A new approach to cancer treatment called immunotherapy could spare patients at least some of the grueling battery of chemotherapy treatments by retraining the body's own defenders--the cells of the immune system--to recognize and destroy tumors. Now researchers at Harvard University have developed a simple way to do this inside the body: a polymer implant attracts and trains immune-system cells to go after cancer.
The experimental approach has shown great success in animal studies, increasing the survival rate of mice with a deadly melanoma from 0 to 90 percent. The implant could also be used to treat diseases of the immune system such as arthritis and diabetes, and, potentially, to train other kinds of cells, including stem cells used to repair damage to the body.
It is a cancer of the cells which form the structure of the stomach and intestine, not a cancer of the linings of the organ itself (that would be a carcinoma).
Cancer immunology is the study of interactions between the immune system and cancer cells (also called tumors or malignancies). It is also a growing field of research that aims to discover innovative cancer immunotherapies to treat and retard progression of this disease. The immune response, including the recognition of cancer-specific antigens is of particular interest in this field as knowledge gained drives the development of new vaccines and antibody therapies. For instance in 2007, Ohtani published a paper finding tumour infiltrating lymphocytes to be quite significant in human colorectal cancer.[1] The host was given a better chance at survival if the cancer tissue showed infiltration of inflammatory cells, in particular lymphocytic reactions. The results yielded suggest some extent of anti-tumour immunity is present in colorectal cancers in humans.
Interleukin 2-mediated conversion of ovarian cancer-associated CD4+ regulatory T cells into proinflammatory interleukin 17-producing helper T cells.
Leveque L, Deknuydt F, Bioley G, Old LJ, Matsuzaki J, Odunsi K, Ayyoub M, Valmori D.
J Immunother. 2009 Feb-Mar;32(2):101-8.
PMID: 19238008
doi: 10.1097/CJI.0b013e318195b59e
Thus, although the impact of TH17 cells on the evolution of EOC remains to be established, our data suggest that local IL-2 treatment in ovarian cancer may result in the conversion of tumor-associated Treg into TH17 cells, relieve Treg-mediated suppression, and contribute to enhance antitumor immunity.
Inhibition of suppressor T lymphocytes (Ts) by cimetidine.
Sahasrabudhe DM, McCune CS, O'Donnell RW, Henshaw EC.
J Immunol. 1987 May 1;138(9):2760-3.
PMID: 2952721
Cyclophosphamide (CY) is the most extensively studied inhibitor of suppressor T lymphocyte (Ts) function. However, repeated administration of CY can abrogate sensitization. Therefore, we were interested in identifying noncytotoxic inhibitors of Ts function as adjuncts in the immunotherapy of Ts-inducing murine tumors. The effect of cimetidine (a histamine type 2 receptor antagonist) and diphenhydramine (a histamine type 1 receptor antagonist) on the Ts mediating tolerance to 2,4-dinitrofluorobenzene was studied. We report our data regarding the specific inhibition of Ts by cimetidine.
Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease.
Kidd P.
Altern Med Rev. 2003 Aug;8(3):223-46. Review.
PMID: 12946237
Th1 pathways typically produce activation
of cytotoxic T lymphocytes (Tc), NK cells,
macrophages, and monocytes, all of which can
attack cancer cells and generally defend against
tumors.55 IFN-gamma and other Th1 cytokines are
typically lower in advanced cancer patients, while
the Th2 marker IL-4 can be higher or unchanged
D structure of the virus, known as Seneca Valley Virus-001, reveals that it is unlike any other known member of the Picornaviridae viral family, and confirms its recent designation as a separate genus "Senecavirus." The new study reveals that the virus's outer protein shell looks like a craggy golf ball¬-one with uneven divets and raised spikes-and the RNA strand beneath it is arranged in a round mesh rather like a whiffleball. "It is not at all like other known picornaviruses that we are familiar with, including poliovirus and rhinoviruses, which cause the common cold," says the study's senior author, Associate Professor Vijay S. Reddy, Ph.D., of The Scripps Research Institute. "This crystal structure will now help us understand how Senecavirus works, and how we can take advantage of it."
