Hot answers tagged cancer
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 ...
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 ...
6
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.)
...
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
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 ...
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 ...
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 ...
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
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
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
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 ...
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 ...
2
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 ...
2
Could you define your terms a bit more? How do you define levels?
The most common trait shared by cancerous cells is a regulatory malfunction somewhere. Whether it's a failure to regulate apoptosis, failure to recognize boundaries composed of regular cells, or failure to enter states of the cell cycle - a metabolic process somewhere goes awry, which leads ...
2
Perhaps you mean COSMIC? The EBI Gene Expression Atlas also has pretty charts, but now mutations.
2
There definitely has to be an upstream factor that drives ALL cancers. The fundamental common denominator of all cancers is growth and survival, basic life processes. If you can figure out what ultimately drives these processes, you can figure out what ultimately drives ALL cancer types and subtypes. Cancer is just diversified growth. With an open ...
2
In the most basic sense you want to kill the most cancerous cells whilst minimizing the regular somatic cell death. Almost all cancer medications affect regular cells, too - though the better ones do so at a minimum whilst being effective. In reality, it's also nearly impossible to kill all of the cancerous cells. The goal is to bring them below detectable ...
2
There are good epidemiological data for this.
Links between cancer and inflammation were first made in the
nineteenth century, on the basis of observations that tumours often
arose at sites of chronic inflammation and that inflammatory cells
were present in biopsied samples from tumours.
There are many triggers of chronic inflammation that ...
2
(A)
Will probably not. You inherit blood type, but not actual erythrocytes (though the mother's erythrocytes do interact with a fetus).
(B)
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 myeloid ...
2
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 ...
2
Teratomas are thought to be a particular type of cancer, present from early development. As cells which are essentially developmental cells, they seem to have a fairly unique ability to develop hair follicles, teeth and even structures like organs. Indeed malignant teratomas often require chemotherapy or radiation therapy.
I think this bizzarre quality ...
2
First question:
In general, topoisomerases are enzymes that relieve supercoiling in DNA strands and tangling in chromosomes. Type II topoisomerases is special among eukaryotic topoisomerases, considering they use divalent metal ions and ATP hydrolysis in their active site. The enzyme cuts both strands of the DNA helix simultaneously (double strand break) in ...
2
Wikipedia claims (without reference) that
Metastatic cancer cells often express a high density of sialic
acid-rich glycoproteins. This overexpression of sialic acid on
surfaces creates a negative charge on cell membranes. This creates
repulsion between cells (cell opposition)[5] and helps these
late-stage cancer cells enter the blood stream.
...
2
The T315l mutation of BCR/ABL gene produce the complete resistance of CML leukemia to all currently available BCR/ABL inhibitors.
There is a idea that is not yet tested for such patients - allogenic hematopoietic transplatation.
More information:
http://www.ncbi.nlm.nih.gov/pubmed/20657522
...
2
As you probably know, there is a lot of literature on the correlation between Streptococcus bovis and colorectal cancer, but very little on possible mechanisms.
In an editorial (Streptococcus bovis: Causal or incidental involvement in cancer of the colon? in the International Journal of Cancer 119(9):xi-xii), Harald zur Hausen referring to this paper:
...
1
There is a tremendous amount of information relating to mutations of genes and how they produce cancer. In fact, this is multi-billion area of research.
What is even more interesting, is the aneuploidy hypothesis of cancer, in which it is chromosomal abnormalities, rather than mutations in single genes, that lead to cancer.
I suggest reading about it, ...
1
There aren't many studies which associate between alcohol consumption and cancer to my knowledge. The association is more with metabolic diseases because the liver is affected.
Alcohol is oxidised to acetaldehyde by alcohol dehydrogenase. Acetaldehyde may also, in turn affect the cells by DNA damage if it is not metabolized quickly to acetyl-CoA (perhaps in ...
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