Add BrightSurf on Google Email

A new ending to an old 'tail'

Researchers at the Salk Institute have uncovered a new structural beacon, called the C-tail, which is found in half of all telomeres in alternative lengthening of telomeres (ALT) tumors. This unique feature may be a key to understanding cancer cell immortality and developing effective treatments.

SourceSalk Institute·JournalMolecular Cell·DateApr 21, 2011

Taking aim at tumors

Binghamton University researchers are studying the role of tubulin tyrosine ligase (TTL) in cancer cells, which may lead to more effective treatments. The team has developed a new labeling technique to observe TTL's behavior in live cells, potentially allowing clinicians to personalize cancer therapies.

The sentinel node dilemma in breast cancer surgery

The sentinel node procedure has evolved to limit surgical overtreatment, but isolated tumor cells and micrometastases have led to increased surgeries. Current studies examine the role of radiotherapy, pathologic protocols, and prognostic impact of these findings on breast cancer patients.

SourceIOS Press·JournalBreast Disease·DateApr 12, 2011

JCI online early table of contents: April 11, 2011

Researchers have discovered a protein that improves vascular regeneration in mice with heart attacks, and found that manipulating this protein could be used to treat various vascular diseases. Additionally, studies on mouse models have revealed plasticity in the pathways that control insulin secretion, offering new insights into diabet...

SourceJCI Journals·JournalJournal of Clinical Investigation·DateApr 12, 2011

Tumors resistant to radiation therapy may be controlled by the MET oncogene

Researchers discovered that ionizing radiation drives overexpression and activity of MET through the ATM and NF-κB signaling pathways, making some tumor cells resistant to radiation. Inhibiting MET counteracted this increased invasiveness, promoting apoptosis in tumor cells and enhancing the effect of radiation.

SourceJournal of the National Cancer Institute·JournalJNCI Journal of the National Cancer Institute·DateApr 4, 2011

Call of the riled

Researchers discovered that cancer cells generate a 'stress response' signal that induces nearby macrophages to issue a similar stress response, promoting inflammation and tumor development. This finding presents a potential target for tumor-specific therapies.

SourceUniversity of California - San Diego·JournalProceedings of the National Academy of Sciences·DateApr 4, 2011

Photodynamic therapy against cancer

Researchers found that photodynamic therapy can eliminate tumor-associated lymphatic vessels and in-transit tumor cells, reducing metastasis. This approach could be combined with existing surgical techniques to destroy lymphatic vessels draining from tumors.

SourceUniversity of Helsinki·JournalScience Translational Medicine·DateFeb 9, 2011

JCI online early table of contents: Jan. 18, 2011

Research highlights the key role of estrogen signaling in maintaining energy balance, as well as the propagation of α-synuclein in Parkinson's disease. Additionally, a new immune cell activator has been identified to protect mice from tumors through an IFN-gamma-independent mechanism.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateJan 18, 2011

Cancer cell survival is not 'miR-ly' dependent on p53

A recent study by Leif Ellisen and colleagues found that inhibiting certain microRNAs decreased tumor growth and made cells more sensitive to chemotherapy in a model of squamous cell carcinoma. The researchers identified a feedback loop between p63, microRNAs, and p73 that promotes cancer cell survival and chemoresistance.

SourceJCI Journals·JournalJournal of Clinical Investigation·DateJan 10, 2011

Protective properties of green tea uncovered

Researchers at Newcastle University found that the compounds in green tea are more effective against key triggers of Alzheimer's development when digested by enzymes in the gut. The study also suggests that these compounds have anti-cancer properties, slowing down the growth of tumour cells.

SourceNewcastle University·JournalPhytomedicine·DateJan 5, 2011

The stemness of cancer cells

Researchers found that p53 mutations can allow cancer cells to acquire stem cell-like characteristics, leading to increased tumor heterogeneity and aggressiveness. The study suggests that p53 plays a critical role in preventing the emergence of more aggressive cancer cells.

SourceSalk Institute·JournalProceedings of the National Academy of Sciences·DateDec 13, 2010

Cheek swab may detect lung cancer

A new clinical study reveals a technique called partial wave spectroscopic microscopy can differentiate individuals with lung cancer from those without, even in lifetime smokers or COPD patients. The findings suggest that this minimally invasive test could lead to personalized screening for lung cancer, the leading cause of cancer deat...

SourceU.S. National Science Foundation·JournalCancer Research·DateOct 7, 2010

An IRCM researcher pinpoints the cellular mechanism responsible for modulating the permeability of blood vessels

A new cellular mechanism has been identified for modulating blood vessel permeability, which could have a significant impact on the treatment of cancerous tumours. Nitrosylation of beta-catenin protein by nitric oxide increases vascular permeability, potentially leading to the blockage of tumour growth.

Concentration, timing and interactions are key when it comes to dietary compounds

Agricultural Research Service chemist Thomas Wang found that resveratrol, a bioactive compound in grapes and plant foods, can inhibit cancer cell growth but also increase tumor vessel development with prolonged exposure. The study suggests that diet complexity and gene expression are key layers in cancer development.

How prostate cancer packs a punch

A team of investigators has identified a series of proteins that may make it easier to diagnose the more metastatic forms of prostate cancer. The study uncovers a protein named Siah2, which initiates a cascade of molecular events that turns a non-malignant tumor into a metastatic neuroendocrine tumor.

SourceSanford Burnham Prebys·JournalCancer Cell·DateJul 12, 2010