As a rule, no. That is whycolorectal cancer has to start from polyps. The polyps are a result of GI stem cells that have mutated. The progression from polyp to colorectal cancer takes about five years. The differentiated epithelial cells at the villus never divide again and they are very short lived (~ 3 days).

The entire essence of cancer is uncontrolled proliferation of cells. Replicative potential is the single most important property of cancer cells. Terminally differentiated cells (like neurons) may dedifferentiate to go back to a state where they have unlimited replicative potential. Therefore it immediately follows that it will need less number of aberrations (mutations) for a stem cell (which already have the potential to replicate) to become cancerous than a fully differentiated cell which would first need to reacquire the capability to replicate and then to disregulate the control over replication.

The entire essence of cancer is uncontrolled proliferation of cells. Replicative potential is the single most important property of cancer cells. Terminally differentiated cells (like neurons) may dedifferentiate to go back to a state where they have unlimited replicative potential. Therefore it immediately follows that it will need less number of aberrations (mutations) for a stem cell (which already have the potential to replicate) to become cancerous than a fully differentiated cell which would first need to reacquire the capability to replicate and then to disregulate the control over replication. However, the time span of a living organism would not be enough to accrue the desired mutations (taking into consideration the mutation rates) and thus such transformations are rare, if present at all.

Cell division is a requirement for tumourigenicity. However resting stem cells can accumulate mutations (acquired or inherited). These cells do not become tumourigenic until they divide.

Cell division is the most essential requirement for tumourigenesis, without division no tumour can be formed. Cell division associated with multiplication of the DNA , this process may confer the basis for genetic errors that lead for tumour formation. Hence cancer arise only in tissue where cell division is active.

Kate, I just realised you have asked 2 questions that have different answers, which can lead to confusion. Your 1st question asks "Is replication a fundamental requirement..." to which the answer is Yes. Your 2nd question asks whether "cell types without replicative potential...undergo tumorigenesis in vivo?" to which the answer is No. Lee's answer ("No") is correctly to your 2nd question, not your 1st.

I would encourage future respondents to not simply answer 'Yes' or 'No' out of context, although reading through Lee's answer clarifies what he means.

I agree with the statements above. Below is a link to a helpful review by Hanahan and Weinberg that cover some of the "hallmarks of cancer". However, it has been rewritten in 2011 to include other features of cancer. This article is a good start to understand some of the tumorigenic requirements for cellular transformation and tumor progression.

http://www.sciencedirect.com/science/article/pii/S0092867400816839#

Through my study on the genetic components of colorectal cancer cells I found evety cancer sample contains unlimited number of cancer cell types, every cell contain different genetic changes indicating the presence of large number of sub-clones in every cancer case. These genetic changes definitely possess impact on the cell morphology and express their effect on cell behavior according to the requirements of those cells to confer suitable environment for more carcinogenicity. Consequently we can expect to find different cell size in every cancer sample regardless of their carcinogenicity power.

Tanks Ramona Salcedo v,ery good rewrite in 2011

The answer to the first question is Yes - as others have indicated. A cell requires at least one mitosis to fix any change in the genome, in this case mutations that lead to oncogenic transformation.

Yes, cells must divide for their neoplastic transformation. However, all the cells that are going through the rapid cell division do not neoplastically transform upon oncogenic lesion.

Second, in principle, any differentiated cell that can be reprogrammed to primitive cell state can transform. To explain this I would take the example of Drosophila cancer model. Drosophila life cycle incudes embryo, larvae, pupa and adult. Larvae carries a pair of wing imaginal disc that give rise to adult wings after metamorphosis. Larval stage is highly proliferative and so are the imaginal discs. Wing imaginal disc can be divided into two developmentally restricted cell types: proximal and distal. Both cell types divide rapidly. Simultaneous loss of tumor suppressor gene Lgl and gain of Wingless (Wnt) signaling lead to the neoplastic transformation of proximal cells but not of the distal cells. This presents a case wherein of the two rapidly dividing cell types, only one cell type progress through neoplasia upon oncogenic hit. However, interestingly, when distal cell types are induced to revert back to a developmentally primitive state (loss of lgl and gain of activated Ras), these too transform. Transformation of distal cells presents a case where reversal to a primitive cell state leads to transformation of otherwise non-transforming cells.

You may please refer to our recently published article for the details:

"Epithelial neoplasia in Drosophila entails switch to primitive cell states"

Yes friends, the replicative potential is an essential feature of neoplastic transformation and moreover, this potential ought to be excessive and uncontrolled beyond bodily capacity to handle, eliminate and overcome the proliferation pool. As is currently known, most of the tumors originate from single transformed cell or are monoclonal in origin and the journey of a single transformed cell from covert to overt malignancy is usually long, very complex, multistep, arduous and meets with many checkpoints and obstacles on its pathway. Looking at different body cells from proliferation potential viewpoint, there are three populations viz. labile, stable and permanent cells in the decreasing order of retention of divisibility. Among these, the permanent cells are most differentiated and even within this group, the mature neurons are known to have least replication capacity. Therefore, only a fraction of brain tumors are of neuronal origin, usually arising in embryonic or fetal stages of the children or occasionally in neonatal life, when the neurons continue to divide at a low rate. Looking from yet another angle, even within the labile and stable populations of cells, the most differentiated or mature cells lose the capacity to divide as they are on way to senescence or death. However, some evidences have shown that rarely mature or better call them maturing cells, may dedifferentiate under special conditions and start dividing again, and that too mostly in vitro. This makes us to believe more and more in the basal or stem cell origins of cancer.

Not only replication is needed for cell transformation, REPLICATION ALLOWANCE BY PROLIFERATIVE MUTATIONS is the single cause of tumor formation. A stem cell, a glia cell, even terminally differentiated neuronal cells can become tumor cells by ONE mutation, that allows the replication and forces the cells to polyploidy or cell division, see: Inhibition of Apoptosis in ALL-1 Leukemic Cell Lines: Allowance of Replication, Constant Repair Replication, Defect DNA Damage Control http://www.omicsonline.org/2157-7013/2157-7013-3-133.php?aid=10462

Cell multiplication is the unique essential feature of cancer. That is why antimitotic drugs are used.

http://onlinelibrary.wiley.com/doi/10.1002/cam4.91/abstract

Dear Riede, I think we should not confuse again by drawing too much inferences and similarities between in vitro and in vivo systems. Most of the cell lines we work with in vitro have highly replication capability such as Leukemia cell line you mentioned and even most of the cells that grow in culture medium are not terminally differentiated cells.