Targeted Photodynamic Therapy Shown Highly Effective Against Prostate Cancer

Excerpt:

“Researchers presenting a preclinical study at the 2017 Annual Meeting of the Society of Nuclear Medicine and Molecular Imaging (SNMMI) demonstrated the efficacy and optimal dose for targeted photodynamic therapy (tPDT) to treat prostate cancer before and during surgery. Prostate-specific membrane antigen (PSMA) was targeted with an anti-PSMA antibody radiolabeled with the tracer indium-111 (111In) and coupled with specialized photosensitizers that cause cell destruction upon exposure to near-infrared (NIR). The combined formula is 111In-DTPA-D2B-IRDye700DX.

” ‘Coupling the photosensitizer to an imaging agent that targets PSMA on the tumor surface makes it possible to selectively and effectively destroy prostate tumor remnants and micrometastases while surrounding healthy tissues remain unaffected,’ said Susanne Lütje, MD, PhD, lead author of the study from the Department of Radiology and Nuclear Medicine at Radboud University Medical Center in Nijmegen, the Netherlands, and the Clinic for Nuclear Medicine at University Hospital Essen, Germany.”

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New Transdermal SARM Drug for Muscle-Wasting Offers Hope for Older Cancer Patients

Muscle wasting that occurs as a result of cancer negatively impacts the well-being and recovery prospects of millions of patients, particularly the rapidly-growing elderly populations in Western societies. Drugs called selective androgen receptor modulators (SARMs) offer hope for these patients, and a new SARM for transdermal administration is promising excellent efficacy without harming liver function and HDL levels. Results and conclusions were presented Tuesday at the joint meeting of the International Society of Endocrinology and the Endocrine Society: ICE/ENDO 2014 in Chicago.

SARMs are able to stimulate the growth of muscle with effects similar to those seen by use of traditional anabolic steroids but without the undesirable side effects of those established muscle-building drugs, in particular, the adverse effects on prostate health that can occur from their use.

Editor’s note: As stated above, drugs called SARMs may help counteract harmful muscle loss that occurs as a result of cancer in elderly patients. A new SARM was recently studied in the lab and in mice. Scientists say that it shows promising ability to stimulate growth of muscle, without harming liver function and without lowering blood levels of a molecule called HDL. Clinical trials to test the drug in volunteer patients will be needed to determine if the drug will help people with cancer.


Antioxidants May Actually Speed Lung Cancer Growth in Some Cases

Antioxidants are chemicals that neutralize particles called free radicals that can damage DNA. Preventing such damage may help lower cancer risk for some people. However, tumors themselves can contain high levels of free radicals; by eliminating these free radicals, antioxidants may help cancer cells grow. In a laboratory, lung cancer cells treated with the antioxidants vitamin E and acetylcysteine (ACC) multiplied faster than untreated cells. Vitamin E and ACC also increased tumor growth and decreased survival time in mice with lung cancer. The so-called ‘tumor suppressor’ protein p53 can sense certain free radicals to detect cells with DNA damage and stop their growth. Antioxidants may interfere with this cancer-suppressing mechanism by reducing free radical levels. Taking antioxidants may therefore not be recommended for lung cancer patients and smokers.


New Targeted Drugs May Offer Treatment for KRAS-Mutant Lung Cancer

Abnormalities in the KRAS gene are the most common mutations in lung cancer, especially in lung adenocarcinoma, a type of non-small cell lung cancer (NSCLC). However, no effective targeted therapy directed at KRAS has been found. Instead, researchers have begun to focus on blocking molecules “downstream” in the chain of chemical reactions through which KRAS affects the cell. Two such molecules are TBK1 and MEK. A recent study found that the drug CYT387 blocks TBK1. CYT387 reduced tumor growth in mice with KRAS-mutant lung adenocarcinoma. Also in mice, CYT387 and the MEK inhibitor AZD6244, given together, shrank aggressive lung tumors with mutations in both the KRAS and the TP53 gene. Researchers now hope to investigate the two drugs in people.


Lung Cancer Drug BGB324 May Counteract Drug Resistance

The protein Axl has been associated with cell transformation processes that contribute to the spread of cancer through the body and to cancers becoming drug resistant. A recent study investigated the effect of the Axl inhibitor BGB324 on non-small cell lung cancer (NSCLC) cells that had become resistant to EGFR inhibitors like erlotinib (Tarceva). BGB324 restored the effectiveness of EGFR inhibitors against these cancer cells, which had been grown either in a matrix or as tumors in mice. BGB324 also appeared to enhance the effectiveness of the chemotherapy drug docetaxel (Taxotere) and of bevacizumab (Avastin). BGB324 may therefore be a promising new candidate for treating drug-resistant NSCLC. The drug will be tested in a phase Ib clinical trial for NSCLC in 2014.


E-Cigarette Vapor Promotes Cancer-Like Transformations of Airway Cells with Predisposing Mutations

E-cigarettes (electronic cigarettes that use a battery-powered system to deliver nicotine without producing smoke) are advertised as a safer alternative to tobacco cigarettes. However, very few studies have investigated how e-cigarettes affect lung function and lung cancer risk. Researchers examined human airway cells with mutations in the TP53 and KRAS genes, which are often mutated in the airways of current or former smokers at high risk of lung cancer. When the cells were exposed to e-cigarette vapor, they developed cancer-cell-like behaviors and gene expression changes very similar to what was seen when these cells were exposed to tobacco smoke. E-cigarettes may increase the risk of developing lung cancer in high-risk people, including current and former tobacco smokers.


Attacking Lung Cancer Cells by Blocking Antioxidants

As a byproduct of their rapid metabolism and growth, cancer cells frequently produce high levels of so-called free radicals–highly reactive particles that can damage cells. To protect themselves, cancer cells also produce antioxidants, which deactivate the free radicals. Drugs that block these antioxidants should therefore selectively impair cancer cells, while having relatively little effect on healthy cells that do not experience high levels of free radicals. Researchers found that the antioxidant-inhibiting drug ATN-224 induced the death of non-small lung cancer (NSCLC) cells in cell culture. ATN-224 also decreased the number and size of lung tumors in mice injected with NSCLC cells.


Timing Cancer Treatment for Maximum Effectiveness

Our bodies follow a 24-hour ‘biorhythm’ that affects most of our biological functions. This fact forms the basis of cancer chronotherapy, which takes time of day into account to plan cancer treatment. Administering cancer drugs at the right time can double effectiveness while reducing toxicity up to fivefold. However, individual differences in biorhythms mean that the ‘right time’ varies from one person to another. In a recent study, researchers linked gene expression in mice with the time point at which the chemotherapy agent irinotecan (Camptosar) produced the least toxicity. They developed a mathematical model that predicts each animal’s ideal time point based on the expression of two genes. In the future, they hope to develop similar tools to help predict the best time for cancer treatment in human patients.


Timing Cancer Treatment for Maximum Effectiveness

Our bodies follow a 24-hour ‘biorhythm’ that affects most of our biological functions. This fact forms the basis of cancer chronotherapy, which takes time of day into account to plan cancer treatment. Administering cancer drugs at the right time can double effectiveness while reducing toxicity up to fivefold. However, individual differences in biorhythms mean that the ‘right time’ varies from one person to another. In a recent study, researchers linked gene expression in mice with the time point at which the chemotherapy agent irinotecan (Camptosar) produced the least toxicity. They developed a mathematical model that predicts each animal’s ideal time point based on the expression of two genes. In the future, they hope to develop similar tools to help predict the best time for cancer treatment in human patients.