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TheAspiringDoc

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Pancreatic cancer school project - feedback?
« on: July 15, 2015, 07:04:14 pm »
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Hey,
I was just doing a class presentation on pancreatic cancer, and I was thinking I'd want my facts straight for the competition, so I've attached my script in thte spoiler below if anyone would mind taking a critical look..

Spoiler
Pancreatic cancer is the ninth most common cancer in men and tenth most common cancer in women in Australia.
Unfortunately pancreatic cancer has a low survival rate as it is most often diagnosed at an advanced stage due to its initial lack of  symptoms. Pancreatic cancer is the fifth most common cause of cancer death over all in Australia.
Cancer of the pancreas, and all cancers for that matter, are genetic diseases. This means that it is caused by an abnormality in the genetic material in our cells.
In this presentation, I am going to explain the current stage at which medical treatment of pancreatic cancer is, and what the future holds.

What is cancer?
When most people think of cancer, a malicious, alien-like infestation comes to mind. However, thanks to scientific progress, we know that that is far from being true.
The word cancer, when translated from Latin, literally means ‘crab’.
The condition was called cancer in ancient times because an advanced cancer was thought to resemble a crab with claws reaching out into surrounding tissues.
Cancer is in fact any disease caused by the continuous uncontrolled division and replication of cells in a damaging manner. In other words, cancer is the result of some cells in the body reproducing uncontrollably. Due to this vast, all-encompassing definition, cancer does not come in one form, but rather as a group of over 200 related diseases.

Okay, so let’s take a look at what makes cancerous tissue so distinguishable and dangerous.
Whilst most healthy body tissues contain cells that have the ability to grow, replicate and reproduce, they are programmed to cease once their role has been completed and stasis has maintained. They do this by undergoing "programmed cell death" or "apoptosis", in which the cell sacrifices itself for the good of others around it. For example, cells in tissues such as the skin, which last for an average of two weeks, or the cells in the colon, which have it rough, with a typical span of about four days, are constantly being recycled and replaced. So cells reproduce to meet the needs of the body.
However, in the case of a cancer, cell replication continues unnecessarily, in a positive feedback loop, so as to spread abnormal and unwanted cells into the surrounding tissues, often causing further mutation and replication, along with damage. In many of the most serious cancers, the cancer cells travel from their origin – which is known as the ‘primary tumour’ – through the blood and lymph vessels and begin to colonise secondary, or metastatic tumours.  This process by which the cancer travels is called ‘metastasis’.

It is important to note that when a cancer metastasises, the new tumour, which we know is called a metastatic or secondary tumour, is very similar in its properties to the primary tumour from which it originated. For this reason when pancreatic cancer metastasises to, say, the colon, it is then called metastatic pancreatic cancer, not colon cancer. 

As for the cause of this cellular mutation, factors such as a genetic flaw, exposure to cancer causing agents (which are known as carcinogens), radiation, viruses, and  plenty of further causes are often to blame.

What is the pancreas?
The pancreas is a thin, lumpy, hormone-emitting organ, (making it a gland,) which lies between your stomach and your spine. It is about 13 centimetres long and is joined by a duct, or tube, which connects it to the first part of the small intestine, immediately following the stomach, which is called the duodenum. The pancreas is primarily concerned with your body’s digestive system and plays two key roles; producing insulin, and producing enzymes.


Signs and symptoms
Pancreatic cancer rarely causes symptoms until the cancer is big enough to touch and affect organs nearby.
However, some of the following signs and symptoms are listed on the screen.

A symptom is an abnormality detected by the patient.
A sign is an abnormality detected by their doctor.

