Question: How many cells are necessary to clone something?
About the article "Cloning", section "Cloning unicellular organisms".

Candidate passages:
This concept of clone assumes importance as all the cells that form a clone share common ancestry, which has a very significant consequence: shared genotype.
One of the most prominent usage is in describing a clone of B cells.
The B cells in the body have two important phenotypes (functional forms) -- the antibody secreting, terminally differentiated (that is, they cannot divide further) plasma cells, and the memory and the naive cells—both of which retain their proliferative potential.
Another important area where one can talk of "clones" of cells is neoplasms.
Many of the tumors derive from one (sufficiently) mutated cell, so they are technically a single clone of cells.
However, during course of cell division, one of the cells can get mutated further and acquire new characteristics to diverge as a new clone.
This is how, in fact, drug resistance could be acquired in many cases.
All the granulosa cells in a Graafian follicle are in fact a clone.
Paroxysmal nocturnal hemoglobinuria is a disorder of bone marrow cells resulting in shortened life of red blood cells, which is also a result of clonal expansion, i.e., all the altered cells are originally derived from a single cell, which also somewhat compromises the functioning of other "normal" bone marrow cells.  
Cells in pre-malignant and malignant neoplasms (tumors) evolve by natural selection.
This accounts for how cancer develops from normal tissue and why it has been difficult to cure.
There are three necessary and sufficient conditions for natural selection, all of which are met in a neoplasm:  There must be variation in the population.
Neoplasms are mosaics of different mutant cells with both genetic and epigenetic changes that distinguish them from normal cells.
That variation must be heritable.
When a cancer cell divides, both daughter cells inherit the genetic and epigenetic abnormalities of the parent cell, and may also acquire new genetic and epigenetic abnormalities in the process of cellular reproduction.
That variation must affect survival or reproduction (fitness).
While many of the genetic and epigenetic abnormalities in neoplasms are probably neutral evolution, many have been shown to increase the proliferation of the mutant cells, or decrease their rate of death (apoptosis).
(See Hallmarks below) Cells in neoplasms compete for resources, such as oxygen and glucose, as well as space.
Thus, a cell that acquires a mutation that increases its fitness will generate more daughter cells than competitor cells that lack that mutation.
In this way, a population of mutant cells, called a clone, can expand in the neoplasm.
Clonal expansion is the signature of natural selection in cancer.
Cancer therapies act as a form of artificial selection, killing sensitive cancer cells, but leaving behind resistant cells.
Often the tumor will regrow from those resistant cells, the patient will relapse, and the therapy that had been previously used will no longer kill the cancer cells.
This selection for resistance is similar to the repeatedly spraying crops with a pesticide and selecting for resistant pests until the pesticide is no longer effective. 
It is currently possible to collect two types of stem cells during childbirth: amniotic stem cells or umbilical cord blood stem cells.
To collect amniotic stem cells, it is necessary to do amniocentesis before or during the birth.
Amniotic fluid contains mesenchymal stem cells while umbilical cord blood contains both hematopoietic and mesenchymal stem cells.
Although there are many potential future applications of such stem cells, there are few current therapeutic applications of such stem cells. 
One common feature of neoplastic progression is the expansion of a clone with a genetic or epigenetic alteration.
This may be a matter of chance, but is more likely due to the expanding clone having a competitive advantage (either a reproductive or survival advantage) over other cells in the tissue.
Since clones often have many genetic and epigenetic alterations in their genomes, it is often not clear which of those alterations cause a reproductive or survival advantage and which other alterations are simply hitchhikers or passenger mutations (see Glossary below) on the clonal expansion.
Clonal expansions are most often associated with the loss of the p53 (TP53) or p16 (CDKN2A/INK4a) tumor suppressor genes.
In lung cancer, a clone with a p53 mutation was observed to have spread over the surface of one entire lung and into the other lung.
In bladder cancer, clones with loss of p16 were observed to have spread over the entire surface of the bladder.
Likewise, large expansions of clones with loss of p16 have been observed in the oral cavity and in Barrett's esophagus.
Clonal expansions associated with inactivation of p53 have also appear in skin, Barrett's esophagus, brain, and kidney.
Further clonal expansions have been observed in the stomach, bladder, colon, lung, hematopoietic (blood) cells, and prostate.
These clonal expansions are important for at least two reasons.
First, they generate a large target population of mutant cells and so increase the probability that the multiple mutations necessary to cause cancer will be acquired within that clone.
Second, in at least one case, the size of the clone with loss of p53 has been associated with an increased risk of a pre-malignant tumor becoming cancerous.
It is thought that the process of developing cancer involves successive waves of clonal expansions within the tumor. 
In the field of cellular biology, single-cell analysis refers to the study of individual cells isolated from tissues in multi-cellular organisms.
Single cell analysis is a natural step in the reductionist approach to studying organisms.
By studying one cell at a time, the results are certain to stem from that particular cell.
A cell can for example be monitored as it migrates or divides into two cells, how many divisions that occur over time and the rate of cell division in a specific cell clone.
Cell divisions are interesting in for example cancer, due to the uncontrolled rate of cell proliferation of a cancer cell as compared to a normal cell.
Genetic patterns and protein expression can explain cellular behavior to a large extent, but the dynamic study of living cells can increase the understanding of the interconnecting molecular events continually taking place in each cell .
Each cell is more or less different from the other, even within the same cell type.
Cellular heterogeneity is well known in bacteria and increasingly apparent in eukaryotic cells.
For a long time it was desired as well as assumed that cell cultures were of a homogeneous nature, and that analyzing a collection of cells would give an accurate assessment of the behavior of the cells in that culture or tissue.
The average response of the cells was, and often still is, interpreted as the response of all cells in that sample.
Additionally, the effect of cell number (signaling, interactions, etc.)
on cell behavior was, and is still often, neglected due to difficulties in monitoring such detailed phenomena.
The attitude to ensemble measurements is starting to change; today's researchers are increasingly aware of, hence interested to study, the resulting effects of heterogeneity in cell samples, as mirrored in recent reviews on single-cell analysis.