FDA Grant Forwards Listeria-Based Throat Cancer Vaccine

Source: www.targetedonc.comAuthor: Sandra Kear An experimental immunotherapy for human papillomavirus-, or HPV-, related throat cancers, which is driven by the Listeria bacteria (that wreaks havoc when ingested), may now move forward due to a $1.1 million dollar grant from the FDA to researchers at Baylor College of Medicine.   “Immunotherapy, such as axalimogene filolisbac, which targets HPV proteins expressed in cancer cells is a great example of using a cancer’s own unique biology against it.” said principal investigator Andrew Sikora, MD, PhD, leader of the head and neck cancer program in the NCI Comprehensive Designated Dan L. Duncan Cancer Center and an associate professor of otolaryngology at Baylor College, in an interview with Targeted Oncology.   "This is hopefully the first step toward development of more targeted treatment approaches that reduce side effects and cancer treatment-related morbidity by uniquely targeting only virus-infected cells.” 
The Listeria-based HPV immunotherapy, axalimogene filolisbac (ADXS11-001), is developed by Advaxis, and functions by stimulating an immune response against HPV proteins, thus killing infected cells.   The drug is currently being evaluated in phase I-II study3 alone or in combination with MedImmune’s durvalumab, in patients with cervical or HPV-positive head and neck cancer. The study has three arms: axalimogene filolisbac alone, durvalumab alone, and the two drugs combined. Primary outcomes established for the study are: number of subjects with adverse events (AEs) in each dose level, number of subjects with AEs in the combination dose, and progression-free survival.   Patients must have measurable disease by RECIST criteria, as well [...]

2015-09-17T09:22:55-07:00September, 2015|Oral Cancer News|

Antioxidants May Cause More Harm Than Good in Cancer Patients

Source: medscape.comAuthor: Zosia Chustecka  While alternative health gurus often encourage increasing antioxidants in the diet and the taking of antioxidant nutritional supplements such as beta-carotene, vitamins A, C, and E, and selenium, new research findings suggest that antioxidants could do more harm than good, especially in cancer patients. The idea is discussed in a perspective article on the promise and perils of antioxidants for cancer patients in the July 10 issue of the New England Journal of Medicine. Coauthor David Tuveson, MD, PhD, professor and deputy director of the Cold Spring Harbor Laboratory Cancer Center in New York, explained in an interview with Medscape Medical News that the idea that antioxidants could be useful in cancer goes back to Linus Pauling, and is based on observations that oxidation within cells is needed for cell growth. "As cancer cells growth rapidly, a cancer cell would have more oxidation within it than a normal cell," he added, and the hope was that antioxidants would interfere with these cellular oxidative processes and would suppress the growth. "Although some early preclinical studies supported this concept," the authors write, there have now been several clinical trials that have shown no effect of antioxidants on reducing the incidence of cancer, and there have even been suggestions of harm in persons who are at risk for cancer. Dr. Tuveson noted a clinical trial from Scandinavia in the early 1990s, which found that high doses of antioxidants, particularly beta-carotene, were associated with more lung cancer rather than less as had been hoped for. There was [...]

2014-07-14T15:04:19-07:00July, 2014|Oral Cancer News|

Growing ‘mini tumors’ from patient’s cancer could lead to custom treatments

Source: www.huffingtonpost.com Author: Marilynn Marchione It's a medical nightmare: a 24-year-old man endures 350 surgeries since childhood to remove growths that keep coming back in his throat and have spread to his lungs, threatening his life. Now doctors have found a way to help him by way of a scientific coup that holds promise for millions of cancer patients. The bizarre case is the first use in a patient of a new discovery: how to keep ordinary and cancerous cells alive indefinitely in the lab. The discovery allows doctors to grow "mini tumors" from each patient's cancer in a lab dish, then test various drugs or combinations on them to see which works best. It takes only a few cells from a biopsy and less than two weeks to do, with materials and methods common in most hospitals. Although the approach needs much more testing against many different types of cancer, researchers think it could offer a cheap, simple way to personalize treatment without having to analyze each patient's genes. "We see a lot of potential for it," said one study leader, Dr. Richard Schlegel, pathology chief at Georgetown Lombardi Comprehensive Cancer Center in Washington. "Almost everyone could do it easily." An independent expert agreed. For infections, it's routine to grow bacteria from a patient in lab dishes to see which antibiotics work best, Dr. George Q. Daley of Children's Hospital Boston and the Harvard Stem Cell Institute said in an email. "But this has never been possible with cancer [...]

