What makes cancer cells different from health cells

Lbeard

I specifically want to know, is there any kind of molecule within the cancer cell that makes it distinct from healthy cells?

I know SFA about biology.

Dingle_berry

Had a bing long explanation typed out but lost it.... FML!

Cancer is a very, VERY, broad umbrella term. Kinda like human is an umbrella term for black, white, yellow, European, Asian, Australian, New Yorker, Dubliner, corkonian, north sider... Etc

Every cell goes through a cycle. At the end of the cycle the cell divides into two cells. Bits of DNA control how fast the cycle goes in response to things outside and inside the cell. The bits of DNA are called proto-oncogenes. Textbooks use an analogy of a bus as the cell, the brakes and accelerator are the proto-oncogenes. In the brakes are stopped from working or the accelerator is jammed on the bus goes out of control.

Some cancers like cervical and penile, are caused by "the brakes" being sabotaged. A protein that the cell uses to detect damage and "stop" itself is destroyed by a virus so the cells just keep replicating. The result of this protein/molecule interruption is used to detect and grade the cancer (p16 immunohistochemistry).
Other cancers, like a type of breast cancer, are caused by the cells "accelerator" being too sensitive. Immunohistochemistry for HER2 is used to find these cancers so the patients can be given a drug to "fix" the accelerator (the drug is Trastuzumab/herceptin).
Another example is a type of B cell lymphoma where the genes are re-arranged so that the signal to divide is constantly turned on. A drug called Glivec helps with this.

So yeah - in theory there are molecules in cancer cells that cause them to behave the way they do but there are lots and lots of types of cancer, with every one being different in some way.
EDIT: and these molecules are present in normal healthy cells too - just in different amounts.

Lbeard

I had a particular idea in mind.

Triggering apoptosis. If you had a method for neatly targeting the cancer cells, then your cancer worries would be over.

Dingle_berry

Lbeard wrote: »

I had a particular idea in mind.

Triggering apoptosis. If you had a method for neatly targeting the cancer cells, then your cancer worries would be over.

Yup that's what big pharma is investing in at the moment. Very specifically targeted pharmaceuticals, cytotoxic drugs "labelled" with ligands that are "attracted to" the cancerous cells, etc. the problem is finding a target that is present in every cancerous cell but not present in healthy cells.

It's turning up new difficulties too. Just like antibiotics put selective pressure on bacteria to evolve resistant strains, targeted chemos are, in a way, selecting targeted chemo resistant cancers. Or patients with metastases that have different profiles to the original tumour - give them the targeted drugs or the general chemo?
The big problem is how unique each tumour can be. Even within the same type of cancer.

Capt'n Midnight

Lbeard wrote: »

I had a particular idea in mind.

Triggering apoptosis. If you had a method for neatly targeting the cancer cells, then your cancer worries would be over.

If you had a method to identify them then you could target them.

In most cases it's like trying to separate isotopes like they do when enriching uranium. Very difficult and you have to rely on subtle physical differences. Some cancer treatments rely on the cancer cells not being as efficiently cooled because they have less blood vessels. Others rely on targeting cancer cells because they divide more rapidly, with horrific consequences to other quick dividing cells.

Lbeard

Dingle_berry wrote: »

the problem is finding a target that is present in every cancerous cell but not present in healthy cells.
.

And that is the holy grail of cancer research. If you could just hit the cancer cells while leaving the healthy cells, then you'd have a cure.

The current methods are pretty brutal. If you're diagnosed and the prognosis isn't good, you might be better to refuse treatment. 2 months of life on painkillers, could be far preferable to six months of living hell on chemo or radio therapy.

The most desirable target is the apoptosis pathway. Apoptosis is different to necrosis. Necrosis is when cells die through injury, it's messy and unhealthy. Apoptosis is when cells commit suicide. And the phages mop up the mess. Normally cells know when to commit suicide if they're abnormal. In cancer cells the mechanism can be blocked, so the faulty cell reproduces itself - with catastrophic consequences.

Lbeard

Capt'n Midnight wrote: »

If you had a method to identify them then you could target them.

I was thinking along the lines of spectral analysis - even spectral targeting.

The current approach is the drug, knife or nuke. I was thinking the compounds in the cells would have unique spectral signatures. Then it's a question of manipulating those elements in the while keeping the healthy cells untouched.

