Saving an Endnote Library

Many MSK staff favor Endnote as their citation management software. Saving an Endnote Library is one of the issues that requires special attention from the Endnote user.

In the desktop version of EndNote, a Library is saved with the extension .enl after its name, and its associated Data folder, with the extension .Data after its name. (NOTE: On Mac computers there is also an option to save your Library as a .enpl file, which combines both the library and the data file into one.)

The Library contains the records and the Data folder is intended for PDFs of the full text associated with the Endnote Library records, as well as anything inserted into the Image field of a reference. Even if no PDFs or images are available, the Data folder will still be there; however a Data folder should never be deleted. Data folders should never be moved or copied without first compressing them into a .enlx file. From there, the compressed zip file can be moved, copied, and shared.

Endnote library (.enl), associated data folder (.Data) and the compressed zip file of both (.enlx)

It is important to know that saving an Endnote Library to any network drive does not work well. There is a very high chance of getting a pop-up Damaged Library message at some point if the Library is saved to any drive other than your local drive, i.e. to your computer. On a PC you may consider This PC>Documents for saving an Endnote Library. If you want to save a Library to a network drive for better security you can save a backup copy either as a Compressed Library as explained above or by using the Endnote File>Save a Copy feature. You can save the backup copy to your personal drive or, as a Read Only copy, to a shared drive for your collaborators’ use (but not for their adding/removing the content). As an alternative, instead of using a shared drive for sharing your Endnote Library with others, you can use the Endnote Online companion to your desktop Endnote for collaboration.


  • Don’t save an Endnote Library to a network drive.
  • Never delete the .Data folders associated with Endnote Libraries.
  • Don’t try moving the Library separately from its Data Folder, use the Compressed Library feature instead.

A Vaccine as an Immunotherapy Booster, Tumor’s Impact on Healthy Tissue Metabolism and More

  • An animal study conducted by an international team of scientists led by researchers from the University of Konstanz in Germany demonstrated that combining a new cancer vaccine with an immune checkpoint inhibitor can dramatically increase the response to therapy rate. The new vaccine is a microparticle-based cancer vaccine, which uses the immunostimulant Riboxxim that has been already approved for application in humans. Combining a cancer vaccine with established drugs creates a foundation for human trials and, eventually, for improving the efficacy of immunotherapies in humans. The study was published in Nature Communications.
  • Researchers from the Washington University in St. Louis conducted an animal study that revealed the impact of melanoma on the metabolism in tissues outside of the tumor. While most of the previous research on cancer metabolism concentrated on the tumor metabolism itself, this study looked at the relationship of the tumor with metabolism in non-malignant tissues. It demonstrated that cancers affect metabolic processes in healthy tissue elsewhere in the body and that, at least in some instances, these metabolic changes take place to support the tumor. The study authors hope that their findings would lead to targeting the metabolism of healthy tissues as a potential treatment for cancer. The study was published in Cell Metabolism.
  • A study by the researchers at UVA Cancer Center shed new light on the intercellular interactions of androgen hormones and their receptors. The study offers new insight into the mechanism of androgen-regulated communication within prostate cancer cells. Its findings could be instrumental for perfecting anti-androgen therapies that are at the core of prostate cancer treatment.  The study was also published in Nature Communications.
  • In an animal glioblastoma study, scientists from the Massachusetts General Hospital reprogrammed the host’s immune cells called regulatory T-cells (Tregs) manipulated and hijacked by cancer to assist in its growth and turned them back into cancer killers. It remains to be seen whether this success can be translated into treating humans, and further testing is necessary. This study was also published in Nature Communications.
  • A recent meta-analysis of 17 observational studies found an association between higher mushroom consumption and decreased cancer risk. While observational studies typically only help establish a correlation between the exposure and the outcomes but not prove causation, this meta-analysis, published in Advances in Nutrition, may boost further research into the protective effects of mushrooms and their potential for cancer prevention.
  • Researchers from Brazil and the U.S. developed a low-dose four-drug combination to help prevent metastasizing of cancer by simultaneously targeting multiple pathways in the metastasis-promoting network without triggering drug resistance. The authors hope that their findings, challenging current cancer treatment approaches, “could lead to a new cancer treatment strategy where patients first receive low-dose combination drugs that block metastasis and then receive traditional cancer treatments such as radiation, chemotherapy, or immunotherapy.” This animal study was published in eLife.

Prolactin in Breast Cancer Development, Dietary Methionine in Oncogenesis and More

  • Researchers from Virginia Commonwealth University conducted studies that shed new light on the role of the hormone prolactin. While prolactin has been known for its role in breast development and milk production in pregnancy, this new research established that it also plays an important part in breast cancer development. This finding may lay the foundation for creating new targeted drug therapies to treat breast cancer. The study was published in NPJ Breast Cancer.
  • Two researchers from Germany conducted a study revealing a new understanding of the activation mechanism of a cell growth protein SHP2. The excessive activity of this protein stimulates increased cell proliferation thus triggering cancers such as leukemia. Knowing the mechanism of activation of this protein is crucial for designing therapeutic strategies to inhibit this protein. The study proves wrong the prior understanding of this mechanism. The new insight paves the way for developing new targeted therapies to prevent excessive cell proliferation caused by this protein. The study was published in PNAS.
  • A researcher from the Purdue University found a way to synthesize a compound that can fight a protein involved in multiple cancers, including breast, brain, colorectal, prostate, lung, and liver cancers. The protein, called BRAT1, was previously considered unsuitable as a drug target because of its chemical properties. The compound, Curcusone D, which belongs to a Curcusone family of compounds and originally came from a shrub named Jatropha curca, can now be synthesized in a lab. The compound kills cancer cells and can keep cancer from metastasizing. As Curcusone D compound is very hard to extract from the plant and since it is the only compound that can inhibit BRAT1 protein, synthesizing it in a lab is a very important discovery. Pending some toxicity studies, this compound could be a significant addition to the therapeutics against cancer. This research was reported in the Journal of the American Chemical Society.
  • A group of scientists from Japan conducted a study on how cell proliferation (oncogenesis) and cell death were regulated, focusing on genes p38, JNK, and slpr. Based on the knowledge that dietary nutrients can control p38, the study was done on fruit flies. Researchers manipulated the amount of dietary amino acid methionine and established that decreasing the amount of the methionine in the diet prevented p38-controlled oncogenesis. One of the study findings was that the oncogene slpr could mediate the signaling pathways controlled by other oncogenes. The researchers hope that their findings can be translated to human cancers and help explain how they develop. The study was published in eLIfe.