2012-09-28T07:16:28-07:00September, 2012|Oral Cancer News|

A New Treatment’s Tantalizing Promise Brings Heartbreaking Ups and Downs

Source: The New York Times Beth McDaniel’s oncologist, a bear of a man, hugged her and twirled her around. “Holy cow, Beth!” Dr. John J. Gohmann exclaimed. For the first time since a rare cancer appeared eight years before, her lymph nodes had shrunk to a normal size, her skin was no longer bright red and inflamed, and the itchiness that plagued her had subsided. Mrs. McDaniel, the 69-year-old wife of a retired corporate executive, had gambled on the ultimate in personalized medicine, an approach known as whole genome sequencing, and it seemed to be paying off. Scientists had compared the entire genetic sequences of the tumor cells invading her body with those in her healthy cells, searching for mutated tumor genes that could be thwarted by drugs approved for other cancers or even other diseases. That had led them to give her an expensive drug approved just a month earlier for melanoma patients. It had never been given to anyone with a blood cell cancer like hers. In theory, the drug should have killed her. Instead, it seemed to have halted or even reversed her cancer. But would it last? And what would it mean if it did not? In the end, Mrs. McDaniel’s journey to the edge of genetics research turned out to be a decidedly mixed experience. It was hard — much harder than anyone in her family had imagined — to get the sequencing and analysis done. It was breathtaking to see the results, which indicated [...]

2012-07-09T09:31:57-07:00July, 2012|Oral Cancer News|

Queensland researchers make cancer treatment breakthrough

Source: HealthCanal.com The culmination of 10 years of collaborative research between scientists from the Queensland Institute of Medical Research (QIMR) and The University of Hong Kong (HKU) Li Ka Shing Faculty of Medicine has led to a significant breakthrough in the treatment of nasopharyngeal carcinoma (NPC), an aggressive throat cancer with a high prevalence in South-East Asia. NPC is associated with Epstein-Barr virus infection in a manner similar to the association of hepatitis B virus and liver cancer. By using immunotherapy, the human body’s own immune system was used to successfully fight the disease. Professor Rajiv Khanna who heads the Australian Centre for Vaccine Development at QIMR said by enhancing the immune cells of NPC patients they have doubled the survival time of terminally ill patients. “The presence of EBV in the cancer cells gives the body’s immune system a definite target to help battle the NPC, resulting in few side-effects,” Professor Khanna said. “Patients who participated in the trial were in the late stages of the cancer and quite unwell, so it was important to ensure the treatment was non-invasive, non toxic and did not damage healthy cells. “By offering such targeted treatment, we were able to increase the expected time of patient survival from 200 to over 500 days, which is an extremely positive result. “We believe that if we offer this treatment in the earlier stages of NPC, accompanied with chemotherapy and radiation, we can further enhance survival rates.” Twenty four NPC patients were recruited at the [...]

2012-02-01T17:06:54-07:00February, 2012|Oral Cancer News|

Grape seed extract kills head and neck cancer cells, leaves healthy cells unharmed

Source: Colorado Cancer Blog Nearly 12,000 people will die of head and neck cancer in the United States this year and worldwide cases will exceed half a million. A study published this week in the journal Carcinogenesis shows that in both cell lines and mouse models, grape seed extract (GSE) kills head and neck squamous cell carcinoma cells, while leaving healthy cells unharmed. “It’s a rather dramatic effect,” says Rajesh Agarwal, PhD, investigator at the University of Colorado Cancer Center and professor at the Skaggs School of Pharmaceutical Sciences. It depends in large part, says Agarwal, on a healthy cell’s ability to wait out damage. “Cancer cells are fast-growing cells,” Agarwal says. “Not only that, but they are necessarily fast growing. When conditions exist in which they can’t grow, they die.” Grape seed extract creates these conditions that are unfavorable to growth. Specifically, the paper shows that grape seed extract both damages cancer cells’ DNA (via increased reactive oxygen species) and stops the pathways that allow repair (as seen by decreased levels of the DNA repair molecules Brca1 and Rad51 and DNA repair foci). “Yet we saw absolutely no toxicity to the mice, themselves,” Agarwal says. Grape seed extract kills head and neck squamous cell carcinoma cells while leaving healthy cells unharmed (image courtesy of Flickr user Anders Ljungberg) Again, the grape seed extract killed the cancer cells but not the healthy cells. “I think the whole point is that cancer cells have a lot of defective pathways and they [...]

2012-01-27T11:17:39-07:00January, 2012|Oral Cancer News|

Cancer drug resistance strategy uncovered

Source: Cancer Research UK Author: Staff   Friday 9 September 2011- US scientists have identified a way in which cancer cells can become resistant to the cancer drug cetuximab (Erbitux), and suggest that treatments that are already available might be able to overcome this resistance. Researchers from the Dana-Farber Cancer Institute in Boston, US, have been studying why some patients only experience short-term benefits with cetuximab, or none at all. Cetuximab is an antibody that interferes with cancer cell growth. It can be given in combination with chemotherapy to patients with bowel cancer or head and neck cancer. Until now, scientists didn't know why some cancers failed to respond to the drug, or initially responded but then became resistant. The new study, published in Science Translational Medicine, found that in some of the drug-resistant cells, a protein known as ErbB2 (also known as HER2/neu) was sending 'grow' signals. These were bypassing the 'stop growing' signals caused by the drug. Pasi Janne, the study's co-senior author, said: "ErbB2 activates a critical signalling pathway that is not normally blocked by cetuximab, and in this way subverts cetuximab's function. "Because ErbB2 isn't affected by cetuximab, this is an easy way for cancers to become resistant to the drug." The researchers suggest that combining cetuximab with already available ErbB2 inhibitors such as trastuzumab (Herceptin) could produce an effective therapy to tackle cancers that previously showed resistance to cetuximab. Henry Scowcroft, science information manager at Cancer Research UK, said: "Unfortunately, patients's tumours can become resistant to treatment, and understanding why this happens is a [...]

