relationship to stated outcomes. In doing this, it has to tease apart real risk factors, and co-incidental factors. We also briefly cover some of the best known risk factors for cancers.
Cancer Screening part 1: Principles of Screening
 
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Screening tests are the source of quite a lot of confusion and controversy – mostly as a result of a widespread misunderstanding of exactly how they work and what their limitations are. This video aims to explain what exactly is a screening test, the major issues surrounding screening tests and the list of criteria that define what a good or acceptable screening test, as described by Wilson and Junger in 1968.
Cancer screening part 3: Sensitivity / specificity trade off
 
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This video describes the issue of the sensitivity/specificity trade off. When we develop a screening test, we have to decide the cut off value that indicates a positive result ourselves. Where we decide to place this cut off has implications in terms of the sensitivity and specificity.
Colorectal Cancer: An overview
 
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An overview of the epidemiology, pathology, symptoms, diagnosis, and treatment of colorectal cancers. Colorectal cancers are more common in older people and those with a family history. Red meat, obesity, cigarette smoking and alcohol are known to be risk factors. The vast majority of colorectal cancers are adenocarcinomas, and over 60% of cancers are found in the rectum or sigmoid colon. Diagnosis is by means of colonoscopy and biopsy, CT and MRI. Treatment options include surgery, radiotherapy, chemotherapy and targeted therapies.
Cancer Diagnosis: initial tests, biopsy and tissue diagnosis, staging and the MDT
 
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How are cancers diagnosed? When a doctor suspects that a patient may have cancer, they will order initial tests, depending on exactly what is suspected, in order to further investigate their concern. They will then refer their patient to the relevant specialty doctor. If a suspicious lesion is seen on a scan or other investigation, a tissue sample, also known as a biopsy, needs to be taken in order to see under the microscope whether the tissue is indeed cancerous. A team of clinicians involved in the care will meet and discuss the case - this is known as a multi-disciplinary meeting or MDT. MDTs often contain physicians, histopathologists (who look at biopsy samples to give a tissue diagnosis), radiologists (who look at scans to stage cancers), surgeons, oncologists and specialist nurses.
Cancer screening part 2: Validity - sensitivity and specificity
 
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This video, the second in a section about cancer screening, describes measures of the validity of a screening test - sensitivity and specificity. Validity measures are useful in telling us how good a test is, by describing how good they are at identifying people with the disease with a positive result, and those without it with a negative result. Sensitivity is the probability that a test will correctly identify people who have the disease with a positive result. A test with a high sensitivity will ensure people with the disease aren’t missed by a test. Specificity on the other hand, is the probability that the test will correctly identify people who don’t have the disease with a negative result. A test with high specificity will ensure we don’t have many people who don’t have the disease going on to have unnecessary further testing.
Clinical features of cancer: how cancers cause clinical symptoms
 
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This video covers some of the mechanisms through which cancers cause symptomatic illness. This includes local effects of tumours, hormone release, infection ulceration and bleeding, cachexia and paraneoplastic syndromes.
Hypercalcaemia of malignancy
 
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This video will cover a bit of the pathophysiology of cancer related hypercalcaemia, the common symptoms, and management. It forms part of a series on common oncological emergencies.