New method better predicts tumour growth rate in 12 cancers

In a new research, scientists have come up with a new formula that predicts tumour growth rate more accurately, a crucial statistic used to schedule screenings and set dosing regimens in cancer treatment.

The mathematical method successfully estimated the doubling time, the amount of time for a tumour to double in size, for 12 types of cancer, ranging from breast and prostate cancers to melanoma.

"This novel method allows clinicians and drug development scientists to use routinely-generated clinical data to infer doubling times of solid tumours. This parameter can be used to design individualised dosing regimens and develop reliable models for anticancer therapeutics," said the Dr.

Tumour doubling time can significantly affect the outcome of anticancer therapy, but the rate is challenging to determine. Current methods calculate doubling time by measuring the size of a tumour at two points in time and assuming cancer will grow at an exponential rate.

However, most doubling times calculated using this method are overestimated, and tiny changes in tumour size can make determining growth rates difficult.

The error impacts the ability of clinicians to schedule optimal follow-up screenings, set effective dosing regimens, and determine whether surgery, chemotherapy or radiation therapy  is the best form of treatment.
 
The researchers instead base their method on data extracted from progression-free survival  plots - the length of time during and after treatment that cancer does not grow or spread.

Progression-free survival plots explained the Dr., inherently contain information that could help identify tumour growth rates.

The investigators examined data from 47 clinical trials that reported plots for any of 12 cancer types: melanoma; pancreatic, lung, prostate, gastric, colorectal and three forms of breast cancer; hepatocellular (liver) and renal cell (kidney) carcinoma; and glioblastoma multiforme (brain).

The cancer growth rates predicted by the researchers using progression-free survival plots were within close range to the reported actual tumour doubling times. 

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Nutrient deprivation triggers cell death in cancers

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 Focusing their research on the kidney cancer renal cell carcinomas, the researchers discovered that majority of these cancer cells rewire their metabolism in a way that leaves them addicted to an outside nutrient called cystine.

By depriving the cancer cells of the amino acid cystine, the researchers were able to trigger a form of cell death called necrosis in mouse models of the disease.

"We found that the same machinery that makes these tumours so aggressive also makes them vulnerable to nutrient deprivation," said senior study author Jen-Tsan Ashley Chi, associate professor at Duke University School of Medicine in North Carolina, US.

"It is like we are beating it at its own game," Chi noted.

The findings appeared online in the journal Cancer Research.

Chi said the study points to a promising new approach for the treatment of renal cell carcinoma, a form of kidney cancer that has historically been very difficult to cure.

 About three-fourths of renal cell carcinoma cases are marked by a missing VHL tumour-suppressor gene, which keeps healthy cells from developing into tumours.


The researchers decided to investigate how this single genetic change could affect the metabolism and nutrient requirement of cancer cells.

They subjected the cancer cells to a nutrient deprivation test, removing each of the 15 amino acids from their growth media, one by one.

Most of the time, the cells weathered the change quite well, slowing down their growth but otherwise remaining healthy.

But the researchers found that when cystine was removed, the cells swelled up and floated to the surface, a sure sign of necrotic death.

Gastrointestinal tumours can lead to additional cancers

Patients suffering from gastrointestinal tumours are at increased risk of contracting other cancers, says a study.

One in 5.8 patients with gastrointestinal stromal tumours (GIST) will develop additional malignancies before and after their diagnosis, the results indicated.

Specifically, patients with GIST are more likely to develop other sarcomas, non-Hodgkin's lymphoma, carcinoid tumours, melanoma, colorectal, oesophageal, pancreatic, hepatobiliary, prostate and renal cell cancers.

"The research indicates that these patients may develop cancers outside these syndromes but the exact mechanisms are not yet known," said Jason Sicklick, assistant professor of surgery at the University of California's San Diego School of Medicine.

"Only five percent of patients with gastrointestinal stromal tumours have a hereditary disorder that predisposes them to develop multiple benign and malignant tumours," Sicklick added.

The researchers said further studies are needed to understand the connection between GIST and other cancers.

When compared to the United States population, the researchers found that people with GIST had a 44 percent increased prevalence of cancers occurring before a GIST diagnosis and a 66 percent higher risk of developing cancers after diagnosis.

The most common tumours were those of the genitourinary tract, breast, respiratory and blood.
"Patients diagnosed with gastrointestinal stromal tumours may warrant consideration for additional screenings based on the other cancers that they are most susceptible to contract," said co-author James Murphy from the University of California.

The study appeared in the journal Cancer.

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