Curing cancer is easier said than done. Constantly evolving, recklessly resilient, and unpredictably nuanced, stopping one type of cancer in its tracks does not mean all other types of cancer can be stopped by the same means. No one scientist, doctor, engineer, or luminary has the sole title of eradicating the unrelenting disease, and it’s unlikely no one human ever will. A recent milestone in cancer research, though, seems to be evidence that even the smallest steps can be groundbreaking for future preventative developments.


Just last year, a leading MIT-affiliated research institute, the Broad Institute, released its recent findings on different proteins and genes related to facilitated cancer development — specifically, biomolecules different cancers are likely to depend on to grow and metastasize throughout the body (1). These kinds of dependencies are different from the occasional genetic mutations that are responsible for triggering cancerous growth. These genetic mutations are often unpredictable, but this newly discovered category of proteins and genes can increase the success of cancer metastasis by providing supplementary functions that might have been inhibited during mutation.


These supplementary functions are what allow the cancerous cells to survive, especially if the mutations silence other genes that would normally be enabling these functions. To be clear, these supplementary functions are not always not provided by new mutated genes, but can also be provided by portions of the genome that were unaffected by the mutation — because these genes are already present in the human genome, researchers at the Broad believe targeting these critical genes could be the key to inhibiting growth of a number of cancers (1). These genetic dependencies come in the form of different proteins and genes that assisted in cancerous cell development that were either mutations themselves, reduced or increased expression of another gene, and may have affected the level of reliance on other genes too.


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Though the research is still in fairly early stages, a number of the found dependencies so far have already been categorized as drug targets, meaning that drugs have been previously developed to inhibit these genes providing the supplementary functions these cancerous cells can’t survive without. Even if these drugs were developed with the purpose of inhibiting other disease growth, the right testing and development could lead to the drug being used in controlling cancerous growth. Other genetic dependencies are still in the process of being researched, and it’s possible drugs may be developed in the future to silence these ones too.


The process to find these dependencies consisted of scrutinizing data from cell lines, analyzing RNA interference (RNAi) patterns apparent in the cell cultures to see what inhibited different types of cancers. To do so, different genes were changed in sample cell cultures (the interfering process of RNAi) and cell behavior was analyzed as a result (2). From statistical analysis, causalities between certain genes and developmental behavior could then be determined. To reduce the presence of statistically insignificant patterns and other noise produced by false positives, one scientist developed the DEMETER tool, which modeled the impact of the interference patterns to see if they really were significant.


Scientist David Root of the Broad does note the importance of analyzing how these genetic dependencies influence cancerous growth based on other environmental factors; each case is unique and the level of dependency may differ as a result (1). Regardless, there are many opportunities for future innovation hidden in each of these dependencies, which you can explore here! Exploring each of these may be the next step in a series of many to tearing down the plaguing disease once and for all.



References and Footnotes

  1. Ulrich, Tom. “Here There Be Dependencies: Putting Cancers’ Vulnerabilities on the Map.” Broad Institute, 5 Apr. 2018,
  2. Ulrich, Tom. “First Draft of Genome-Wide Cancer ‘Dependency Map’ Released.” Harvard Gazette, Harvard University, 27 July 2017,

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