In most cases it's like trying to separate isotopes like they do when enriching uranium.

And one of the things isotopes have to differentiate themselves is unique spectral signatures.

Very difficult and you have to rely on subtle physical differences. Some cancer treatments rely on the cancer cells not being as efficiently cooled because they have less blood vessels. Others rely on targeting cancer cells because they divide more rapidly, with horrific consequences to other quick dividing cells.

I had a very loose and crude idea. If the cells could be differentiated by spectra, and then spectra used to stimulate apoptosis in the cancer cells. Bang, you've got a cure.

Capt'n Midnight

Lbeard wrote: »

The most desirable target is the apoptosis pathway.

even if the "pathway" was working the problem could be with cells not detecting or receiving external or internal clues.

It's really amazing when it works that your arms are the same length despite the cells not having any direct contact since you were a blob of cells in the womb

Dingle_berry

Lbeard wrote: »

I was thinking along the lines of spectral analysis - even spectral targeting.

I know some work has been done on ramen(?) spectroscopy to detect tumours. I've no idea where it's at, how feasible it is for diagnostics or therapeutics - no idea what ramen(?) spectroscopy is!

The new generations of targeted chemo therapies are more "elegant" than the brutal general cytotoxic drugs. They just don't work for every cancer, require "companion diagnostics" and often cost a fortune. They don't result in the hair loss, nausea, lowered immunity etc of traditional chemo.

There is a theory that cancerous cells continually "pop up" in all our bodies, just our immune system normally detects the rogue cells and destroys them before they become a tumour. So if you could develop a vaccine to the tumour cell, or somehow label it to bring it to the attention of the immune system for destruction, the body could rid itself of the cancer.

Lbeard

Dingle_berry wrote: »

I know some work has been done on ramen(?) spectroscopy to detect tumours. I've no idea where it's at, how feasible it is for diagnostics or therapeutics - no idea what ramen(?) spectroscopy is!

Ramen sounds interesting. I was thinking about using more than one technique to manipulate the cells. I think nowadays you could do a much quicker spectroscopy than years ago - literally do stuff that was impossible. Cervical smears were (I don't know if they still are) examined by hand and eye - lots of mistakes.

But they've literally thrown the kitchen sink at cancer.

There is a theory that cancerous cells continually "pop up" in all our bodies, just our immune system normally detects the rogue cells and destroys them before they become a tumour. So if you could develop a vaccine to the tumour cell, or somehow label it to bring it to the attention of the immune system for destruction, the body could rid itself of the cancer.

Normally, an apoptosis pathway, or mechanism, kicks in to get rid of the mutant cell.

I've read some of the research on it. The experiments with mice. They find that they can target something well, like a tumour, with a drug but then the drug causes a pathway elsewhere to deform. So you could kill a tumour but give the mouse a deformed brain. Once you put a drug in the body it goes everywhere. Mutations serve a purpose. They may be need to trigger bifurcation - like fingers developing from the paws or claws, or whatever it is we have in the womb.

Dingle_berry

Lbeard wrote: »

.... Cervical smears were (I don't know if they still are) examined by hand and eye - lots of.....

Yeah smears are still read by human eye. Not as many mistakes as the image recognition software makes when left to its own! AFAIK the current protocol is smears with no history of abnormality are screened by image recognition, a certain amount of these and any abnormals are read by a cytologist, any malignancies are referred to a consultant cytopathologist for confirmation. No computer is able to grasp all the factors that make a human call something benign or malignant. It's not something that's easily taught either. Its not a matter of nuclear to cytoplasmic ratios or shapes. It takes a lot of hands on practise to become good at examining cytology. (A skill set that was present in Ireland but that the previous government/HSE executed and sold to America)

Lbeard wrote: »

Normally, an apoptosis pathway, or mechanism, kicks in to get rid of the mutant cell.

I've read some of the research on it. The experiments with mice. They find that they can target something well, like a tumour, with a drug but then the drug causes a pathway elsewhere to deform. So you could kill a tumour but give the mouse a deformed brain. Once you put a drug in the body it goes everywhere. Mutations serve a purpose. They may be need to trigger bifurcation - like fingers developing from the paws or claws, or whatever it is we have in the womb.

