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12

Yes. The very first cells used to study cancer are still around (HeLa Immortal Cells - Named for the subject Henrietta Lacks) and are basically immortal as long as they're fed. As for tumors, whether cancerous or not they most definitely can continue to grow until they become a serious medical issue (WARNING: GRAPHIC - 3 Largest Tumors Recorded). One of the ...


11

Actually we aren't that good at localizing cancer cells. There need to be around 100,000 cancer cells at a single location for the cancer to be visible on fMRI. If you want to treat a cancer via chemotherapy it's good to be able to see the cancer. It allows you to see whether the drug you are giving works. When dealing with a metastasized cancer where you ...


10

Hanahan and Weinberg's "Hallmarks of Cancer" articles should answer your question. Their original, highly cited (14k+ citations), [Six] Hallmarks of Cancer article list these six common attributes of all cancers: Sustaining proliferative signaling Evading growth suppressors Activating invasion and metastasis Enabling replicative immortality Inducing ...


10

Yes, plants of all sizes can have cancerous growths. Agrobacterium tumifaciens, the causative agent of crown gall disease, produces what is called a tumor. See this link for detailed information on these growths. Alternatively, use a plant physiology textbook to look up the above terms. (Here, is where a textbook is better than a single abstract in PubMed.) ...


8

To answer this question in its entirety we have to split it into two questions: What are the underlying mechanisms of carcinogenity? One of the main mechanism behind carcinogenity is the mutagenity of the cancerogens, i.e. the ability to cause mutations, that are abberations of the cell DNA leading to uncontrolled proliferation. This classical paper ...


7

Yes, this is mostly about estrogen. Most breast cancers rely on endogenous estrogen to sustain proliferation. Some general reading: Cancer Medicine, Chapter 18 More in-depth reading: Endogenous Hormones as a Major Factor in Human Cancer Requested summary of mentioned readings: First of all, there is an established link between breast cancer cell ...


7

Interesting question. My answer is no, but it requires a rather science-fiction style answer - at least it's beyond current technology, but here goes: My Assumptions I make the simplifying assumption that ageing is only related to telomere length. Thus by "avoid ageing" I assume you mean "avoid telomere shortening". Also to clarify things for others, I'll ...


7

Cancer cells and normal cells differ on the genetic basis but they share the same genetic background, so they have not different DNA in the sense of two different people. They have to be different, since cancer cells have to accumulate mutations on a number of genes to become a cancer cell, which can survive and will not directed into apoptosis. These are ...


6

Cancer is such a diverse group of diseases that they really only share one commonality, unregulated cell growth with the potential ability to invade or transfer to other tissue types. Many types of cancer share certain characteristics and can thus be grouped, but as a whole the only characteristic all cancers share is that they are classified as cancer. ...


6

I'm assuming you are not talking about a single solid tumor, but rather one where the tumor is loose and is distributed throughout the tissue, or has metastasized I guess the answer is you could, but it would be one amazing machine. This robot would have to examine each individual cell and destroy it based on what you could sense about the surface ...


5

The answer is b, as the mutation constantly activates the RAS protein. RAS is part of the MAP-Kinase pathway, constant signaling of it permanently activates this pathway and leads to changes in gene expression. See the image below: If you are interested in more details, have a look at these papers: RAS oncogenes: weaving a tumorigenic web RAS mutations ...


5

Teflon is a polymer of perfluorooctanoic acid (PFOA) and related compounds. PFOA is thought to be a carcinogen. I think there's an urban legend that if you really heat teflon up or burn it (it doesn't burn as flouroxides are not stable in air) that you might get some of the constituent chemicals out into the air. Once the flourocarbons are polymerized ...


4

As mentioned in the comments, this question is quite complicated. If the chance of a single cell from different organisms getting cancer was the same, then you would be correct, but this is not the case. Different organisms have evolved to live different lengths of time. This is rather obvious when you think about it: mice have a maximum lifespan of ~3 ...


4

We can manufacture materials thin and hard enough to penetrate the body without harming it. It’s not a question of materials. After all, we have the materials to build flying cars – so why are there no flying cars? The problem is reliably locating, recognising and selectively killing tumour cells. using micro tubes, kills them one by one? “one by ...