The Senecavirus is a "new" virus, discovered several years ago by Neotropix Inc., a biotech company in Malvern, Pennsylvania. It was at first thought to be a laboratory contaminant, but researchers found it was a pathogen, now believed to originate from cows or pigs. Further investigation found that the virus was harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer.
Dietary omega-3 polyunsaturated fatty acids plus vitamin E restore immunodeficiency and prolong survival for severely ill patients with generalized malignancy: a randomized control trial.
Gogos CA, Ginopoulos P, Salsa B, Apostolidou E, Zoumbos NC, Kalfarentzos F.
Cancer. 1998 Jan 15;82(2):395-402.
PMID: 9445198
...has been the number one Google search term leading people to the blog this week - and that worries me.
As I wrote about a week ago, dichloroacetate, or DCA, is the molecule tested recently by a team at University of Alberta for its ability to slow the growth of human lung cancer in immunocompromised rats. Among DCA's action is the ability to prevent cancer cells from producing lactic acid via aerobic glycolysis, a process used by more than half (but not all) tumors. Scientists continue to debate whether this process is a cause of cancer, or just a byproduct of malignant cell transformation.
I am deeply concerned that desperate cancer patients may be trying to purchase dichloroacetate (DCA) and self-treat for cancer based on this highly-hyped single paper. To the credit of the researchers and their institution, who have set up a website to address the intense interest, they discourage such practice:
Cancer immunotherapies, including cancer vaccines, are novel investigational cancer therapies. In contrast to chemotherapy and radiotherapy regimens that are often associated with severe side effects, cancer immunotherapy stimulates the body's immune system and natural resistance to cancer, thus offering a gentler means of cancer treatment that is less damaging to the rest of the body. Surgery is generally (but not always) performed, prior to immunotherapy, to remove most of the tumor (Hanna MG, Jr. et al 2001; Jocham D et al 2004). Vaccination or immunotherapy prompts the immune system to kill residual cancer cells that persist after surgery and could result in the cancer recurring.
It was concluded that omega-3 fatty acid could inhibit the proliferation of pancreatic cancer cell line SW1990 cells and promote their apoptosis. The down-regulation of the cyclin E expression by omega-3 fatty acid might be one of the mechanisms for its anti-tumor effect on pancreatic cancer.
Modulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells.
Zhang W, Long Y, Zhang J, Wang C.
J Huazhong Univ Sci Technolog Med Sci. 2007 Oct;27(5):547-50.
PMID: 18060632
Derived from the cap and stem of the mushroom. The active constituent is thought to be a beta-glucan polysaccharide. The whole mushroom is used primarily as a dietary element, but extracts and supplements are sold as immune stimulants for patients with HIV or cancer. While no adverse effects have been reported, some studies reveal a hypoglycemic effect following administration of maitake extract (9) (12). Maitake was shown to enhance bone marrow colony formation, reduce doxorubicin toxicity in vitro (11), and to inhibit tumor metastasis
A recently published study in Nutrition and Cancer (60(5), 643-651) by researchers at Kansai Medical University in Osaka, Japan has shown that AHCC (Active Hexose Correlated Compound) enhances immune function by increasing the number of dendritic cells (DCs).
DCs are a key part of the immune system responsible for presenting foreign substances to other immune system cells.
The study was conducted in a double-blind randomized fashion where twenty-one healthy subjects received a placebo or AHCC at 3.0 g/day for 4 weeks. Blood samples were obtained and measured at baseline and at 4 weeks. The number of circulating types of DCs was measured which included CD 11c+ DCs (myeloid DC population; DC1) and CD11c- DCs (lymphoid DC population; DC2). Other parameters measured included mixed-leukocyte reaction (MLR), natural killer (NK) cell activity, the proliferative response of T lymphocytes toward mitogen (phytohemagglutinin [PHA]) and cytokine production of interleukin (IL)-2, IL-4, IL-6, IL-10, interferon gamma-gamma, and (alpha)-tumor necrosis factor.
Vitamin D and intervention trials in prostate cancer: from theory to therapy.
Schwartz GG.
Ann Epidemiol. 2009 Feb;19(2):96-102. Epub 2008 Jul 10.