Pain in the lower back and upper abdomen (indicative of the tumour’s location)(worse at night)
Jaundice – a yellow to the eyes or skin (due to obstruction of the bile ducts located near to the pancreas)
 
Diagnosis
Blood tests
Imaging;
Ultrasound - which uses the reflections of very high frequency sound to construct an image of the body.
 MRI - which monitors the resonance of protons in a magnetic field, allowing it to figure out the densities of protons in different areas, and hence creating an image.
CT which uses lots of X-rays from different perspectives, and
PET scanning, which uses a similar technique as CT scanning in that it constructs a 3D image from lots of 2D 'slices', only a PET scan measures an organ's metabolic rate - how 'active' it is.
Tissue sampling – needle biopsy, endoscopy and laparoscopy


Causes
The specific cause are not known but factors known to increase the risk of developing the disease are..
smoking
age (it occurs mostly in people over the  age of 65)
diabetes
a family history of pancreatic, ovarian or colon cancer
chronic pancreatitis – the inflammation of the pancreas.
 And patients who have undergone a gastrectomy – a procedure in which some or all of the stomach is removed.

Prevention
As there is still relatively little known about what causes pancreatic cancer, there is not yet much knowledge as to what can be done to prevent it. The exception to this is quitting or not smoking in the first place - smokers are two to three times more likely to develop pancreatic cancer.


Treatment and management
Over the years, many treatments for cancer have been developed, most notably surgery, chemotherapy, radiation therapy, hormonal therapy and targeted therapy. These different treatments are prescribed and applied based upon the form of cancer, the location, and grade of cancer, as well as the patient’s individual preferences and separate health conditions.
The most common treatments for pancreatic cancer are include
 surgical removal of the tumour,

 an endoscopic stent – in which a stent, or small tube (as pictured) is inserted into the bile duct, allowing bile to drain away, preventing symptoms of jaundice as seen earlier. This is done during an endoscopy, (pictured here again), while the doctor guides the stent into position using an X-ray.

,chemotherapy, which is the use of chemical substances – an unfortunate side-effect of which is that patients undergoing this treatment often lose their hair.

 or radiotherapy, the use of ionising radiation to kill or control cancerous cells.

These treatments are often given as a combination, so as to be more effective.

For early disease, surgery is the most common treatment – usually the Whipple operation, which is removal of part of the pancreas, the first part of the small bowel (duodenum), part of the stomach and the gall bladder, and part of the bile duct. Enough of the pancreas is left to allow the pancreas to still produce digestive enzymes and hormones.







The future of cancer research and treatment.
-nanobots
nanobots are cylindrical clamshells on flexible DNA hinges. They carry a molecular payload, like a cancer drug, inside. The cancer drugs are engineered to react only with specific molecules or proteins on the surfaces of cancer cells.

High intensity focused ultrasound.
A treatment given using a machine that gives off high frequency sound waves. These waves deliver a strong, concentrated beam to a specific part of the cancer. Some cells die when this high intensity ultrasound beam is focused directly onto them.
Doctors have been interested in this type of treatment for nearly 50 years. But it is only in recent years that they have been seriously investigating its use in treating different types of cancer. One advantage of this type of treatment is that because it only uses sound waves to kill the cancer cells,  it doesn’t have as many side effects as other types of cancer treatments already in use.

Lasers
‘laser’ stands for light amplification by stimulated emission of radiation. Laser light is a very focused, high intensity beam that can cut through steel or even diamonds. Because of this, it has become a major area of interest due to its potential surgical uses as a very precise scalpel.

Cheers :)
« Last Edit: July 26, 2015, 03:43:47 pm by TheAspiringDoc »

pi

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Re: Pancreatic cancer school project - feedback?
« Reply #1 on: July 25, 2015, 08:53:02 pm »
+2
Probably a bit late, but I thought this was pretty good.

Maybe a bit boring if read verbatim without some exciting slides to visually depict some of the concepts (eg. the Whipple's procedure probably wouldn't make sense to the average high schooler, even with your explanation, without diagrammatic representation), but quite informative and accurate.