2011-09-09T12:20:44-07:00September, 2011|Oral Cancer News|

Immunity Drugs Used to Fight Cancer

Source: The Wall Street Journal Scientists are scrambling to develop medications that fight cancer by spurring the body's immune system, a form of treatment that some cancer specialists believe may hold the key to keeping a patient permanently disease-free. The new efforts come in the wake of recent Food and Drug Administration approvals of Dendreon Corp.'s Provenge, an immunotherapy drug used to treat prostate cancer, and Bristol-Myers Squibb Co.'s Yervoy, for melanoma. Other immunotherapy drugs are being developed for a number of other cancers, including lung, brain and kidney cancers. Unlike most traditional therapies that attack a cancer directly, immunotherapy uses the body's own internal defenses to ward off the disease, with the ultimate hope of building up a long-term resistance to the cancer. "If we are ever going to use the word 'cure', the immune system is going to have to come into play," says Stephen Hodi, director of the melanoma center at Dana-Farber Cancer Institute in Boston. One of the ways that cancer survives and ultimately spreads through the body is by exploiting a function in all cells that prevents the immune system from killing them. Researchers have found that cancer cells have multiple methods of avoiding detection and suppressing the immune system's response. "Why would cancer devote so much energy to avoid the immune system if the immune system didn't have the potential to reject the cancer?" says Robert Vonderheide from the Abramson Cancer Center of the University of Pennsylvania. There are big hurdles to advancing the [...]

Targeting Cancer Treatment

Source: Medical News Today Cancer treatment is depending more and more today on specific factors of a patient's tumor, including gene mutations, or proteins that are commonly typical of certain cancer cells, rather than focusing on where in the body the cancer started. Before, treatment was based on finding where in the body the cancer originated, such as the breast or lung. Targeted therapy is all about the cancer's genes, tissue environment that contributes the tumor's growth and survival, and its proteins. Nowadays, cancer therapy is designed to interfere with a signal that tells the cancer cells not to die or tells it to divide, while before, chemotherapies had the goal of interfering with cancer cells as division was already underway, when the cells were dividing into new ones. The human body is made of various types of cells, including skin cells, brain cells, or blood cells. Each one has a specific function. Cancer occurs when healthy cells change and start growing out of control; they eventually form a tumor - a mass. A benign tumor is noncancerous, whereas a malignant one is cancerous, it can spread to other parts of the body. Cancer cells either divide too quickly or do not die when they should do Specific genetic mutations within a cell change the way it behaves. When the genes that control cell division mutate (change), they can multiply too quickly; the cell has become cancerous. Cells are genetically programmed to die, when the specific genes that tell the [...]

Sensitization of Head and Neck Cancer to Cisplatin Through the Use of a Novel Curcumin Analog

Source: EthiconEndo-Surgery.com Objective To determine whether a novel small molecule inhibitor derived from curcumin (FLLL32) that targets signal transducer and activator of transcription (STAT) 3 would induce cytotoxic effects in STAT3-dependent head and neck squamous cell cancer (HNSCC) cells and would sensitize tumors to cisplatin. Design Basic science. Two HNSCC cell lines, UM-SCC-29 and UM-SCC-74B, were characterized for cisplatin [cis-diammineplatinum(II) dichloride] sensitivity. Baseline expression of STAT3 and other apoptosis proteins was determined. The FLLL32 50% inhibitory concentration (IC50) dose was determined for each cell line, and the effect of FLLL32 treatment on the expression of phosphorylated STAT3 and other key proteins was elucidated. The antitumor efficacy of cisplatin, FLLL32, and combination treatment was measured. The proportion of apoptotic cells after cisplatin, FLLL32, or combination therapy was determined. Results The UM-SCC-29 cell line is cisplatin resistant, and the UM-SCC-74B cell line is cisplatin sensitive. Both cell lines express STAT3, phosphorylated STAT3 (pSTAT3), and key apoptotic proteins. FLLL32 downregulates the active form of STAT3, pSTAT3, in HNSCC cells and induces a potent antitumor effect. FLLL32, alone or with cisplatin, increases the proportion of apoptotic cells. FLLL32 sensitized cisplatin-resistant cancer cells, achieving an equivalent tumor kill with a 4-fold lower dose of cisplatin. Conclusions FLLL32 monotherapy induces a potent antitumor effect and sensitizes cancer cells to cisplatin, permitting an equivalent or improved antitumor effect at lower doses of cisplatin. Our results suggest that FLLL32 acts by inhibiting STAT3 phosphorylation, reduced survival signaling, increased susceptibility to apoptosis, and sensitization to cisplatin.      

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