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Hedgehog signalling pathway is also important in cellular differentiation. However, it is not only in embryonic cells, but also in adult organisms being silenced in most adult tissues. Hedgehog signalling pathway can be divided into Sonic Hedgehog (SHH), Indian Hedgehog (IHH) and Desert Hedgehog (DHH), and the SHH has the most research. Hh pathways are mainly controlled by two receptors, Patched and Smoothened. Binding with Patched receptors can inhibit the Smoothened pathway, so there are some points that the Hh pathway can not be inhibited normally in cancer cells and lead to cell over-proliferation. Some inhibitors of Hh pathways like SMO antagonists and Hh ligand antagonists are also ongoing the trials (Ruch & Kim, 2013). This research may treat cancer by creating balance in Hh pathway.

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Notch signaling pathway regulates cell fates and proliferation. Notch signalling pathway plays key role in neural differentiation, especially in embryonic development, including development of heart and stem cells. An essential point of Notch signaling pathway is its specific receptor, which is a single membrane subunit containing protein, and most Notch receptors are outside the cell and the other are inside the cell. Specially, the Notch receptors are also the Notch ligand which can bind with Notch receptors on other cell membrane and form Notch-Notch ligands. This process can start the Notch signalling pathway and finally start reactions in target genes. Another important point is a small subunit called the NCID, it can combine with Notch receptors and activate some functions in stream target. The aberrantly expression of Notch receptors and ligands is found in many cancers, so the Notch signalling pathway is vital direction in cancer study. The Notch receptor or ligand, NICD and its stream targets could provide some drug targets to treat cancers. Moreover, as Sethi & Vidal-Puig (2010) states, NICD and β-catenin have interaction effects and can cause opposing responses. It suggests that Notch signalling pathway and wnt signalling pathway are not noninterference and could affect each other.

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Wnt pathway is one of the common cell signalling pathways working on cell cycle and cell proliferation. Wnt always work with β-catenin as a signalling network, which is called Canonical Wnt Pathway. Wnt binds with receptor on cell membranes and lead to β-catenin increasing in the cytoplasm and then move into the nucleus to activate target genes. In addition, frizzled as membrane receptor and dishevelled in the cytoplasm are both significant steps of this pathway. Abnormal Wnt signaling pathways leads to excessive cell division and cancer (Sethi & Vidal-Puig, 2010). For treating cancers, controlling cell signaling pathways is effective. An example of this is regulating the activity of Notum, which is a phospholipase enzyme and can make the proteins in Wnt pathways deactivates, is a good drug target to control Wnt pathways (Nusse, 2015).
Figure - The Wnt signalling pathway (Reya & Clevers, 2005)

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Introductory paragraph - what is cancer, how does it come about? How long have we known about it? What measures are there for treatments of cancer? Some specific examples of cancer and of course an outline to the structure of your essay.
Main body (1) cellular mechanisms in cell-signalling e.g. ligand binding/protein -protein interactions and shape changes/cascades of interactions/protein phosphorylation - state that failures in any one of these can results in things going wrong in the body, including cancer
Main body (2) Genes and their receptors that regulate normal cell growth and cell division e.g. growth factors and their receptors, intracellular molecules of signalling pathways. One example in the plasms membrane is the G-protein coupled rectors - receptor tyrosine kinases and ion channel receptors
Main body (3) transcription and translation pathways and failures e.g. hormones receptors complex, or even some non-protein ions known as second messengers
Main body (4) controls on regulation and their failures - signalling pathways amplify the cell's response, the degree of which depends on the specific function of the molecules in the pathway, the many steps, in the multi-step pathway provide point control points for further regulation, overall efficiency is enhanced by presence of scaffolding proteins and the termination of the signal - errors in any of these steps can cause diseases/disorders
Main body (5) - inactivation mechanisms - For a multicellular organism to remain capable of responding to incoming signals, each molecular change in its signalling pathways must only last a short time. If a signalling pathway component becomes locked into one state, whether inactive, or active, consequences can be devastating
Main body (6) - apoptosis features - Cells that are damaged, infected or have reached the end of the functional life span often undergo programmed cell death known as apoptosis. The signal that triggers apoptosis can come from either inside or outside the cell. Outside the cell, signalling molecules released from other cells can initiate a signal transductions pathway that activates the genes and proteins responsible for apoptosis. Within a cell whose DNA has been irretrievably damaged, a series of protein-protein interactions can pass along a signal that similarly triggers apoptosis
Main body (7) - oncogenes and their cause - genes that code for proteins that stimulate normal cell growth and cell division. Oncogenes arise from genetic mutations and fall into 3 categories -
movement of DNA within the genome, amplifications of a proto-oncogene, and point mutations in a control element or in the proto-oncogenes itself
Main body (8) - Mutations in genes that normally regulate cell growth and division
Main body (9) - mutations in genes that usually inhibit cell division e.g. tumour suppressor genes
Main body (10, 11, 12) - NOTCH, WNT and hedgehog
Final conclusion paragraph - future developments? Importance of understanding these pathways etc.?

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Many proto-oncogenes and tumor-suppressor genes are part of cell signalling pathway, and their abnormal expression leads to excessive cell division and even cancers. One idea is the protooncogene is a normal cellular gene that regulate cell proliferation and differentiation. An example of this is ras proto-oncogene gene, which can be transcribed and translated into a G protein, Ras protein, working as growth factor to stimulates the cell cycle. This protein triggers the kinase cascade and its express malfunction causes abnormal cell division. Previous research by Campbell (2014) supports the idea that 30% of cancers have ras proto-oncogene gene mutations and more than 50% cancers have p53 tumor suppressor gene mutations. This indicates dysregulation in genetic expression causes cancer. In contrast, some failures of gene expression is not as components of signalling pathways, it might be cell signalling pathways lose control in adjust genetic expression or cell apoptosis. Cell signalling pathways can control irreparable, damaged and lost functional cells undergo programmed cell death. The cell apoptosis can avoid accumulated gene mutations, but the losing control of cell apoptosis ensue on cancers. This suggests dysregulation of cell signalling pathways can influence cell normal functions and cause cancers.

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Signalling pathways are a serious of cellular molecules working together to adjust different cellular functions. The normal signalling pathways can use some proteins encoded by genes as signal and relay them to particular receptor, and then cause protein-protein interactions and shape changes, cascades of interactions and protein phosphorylation. The normal signalling pathways control cell cycle and even tissue development, nevertheless some dysregulated activations of signalling pathway may lead to cancers. This essay will look at the dysregulation in cancer cells and some common cell-signaling pathways including Wnt, Notch and Hedgehog (Hh) signaling pathways.