Felt like some parts could have been expanded for the interest of the audience (eg. why does hair fall out in chemo? that would be interesting) and some concepts were not explored in enough depth (eg. lymph + blood are not the only ways to metastasise in general; eg. clinical features of unintentional weight loss or Courvoisier's sign). Also keep in mind that it's quite possible that no one but you might know much about bile ducts, so you may have to explain the phenomenon of "jaundice" in a little more detail haha. But these are very little things and definitely more than anyone your age needs to know about pancreatic cancer!

Maybe for your own learning, you could read up on some of those points. Also have a think about how PET scans work to measure "activity" of organs/tumours, quite fascinating :P

Overall, gw (Y)

(I split this because thread hi-jacking is not ok)

TheAspiringDoc

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Re: Pancreatic cancer school project - feedback?
« Reply #2 on: July 26, 2015, 02:42:30 pm »
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I wonder if anyone'll notice this incredibly small font?
Probably a bit late, but I thought this was pretty good.

Maybe a bit boring if read verbatim without some exciting slides to visually depict some of the concepts (eg. the Whipple's procedure probably wouldn't make sense to the average high schooler, even with your explanation, without diagrammatic representation), but quite informative and accurate.

Felt like some parts could have been expanded for the interest of the audience (eg. why does hair fall out in chemo? that would be interesting) and some concepts were not explored in enough depth (eg. lymph + blood are not the only ways to metastasise in general; eg. clinical features of unintentional weight loss or Courvoisier's sign). Also keep in mind that it's quite possible that no one but you might know much about bile ducts, so you may have to explain the phenomenon of "jaundice" in a little more detail haha. But these are very little things and definitely more than anyone your age needs to know about pancreatic cancer!

Maybe for your own learning, you could read up on some of those points. Also have a think about how PET scans work to measure "activity" of organs/tumours, quite fascinating :P

Overall, gw (Y)

(I split this because thread hi-jacking is not ok)
Thanks Pi!!
I did use this alongside a powerpoint packed with pictures and I differed from the script quite a bit, it was just supposed to be a rough guide to remind where I was up to and what to speak about next.
I'm not too fussed about my actual presentation though; I just posted it up here so I could learn more about cancer.

Here's some more if anyone feels like taking a look:


Hair falls out in chemo because chemotherapy generally (or is it always?) targets rapidly dividing cells and stops their division. As chemo targets rapidly dividing cells, and since hair growth, like cancer, is also governed by a set of rapidly dividing cells, it too is effected. (is that right?)

Other than local invasion, and my two previously stated metastatic pathways (the lymphatic and blood vessels) how else can cancer metastasise?

Almost all cancers can quite often cause weight loss. This can be be due to an array of reasons, including; inadequate food ingestion (or lack of the desire to eat, or 'anorexia'); reduced ability of the body to digest and absorb food; a lot of nutrients are taken by the tumour, which doesn't convert it (the nutrients) into weight as effectively; increased energy required of the hosts body to fight of the tumour; and the body can produce cytokines in an effort to fend of the tumour (cytokines can lead to weight loss).  Did I miss any?

Bilirubin, a substance often found in the bile and urine, is a yellow pigment. Bilirubin's main function is thought to be as a cellular antioxidant. Jaundice is the yellowing of the eyes and skin due to an excess concentration of bilirubin in the blood. A tumour in the pancreas can cause the bile duct to become blocked. The bile duct leads into the small intestine, where the bile secreted will leave the body in faecal matter. However, if the bile duct is blocked, the levels of bile, and hence bilirubin levels, will increase and remain in the body. This inevitably causes the aforementioned symptom, jaundice.
Excess of bilirubin can also cause darkened urine, light coloured stools (due to the lack of bilirubin), and itchy skin.

Courvoisier's sign/law relates to a bloated and palpable (able to be felt) gallbladder in those with jaundice caused by an obstruction of the bile duct due to cancers and tumours located either in the gallbladder, bile duct, or head of the pancreas.

