No. Cancerous cell can't make the normal cell cancerous, the uncontrolled growth ability will make them dominant at the end.

well this is an interesting question and i would say it may depend on what type of cancer cells you are growing and what type of "normal" cells your growing. One possibility is that cell fusion events may occur between your cancer cells and normal cells, thus creating a few options 1 - making the normal cell cancerous, 2 - making the cancer cell that fused with the normal cell not cancerous anymore. 3 - either way the fused cell will have a different genotype and hence be a different cell

They definitely won't make the healthy cells cancerous but I wouldn't be too sure that they have no effect - have a look at these papers which suggest aggressive cancer cells can drain non-cancer fibroblasts of their resources and damage their mitochondria etc:

http://www.ncbi.nlm.nih.gov/pubmed/21300172

http://www.ncbi.nlm.nih.gov/pubmed/21883043

I haven't worked with tumour/cancer cell lines before but am planning to study around this effect late next year. I wouldn't assume they have no affect. Hope that helps

Definitely. Cancer cells often extrude lactate and acidify their environment. This already can hav an impact.

You get a very good question, that's also a question a lot of scientists try to answer. Base on our research, the answer is positive.

Other than some of the other potential effects mentioned above there is also emerging evidence for cancer cells releasing exosomes with oncogones or oncogenic miRNA, also sometimes called oncosomes, which could be taken up by normal cells.

The cancer cells have effect on surrounding healthy cells to make a suitable Niche for themself, as the process of angiogenesis, but can't "transform" the health cells into cancer cells. Even among cancer cells there exist different. Not all cancer cells will lead to tumor, only parts of them, as cancer stem cell (CSC) have ability to create tumor. If they can, leukemia patient may have many types of the tumor (liver, brain, lung extra) before they die.

@Chaubal, hello~ Nice to hear from you. Maybe the cancer cells may act like Mr Smith in the movie The Matrix Revolutions, they may also release something as signal molecules, DNA or RNA for disturbing the health cells action, but not mean all "Guard" in health cells are useless, they will act too. Most of them will going to die before they are really been "transformed". This maybe a war, but the cancer cells may not always win.

The question is that Will Mr smith change all people smith? the answer is no. But there may exit chances that Mr smith find a way, like cell fusion, everything is possible actually.

Show the evidences when you can prove it. One cancer cell can transform another health cell become another cancer cell. This is a great project!!!

Anyway, I'm reading the paper you suggest, thanks.

I may recommend an excellent paper named: Hallmarks of cancer: The next generation.

The control actions of some kind of cancer cells via micro-molecules more like making slaves working for them than transform them.

I'm not sure if cancerous cell able to make the normal cell cancerous.

But on our researches (not yet published)... YES... cancerous cell can affect normal cells.

Like said Hongjuan Cui a lot of scientists try to answer.

There exist a gap between the real affects and small probability events. I will following up and waiting more evidences.

Yes

Cancer cell has an indirect effect on normal cell through competition to get nutrition. Cancer cell cannot affect normal cell by any means except its ability to invade and control the area to capture all physiological features. Because some viruses are implicated in some cancer types it is thought that the infectious property of the viruses may lead to infect normal cell if the cancer cell is infected. Therefore in such situation cancer cell may affect normal cell.

Your question raises some interesting points. A known effect of carcinogens is increased reactive oxygen species (ROS), which may cause mitochondrial injury. Reactive oxygen species (ROS) are a second messenger in cell signaling and in larger amount cytotoxins. As ROS are usually increased in cancer cells and act in initiation, progression and metastasis, they are considered oncogenic (see Cancer Biol Ther. 2008 Dec;7(12):1875-84). The release of ROS by cells undergoing tumorogenesis may damage bystander cells. You could measure this by examining ROS stress in the bystander cells in the presence and absence of cancer cells.

We cannot expect that naked DNA from cancer cell able to transfect normal cell to change it to cancer cell. This concept may be seen in virus biology but not in normal in vivo human cells. Returning to Rous hypothesis about virus and naked cell DNA , those tests were done in the laboratory but not in vivo. Hence cancer cell has no effect on normal cell but nutrition competition..

Maybe in the study of cell-free nucleic acids circulating in the plasma might add the unresolved problem of the "dormant metastases"? (hereinafter remember an abstract that addresses only a particular case). I understand that this is a way to resize the discussion relating to the capacity of cancer cells to transfect the normal cell to change it, but I think maybe it could be a more easily approachable in vivo.

Metastasis Dormancy in Estrogen Receptor–Positive Breast Cancer

Xiang H.-F. Zhang, Mario Giuliano, Meghana V. Trivedi, Rachel Schiff and C. Kent Osborne

About 20% to 40% of patients with breast cancer eventually develop recurrences in distant organs, which are often not detected until years to decades after the primary tumor diagnosis. This phenomenon is especially pronounced in estrogen receptor–positive (ER+) breast cancer, suggesting that ER+ cancer cells may stay dormant for a protracted period of time, despite adjuvant therapies. Multiple mechanisms have been proposed to explain how cancer cells survive and remain in dormancy, and how they become reactivated and exit dormancy. These mechanisms include angiogenic switch, immunosurveillance, and interaction with extracellular matrix and stromal cells. How to eradicate or suppress these dormant cancer cells remains a major clinical issue because of the lack of knowledge about the biologic and clinical nature of these cells. Herein, we review the clinical manifestation of metastasis dormancy in ER+ tumors, the current biologic insights regarding tumor dormancy obtained from various experimental models, and the clinical challenges to predict, detect, and treat dormant metastases. We also discuss future research directions toward a better understanding of the biologic mechanisms and clinical management of ER+ dormant metastasis. Clin Cancer Res; 19(23); 6389–97. ©2013 AACR.

Early studies have shown that the growth of transformed cells is inhibited when they are in contact with normal cells ( https://www.ncbi.nlm.nih.gov/pubmed/2416473 ), and that chemicals that modulate intercellular communication not only inhibit the induction of transformed foci but also revert transformed cells to the normal phenotypes by establishing intercellular communication with surrounding normal cells ( https://www.ncbi.nlm.nih.gov/pubmed/2836057 ).

From the viewpoint of cellular responses to ionizing radiation, low dose to nontransformed cells stimulates the selective removal of precancerous cells ( https://www.ncbi.nlm.nih.gov/pubmed/17283161 ). Tumor microenvironment plays critical roles in radiation carcinogenesis such that tumor arise from non-irradiated p53 null epithelium transplanted into irradiated mice ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110779/ ).