PMID: 18619854
doi:10.1016/j.annepidem.2008.03.007
This suggests that whereas vitamin D (e.g., cholecalciferol) might prevent prostate cancer, existing prostate tumors likely would require treatment with 1,25(OH)(2)D and/or its analogs. The major obstacle to the use of 1,25(OH)(2)D in patients therapeutically is the risk of hypercalcemia. Several maneuvers to reduce this risk, including pulse dosing and the use of less calcemic 1,25(OH)(2)D analogs, have been explored in Phase I-III clinical trials. Once merely a promise, vitamin D-based therapies for prostate cancer may soon be medical practice.
A heat-stable extract of white button mushrooms (Agaricus bisporus) with potential chemopreventive and immunomodulating activities. Phytochemicals, such as polysaccharides and especially beta-D-glucans found in the white button mushroom extract, bind to and inhibit the activity of aromatase, an enzyme responsible for the conversion of androgens to estrogens and which is often upregulated in breast cancer cells. The consequent decrease in estrogen production may result in the suppression of estrogen-dependent cellular proliferation. In addition, this extract may promote dendritic cell (DC) maturation, increase interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production, and may enhance natural killer (NK) cell activity, thus amplifying both innate and T cell-mediated immune responses against cancer cells. Check for active clinical trials or closed clinical trials using this agent.
Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions.
Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ.
J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17.
PMID: 17704354
doi: 10.1124/jpet.107.128017
The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic "natural" over-the-counter medication.
In this video, Dr. Ramakant Deshpande explaining How does doctor decide Lung cancer treatment for different stages of Lung cancer.
Lung cancer and its adversities can be lethal, if remains undiagnosed or left untreated. A multidisciplinary approach can successfully eliminate the cancer from lungs and patient may resume normal life after recovery,
says Dr. Ramakant Dehspande, Chief of Thoracic Surgical Oncology, Asian Institute of Oncology.
Lung cancer
There are different sizes and stages of lung cancer, which are treated differently. Broadly, specialists categorize various types of lung cancer into two basic forms Non-small cell lung cancer and small cell lung cancer.
The staging of lung cancer helps in deciding the severity of the disease,
course of treatment, and chances of survival. Detection of cancer at an early stage increases the chances of successful treatment and full recovery of the patient. A small legion located in one area is known as the first stage; a little larger tumor is called stage 2; spread within the lungs is called stage 3, and if it spread to other parts then termed as stage 4.
Doctor Profile:
Dr. Ramakant Deshpande
MS; FICS; FAIS; DHA having experience of 31+ years and is a Chief of Thoracic Surgical Oncology, Asian Institute of Oncology.
- Padmashree award by the President of India in 2014
- Lifetime Achievement Award at the Indian National Critical Care Society Annual Meet at Jaipur 2014
- Lifetime Achievement Award by Zee Maaza TV in 2019
- Senior of Robotic surgery at the Asian Cancer Institute
- Established the Minimally Invasive method of Thoracoscopy
- President of the Indian Society of Oncology
- Director - Asian Cancer Institute
- Ex Tata Memorial Doctor
This video is under the "My Health My Right" Initiative of MedicoExperts - A Global Virtual Hospital.
For Inquiry Call or WhatsApp us at +919769516280
#lungcancertreatment #MyHealthMyRight #lungcancer #lungcancerstages #MedicoExperts #lungcancertreatmen
A comprehensive diagnostic and prognostic cancer (oncology) biomarker database with cancer companion diagnostics biomarker pathway maps, which contain protein-protein interactions networks of cancer drug efficacy/response/predictive biomarkers. This database contains discovery, pre-clinical and clinical cancer biomarkers that were identified or validated using patient samples. The biomarkers include blood based cancer biomarkers, tumor biomarkers, urinary cancer biomarkers, fecal cancer biomarkers, saliva cancer biomarkers, breath cancer biomarkers etc. Patient/sample details, experimental results/observations, biological and molecular functional analysis, biological process analysis, protein-protein interaction networks of each biomarker are included in this database.Link (preview is available): http://www.sciclips.com/sciclips/diagnostic-prognostic-cancer-biomarker-main.do