PET Scans (an abbreviation of positron emission tomography), use a radioactive substance called a 'tracer' to enable the PET scanner to identify abnormalities in the body's normal functions. The most commonly used tracer in PET scan is fluorodeoxyglucose (FDG), a radioactive form of glucose. The reason that FDG is used is that cancer cells use a massive amount of glucose compared to normal bodily (or somatic) cells (is it around about 100 times more?). FDG is still used by cells as a source of glucose, only it is also radioactive and hence, can be seen by the PET scanner. Since cancer cells use so much more glucose than normal cells, they show up as having an abnormally high rate of glucose absorption (was that the right word to use?). The physics behind FDG is as follows; FDG is a radioisotope; radioisotopes contain an unstable nucleus that tends to convert protons into their two counterparts - a positron and the remaining neutron. The emission of the positron is detected by the PET (remember 'Positron Emission') scanner.

Don't read the spoiler Pi.
Spoiler
Physics is cool isn't it? I'm looking forward to VCE physics :P

Does that all seem right? Have I left any gaps or not explained anything properly/thoroughly enough?
 
 T
Thanks
  a
  n
  k
  s
;)

pi

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Re: Pancreatic cancer school project - feedback?
« Reply #3 on: July 26, 2015, 03:08:59 pm »
+2
I wonder if anyone'll notice this incredibly small font?

Noticed.

That explanation of how hair falls out is fine. I myself aren't familiar with all chemotherapy, but most of the ones I know do indeed effect rapidly dividing cells and hence your explanation would be in-line with that.

In terms of metastasis, look up transcoelomic spread ;)

Good reasons for weight loss, that's a pretty solid list imo.

Good logic for jaundice (obviously would help with a picture, but no doubt you'd have googled one in your research).

That's a good definition of Courvoisier's law, it's a classic sign for pancreatic cancer (but as you said, also for cancers such as cholangiocarcinoma as well!).

As for PET, what you have written is correct, but think about why tumour cells use so much more glucose. Obviously the fact that they divide in an unregulated fashion is a factor, but think about the biochem. Do cancer cells, which PET would be useful for, go through the full aerobic respiration? Chuck the "Warburg Effect" a google :)

And that spoiler is disgusting, I don't think you'll find physics as interesting as you hope it will be :P

Everything I have written is far beyond school-level knowledge, but hey, learning shouldn't be bound by semesters or textbooks, and it's refreshing to see a young person on AN not strictly care about their predicted study score! :D

TheAspiringDoc

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Re: Pancreatic cancer school project - feedback?
« Reply #4 on: July 26, 2015, 03:42:46 pm »
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Noticed.

That explanation of how hair falls out is fine. I myself aren't familiar with all chemotherapy, but most of the ones I know do indeed effect rapidly dividing cells and hence your explanation would be in-line with that.

In terms of metastasis, look up transcoelomic spread ;)

Good reasons for weight loss, that's a pretty solid list imo.

Good logic for jaundice (obviously would help with a picture, but no doubt you'd have googled one in your research).

That's a good definition of Courvoisier's law, it's a classic sign for pancreatic cancer (but as you said, also for cancers such as cholangiocarcinoma as well!).

As for PET, what you have written is correct, but think about why tumour cells use so much more glucose. Obviously the fact that they divide in an unregulated fashion is a factor, but think about the biochem. Do cancer cells, which PET would be useful for, go through the full aerobic respiration? Chuck the "Warburg Effect" a google :)

And that spoiler is disgusting, I don't think you'll find physics as interesting as you hope it will be :P

Everything I have written is far beyond school-level knowledge, but hey, learning shouldn't be bound by semesters or textbooks, and it's refreshing to see a young person on AN not strictly care about their predicted study score! :D
Transcoelomic spread
Transcoelomic spread is the spread of a cancer (it has to be cancer as it's spreading - right?) by means of travel through the peritoneum - the smooth, transparent membrane that lines the cavity of the abdomen and coats the abdominal organs.