4

There are several competing models of metastasis, and this question does go right to the differences between them. The primary thing to remember about CSCs is that all evidence suggests that they are a tiny, tiny subset of tumor cells. CTCs, meanwhile, consist of whichever cells manage to acquire the right combination of motility, invasiveness, and ...


4

Red blood cell Will probably not. You inherit blood type, but not actual erythrocytes (though the mother's erythrocytes do interact with a fetus). T cell Will probably not. However, while in the uterus and for the first few weeks outside the uterus the Mother's immune system is effectively the newborn's immune system. While the mother doesn't pass on any ...


4

There seems to be some solid evidence that transcription promotes mutation because the untranscribed strand is able to form secondary structures which expose bases to chemical mutagenesis. Here is a recent paper about transcription-associated mutagenesis: Kim H et al.(2010) Transcription-associated mutagenesis increases protein sequence diversity more ...


4

interesting question.. i believe it definitely is an evolutionary process.. unicellularity breaking away from a multicellular life. there are two examples that i can think of, which can support this argument: Hela cells: hela cells have been classified as a different organism because they have the ability to grow outside the host indefinitely and their ...


4

This is a specific version of the great cancer question: "Why are some cancers more common than others?" The answer is either "Some have more common causes", and (or) "Some are cured spontaneously more often". So now all you are asking is "What causes cancer?" and "How do we cure it?" Given that, I don't expect a general definitive answer will be ...


4

Infecting tumor cells with viruses to provoke an immune response used to be termed (tumor / immune ) 'xenogenization'. The approach may now fall under the general headings of tumor immunology, immune modifiers or tumor vaccines. Xenogenization been explored for decades (with only moderate success). Some modern approaches include adding immune ...


4

Usually the cell death mechanisms are overridden and therefore oncogenesis. The pathway components themselves are not mutated. One classical case I can cite is that of Ras-oncogene. See this article for details. Usually the survival/growth signals (MAP-kinase) are activated with simultaneous inactivation of apoptotic regulators (Akt-pathway). A mutation of ...


3

I tried to comment but what I wrote is too long, so here it is as an answer of sorts. If I understand the question, you are asking: has anyone done a prospective study where they store the DNA of individuals and then later, when some of these individuals get cancer, have a look for mutations that are associated with that cancer. In fact this is done all of ...


3

If you look at a cancer textbook (eg. Robert A. Weinberg's The Biology of Cancer), you'll find that by definition, a tumor arises from tissues normally found in the patient's body. There's a great deal more to it than just that simple statement, but given the context of the question, I think that answer should suffice. In writing, "...tumors growing a ...


3

The Ames test aims to find out if a chemical (not yet known to be mutagen) is indeed a mutagen, either directly, or following treatment with liver enzymes (which may metabolise a chemical to mutagenic derivatives during "detoxification"). As you explain, the test involves looking for reversion of various histidine auxotrophic strains of Salmonella. If the ...


3

There are a number of reasons, generally, why a screening test may fail to decrease cancer mortality rates: The screening test may not be very good. I know this seems like an obvious one, but its something of a problem - a screening test will only reduce mortality if it catches cases that are both treatable and wouldn't be detected in time to treat using ...


3

This article covers some of the key issues of cancer in layman's terms. Essential, cancer is caused by multiple mutations in key regulatory genes which function in maintaining the cell cycle. This provokes uncontrollably rapid cell division, with only furthers the problem with genetic mutation. Here are some quotes from the article to strengthen your ...


3

Burls/Burrs are often defined as tree tumours, and as analogous to cancer in animals. There seems to be numerous reasons why burls are formed (more research is needed on the topic), which include wounds, insects, fungi, DNA changes, environmental stress and viruses. However, burls are localized and often relatively benign, and since plant cells do not move ...


3

Cancer is a highly genetic disease, and much is known about how different genetic mutations contribute to the generation, growth, proliferation, metastasis, and control of tumors. Jackson Labs (commonly known as Jax in the research community) provides literally thousands of strains of mice, each bred/genetically engineered to have certain genotypes and/or ...


3

In the Sanger approach, DNA would be isolated from the biopsy and would contain both normal alleles and mutant alleles of genes associated with the development of the tumour. If, for example, PCR amplification was then used to derive a sample of a target template region, this material would end up being sequenced as a mixed population: the derived sequence ...



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