Yes the theory goes that the immune system instructs these cancer cells to apoptise. It's when the immune system fails to recognise the cancerous cell that a tumour grows.
Not every drug goes everywhere. And drugs may cause developmental abnormalities but that's only relevant for pregnant women and foetuses. Once you have non-webbed toes no amount of mutagens will make them webbed. The problem is finding the target that's expressed exclusively in a type of cancer or expressed a lot more than in normal cells. Like with BRAF/Vemurafenib.

cgc5483

There are several different characteristics that distinguish cancer cells from normal cells. There is a very famous review which was written first in the early 2000's and updated recently called "Hallmarks of Cancer" by Hanahan and Weinberg which is quite an extensive review of what enables a cancer cell to survive and thrive. Essentially they describe 6 different characteristics of a cancer cell which are 1. the ability to continually divide 2. evade the action of factors telling them to stop dividing 3. resist undergoing cell death 4. an ability to invade other tissues and regions 5. ability to induce the formation of new blood vessels (angiogenesis) and 6. can undergo unlimited cell division cycles.

The vast majority of chemotherapeutic agents tend to work by inducing apoptosis or cell death and primarily by targeting the rapidly dividing cells. Some of these drugs have been used for more than 50 years and were used at a time when the understanding of how they worked was unknown.

Nowadays researchers are trying to focus much more on developing drugs that target specific molecules that are modified in certain cancer cells and not just trying to kill the cells but also targeting the other hallmarks (Avastin being an example which tries to limit the ability of tumour cells to grow blood vessels). This works well in certain settings but we still have the same problems with adverse effects and the fact that these drugs can get to all of the cancer cells and what happens is as previously suggested you end up creating resistant sub-populations of cancer cells. For instance the BRAF inhibitor mentioned above has been shown to result in populations of cancer cells which become resistant by activating an alternative EGFR signalling pathway.

Also mentioned was that the primary tumour has spread it often has different characteristics in the new site of growth and this can affect the efficiency of treatments. Unfortunately some cancer cells are just so adapted to divide and survive that it is very hard to kill or even suppress their growth. I can never see their being a miracle cure that will work on all cacner but with more work and a better understanding we can at the very least prolong survival in a meaningful manner. They are many different theories and ideas coming out as well that will hopefully help. For instance they have been studies which has demonstrated that in some cases inducing apoptosis can be a bad thing for increasing survival as the dying cells can release factors which help the survival and growth of nearby cancer cells. Other studies have showed that if you use low dose chemotherapy to keep cancers in check you can have much better responses that using very severe treatments where you get an initial response that ultimately results in relapse and death.

lindade

The normal and the healthy cells have the propery of cell reproduction, cell destruction, cell communication, cell adhesion etc. The healthy cell reproduce normally but the reproduction in cancer cells are uncontrollable. the normal cells communicate with other cells and there is adhesion quality. These qualities can't seen in the cancer cells. The healthy cells have property of self destruction. But the cancer cell will not have this property.

Kevster

I find the thread very interesting and the responses intellectual. Apologies for replying late.

I completed my PhD in breast cancer research and have worked as postdoctoral scientist in lung and colon cancer. I have had the 'great' experience of being able to analyse whole genome sequencing data from 'normal' [healthy] DNA, breast primary tumour DNA, and metastatic breast cancer DNA. What I saw, firstly, was a genome ridden with mutations, translocations, and copy number alterations in the 2 cancer samples. The normal sample also had many mutations, but indeed each of us who are healthy equally harbour mutations that are not necessarily doing us any harm.

The next big thing I noticed was that there were only a handful of mutations in coding regions in the metastatic sample that were not in the primary tumour sample. Some of these were in known oncogenes and one could surely assume they were what conferred metastatic potential to the primary tumour. HOWEVER, the other interesting bit was that there were many mutations in the primary sample that were not in the metastatic, which led me to believe that the metastatic sample that was analysed had not arisen from the primary tumour sample (but had arisen from a different tumour clone not analysed/sequenced).

In my view, cancer will always be with us and -instead of constantly finding drugs to treat/'cure' it- we'd be better off focussing on detecting it earlier and ptting money into national screening programmes. In the UK, the breast screening programme starts at 54 now, I think, but that was no good for the lady of 31 years of age who died in my PhD study from multiple metastases.

Kevin