Warburg effect
Thanks for reminding me about that - it was just starting to escape my memories (I've been watching Ben Garside's cancer series [check him out for maths!]). Anyway, the Warburg effect is the idea that cancer cells produce their energy by a massive amount of glycolysis (the transformation of glucose into pyruvate, along the way creating energy for the cells) and then lactic acid fermentation (the transformation of "six-carbon sugars" [primarily glucose] into energy by a fermentation reaction). Lactic acid fermentation is an anaerobic (non-oxygen requiring) process. But the glyscolysis in cancer cells still is aerobic (hence the need for angiogenesis in tumours for them to become cancerous) right?

Current VCE students, please do not read the following spoiler.
Spoiler
Also, can you please predict me my performance rank in the ACHSC?
I sat an online cancer SAC on Profs Online and scored 7/8.
hehehe


pi

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Re: Pancreatic cancer school project - feedback?
« Reply #5 on: July 26, 2015, 03:55:14 pm »
+1
Transcoelomic spread doesn't have to mean peritoneum, although that's the most common anatomical reference (eg. for ovarian ca).

Warburg effect explanation is pretty good, but now relate that to PET scans and tell me why tumours light up like fireworks :P

Current VCE students, please do not read the following spoiler.
Spoiler
Also, can you please predict me my performance rank in the ACHSC?
I sat an online cancer SAC on Profs Online and scored 7/8.
hehehe

Is that brightsky's competition? I honestly have no idea, I'm not involved with that at all and don't really know what their questions would be like. You're best off asking (or PM-ing) him perhaps?

You definitely have much more knowledge about cancer/medicine than 99% of people your age, so I'd guess you'd fare very well in a general sense.

TheAspiringDoc

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Re: Pancreatic cancer school project - feedback?
« Reply #6 on: July 26, 2015, 04:19:36 pm »
+1
Transcoelomic spread doesn't have to mean peritoneum, although that's the most common anatomical reference (eg. for ovarian ca).

Warburg effect explanation is pretty good, but now relate that to PET scans and tell me why tumours light up like fireworks :P

Is that brightsky's competition? I honestly have no idea, I'm not involved with that at all and don't really know what their questions would be like. You're best off asking (or PM-ing) him perhaps?

You definitely have much more knowledge about cancer/medicine than 99% of people your age, so I'd guess you'd fare very well in a general sense.
kay, so a main principle in the Warburg effect is that cancer cells use heaps of glucose. PET scans using FDG (a radioisomer of glucose), show "firework" areas where there is a high rate of glycolysis. So,
Cancer cells => high rate of glycolysis (Warburg's law)
PETFDG => glycolysis rate detection
Therefore Cancer cell clusters show up very noticeably on PETFDG

Oh, and that previous spoiler was a joke, I figure I'll just give the competition my all and see what happens, as opposed to worrying about my scores (I've got enough of that in my life already I'm looking at you ANCQ).

pi

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Re: Pancreatic cancer school project - feedback?
« Reply #7 on: July 26, 2015, 04:25:57 pm »
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Great deduction :) This is what learning is all about!

TheAspiringDoc

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Re: Pancreatic cancer school project - feedback?
« Reply #8 on: July 26, 2015, 07:09:30 pm »
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Thank you for your wonderfulness Pi.

I'm going to try and make a venn-diagram type thing that compares normal cells and cancer cells. I'll  jut keep updating. I plan on writing approx. 1 small paragraph on each point.

Normal cells
Limited replicative potential
This is necessary to stop the overproduction of cells and promotes genomic stability. Telomeres, located on the end of chromatids, act as a form of protective cap to prevent the deterioration of the genetic material in the cells. However, the telomeres themselves deteriorate through divisions and eventually become non-existent. This phenomenon usually occurs somewhere between 40 to 60 divisions (this is called the 'Hayflick limit'). Once the telomeres are gone, the chromatids (at least those in normally functioning cells) will cease from replicating. Limited replicative potential is involved in ageing.
Normally functioning tumour suppressor genes, DNA repair genes and proto-oncogenes.
Stop dividing when the reach the basement membrane/other cells (what's the formal name for that?)




Intersection
Do they both contain the same organelles?
Do they both have a cell nucleus?


Cancer cells

Evade apoptosis
Apoptosis is the process of 'programmed cell death' that may occur in multicellular organisms. There are two main forms of apoptotic machinery; sensors, which monitor the cell for abnormal behaviour and effectors, which induce apoptosis.
Sensors include:
IGF-1/IGF-2
IL-3
Effectors include:
FAS
TNF-alpha

The p53 tumour suppresor protein evokes apoptosis in response to DNA abnormalities, and is a major playere in the prevention of cancer. p53 is mutated in >50% of cancers.

Cancer cells characteristically overcome and avoid apoptosis.

Sustained angiogenesis
Angiogenesis refers to the formation of new blood vessels. There is much debate of the topic, but the general scientific consensus seems to be that the tumour itself can induce angiogenesis. Angiogenesis is a necessary development in order for the tumour to grow and become malignant as it delivers nutrients and oxygen. 98% of adults aged 40 to 50 have a tumour in their thyroid, but only rarely is this actually an issue as the tumour can not grow to a harmful form without angiogenesis. Angiogenesis also allows the tumour with a method of metastasis, making it a cancer. Inhibitors such as thrombospondin-1 are thought to inhibit angiogenesis. The tumour suppressor p53 regulates thrombospondin-1 production, so for this reason the loss of function of p53 can lead to angiogenesis. Drugs such as Endostatin and Angiostatin are used to inhibit angiogenesis.
Evading immune surveillance
Oxidative stress
Metabolic stress
Proteotoxic stress
Mitotic stress
DNA damage stress
Tissue invasion & metastasis
Cancerous cells can break away from their primary site and metastasise to new locations. They can do this by spread through the blood or lymphatic vessels or transcoelomic spread. They then form new, 'secondary tumours'.
Unlimited replicative potential
Cancer cells are thought to use the enzyme telomerase (which produces telomeric material) to lengthen their telomeres and allow for unlimited replication and evasion from the hayflick limit that governs the replication of normal cells.
Insensitivity to anti-growth signals
Normal cells stop dividing when they start to invade the the area taken up by neighbouring cells. This is because neighbouring cells have 'anti-growth signals' that act upon other cells by stopping mitosis. Cancer cells however, are able to bypass this and keep replicating and growing.  RB is an example of a tumour suppressor gene that stops the progession of the cell cycle from G1 to the S-phase.
Self sufficiency in growth signals

P.S. Since "stress" is turning up so often, I though I should add a definition from cellular stress (it's not mine btw; I got it from Stomp On Step 1)
Cellular stress occurs when a cell is in an inhospitable environment or is asked to do something it can't.
Please, anyone and everyone let me know if you think I've left anything out.
 
« Last Edit: July 27, 2015, 10:52:30 am by TheAspiringDoc »

odeaa

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Re: Pancreatic cancer school project - feedback?
« Reply #9 on: July 26, 2015, 07:13:02 pm »
+1
When I was in year 10 all I knew about biology was that mitochondria is the powerhouse of the cell
VCE Class of 2015

Monash Uni

TheAspiringDoc

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Re: Pancreatic cancer school project - feedback?
« Reply #10 on: August 03, 2015, 06:53:06 pm »
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Wikipedia:
Quote
Ras-regulated signal pathways control such processes as actin cytoskeletal integrity, proliferation, differentiation, cell adhesion, apoptosis, and cell migration. Ras and ras-related proteins are often deregulated in cancers, leading to increased invasion and metastasis, and decreased apoptosis
Doesn't that make Ras a tumour suppressor gene (which I know it isn't)?
'Cos I thought that TS genes experienced a loss of function and proto-oncogenes experienced a gain of function for cancer to occur - not a LOF in a proto-oncogene..?