The research team confirmed those results by testing the four compounds at a low dose in mice injected
with ovarian cancer cells.
This research was done
with ovarian cancer cells.
They then tested the circuit in mice implanted
with ovarian cancer cells, and demonstrated that it could trigger T cells to seek out and kill the cancer cells without harming other cells around them.
Their theory was first confirmed
with ovarian cancer cell lines and then the Peter / Lengyel team tested HGMA2 protein levels in tumor samples from 100 patients with ovarian cancer.
Not exact matches
Mutations in these genes have been associated
with one of the deadliest types of
ovarian cancer, called clear
cell carcinoma.
Based on results of the current study described in a report online June 18 in the journal
Cancer Cell, Johns Hopkins researchers say they are planning a phase I clinical trial to test the paclitaxel - fostamatinib combination therapy in patients with recurrent advanced ovarian c
Cancer Cell, Johns Hopkins researchers say they are planning a phase I clinical trial to test the paclitaxel - fostamatinib combination therapy in patients
with recurrent advanced
ovarian cancercancer.
Working in
cell cultures and mice, researchers at Johns Hopkins have found that an experimental drug called fostamatinib combined
with the chemotherapy drug paclitaxel may overcome
ovarian cancer cells» resistance to paclitaxel.
Shih, Wang and their colleagues tested fostamatinib's power to reduce tumor size in mice implanted
with human
ovarian cancer cells that were resistant to paclitaxel.
The research shows that ONA reduces the progression of malignant
ovarian cancer tumors by interfering
with the pro-tumor function of myeloid
cells.
«For this reason, we decided to combine vitamin C
with a PARP inhibitor, a drug type known to cause
cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients
with ovarian cancer.»
«While the presence of lymphocytes in tumors is often associated
with better clinical outcomes, this research adds clarity on the diversity of T
cells within the tumor environment and their influence on
ovarian cancer outcomes,» says first author Kunle Odunsi, MD, PhD, FRCOG, FACOG, Deputy Director, M. Steven Piver Professor and Chair of Gynecologic Oncology, and Executive Director of the Center for Immunotherapy at Roswell Park.
The study evaluated 56 patients
with ovarian clear
cell adenocarcinoma (CCA), an aggressive form of
ovarian cancer that is more likely to be resistant to chemotherapy and to have a poorer prognosis than other forms of this disease.
The researchers treated 63
cancer cell lines (26 breast, 14 colorectal and 23
ovarian)
with low - dose 5 - azacitidine (AZA), an FDA - approved drug for myelodysplastic syndrome, that reverses epigenetic changes by stripping off the methyl group that silences the gene.
Analyzing white blood
cells from 934 patients and 1,698 healthy controls, they found BRCA1 methylation among 6.4 % of patients diagnosed
with ovarian cancer, contrasting 4.2 % among controls.
They systematically deleted genes for secreted effector proteins — molecules that the parasite injects into a host
cell to modulate the immune system during infection — and injected the altered parasites into mice
with aggressive
ovarian cancer.
In particular, it has been shown that
cells with other HR repair pathway defects, such as BRCA mutations frequently found in breast and
ovarian cancer, are sensitive to inhibition of the enzyme PARP, and the PARP inhibitor Olaparib has been approved for treatment of BRCA - mutated
ovarian cancers.
The research team
with international collaborators analysed more than 100 patient samples from
ovarian and other
cancer types to discover a distinct population of
cells found in some tumours.
A section of a tumor organoid grown from
cells derived from a patient
with high - grade serous
ovarian cancer (left) and a mini-tumor treated
with ReACp53, resulting in extensive
cancer cell death.
Analysing certain genes in these
cells enabled them to detect 33 per cent of
ovarian cancers and 81 per cent of endometrial
cancers in Pap test specimens collected from 627 women already diagnosed
with these diseases.
They found that tumor
cells with the mutant genes were particularly sensitive to a drug, olaparib, recently approved for the treatment of hereditary
ovarian cancer.
Ongoing Phase 1b / 2 clinical trials combine entinostat
with KEYTRUDA ® from Merck & Co., Inc. for non-small
cell lung
cancer, melanoma and colorectal
cancer;
with TECENTRIQ ® from Genentech, Inc. for triple negative breast
cancer; and
with BAVENCIO ® from Pfizer Inc. and Merck KGaA, Darmstadt, Germany, for
ovarian cancer.
Next they treated the experimental tumor
cells with MIR506 to determine if it would behave in the same way it had
with ovarian and other
cancers.
In the proposed project, Dr. Lampi Hermanson will produce NK
cells from stem
cells, inserting a chimeric antigen receptor (CAR)
with the capacity to recognize mesothelin
cells, which is expressed in 70 % of
ovarian cancer patients.
The earliest and one of the most striking came from observations that the presence of infiltrating T
cells (called «tumor - infiltrating lymphocytes,» or TILs) in
ovarian tumors is positively and strongly associated
with improved survival of patients
with ovarian cancer [1].
Several phase I and II trials of adoptive T
cell transfer techniques are currently under way for patients
with ovarian cancer, including:
Tanyi said he is eager to explore whether the dendritic -
cell vaccine might also be used as a first - line treatment for women who are newly diagnosed
with ovarian cancer.
[2] Sato E, Olson SH, Ahn J, Bundy B, Nishikawa H, Qian F, Jungbluth AA, Frosina D, Gnjatic S, Ambrosone C, Kepner J, Odunsi T, Ritter G, Lele S, Chen YT, Ohtani H, Old LJ, Odunsi K. Intraepithelial CD8 + tumor - infiltrating lymphocytes and a high CD8 + / regulatory T
cell ratio are associated
with favorable prognosis in
ovarian cancer.
NK
cells are a key part of the innate immune system
with the ability to recognize and kill diverse types of tumor
cells, including
ovarian cancer.
The book introduces the incessant menstruation hypothesis, which may allow physicians to better understand and explain to patients why many serous
ovarian cancers may actually be originating from the fimbriated end of the fallopian tube and why endometrioid and clear
cell cancers may arise in association
with endometriosis.
Interference
with actin dynamics is superior to disturbance of microtubule function in the inhibition of human
ovarian cancer cell motility.
Liron Bar - Peled and Lynne Chantranupong, who are both authors of the Science article and graduate students in Sabatini's lab, found that GATOR1 itself is mutated in several
cancers, including glioblastomas and
ovarian cancers, and that
cancer cells with these mutations are also highly sensitive to treatment
with rapamycin.
In this video Dr. Odunsi discusses a new study that found that higher T -
cell diversity in
ovarian cancer is associated
with poor overall survival.
December 17, 2013
Cancer genetics pioneer Janet Rowley, 1925 - 2013 A pioneer in connecting the development of cancer with genetic abnormalities, Janet D. Rowley, MD, the Blum - Riese Distinguished Service Professor of Medicine, Molecular Genetics & Cell Biology and Human Genetics at the University of Chicago, died from complications of ovarian cancer on December, 17, 2013, at her
Cancer genetics pioneer Janet Rowley, 1925 - 2013 A pioneer in connecting the development of
cancer with genetic abnormalities, Janet D. Rowley, MD, the Blum - Riese Distinguished Service Professor of Medicine, Molecular Genetics & Cell Biology and Human Genetics at the University of Chicago, died from complications of ovarian cancer on December, 17, 2013, at her
cancer with genetic abnormalities, Janet D. Rowley, MD, the Blum - Riese Distinguished Service Professor of Medicine, Molecular Genetics &
Cell Biology and Human Genetics at the University of Chicago, died from complications of
ovarian cancer on December, 17, 2013, at her
cancer on December, 17, 2013, at her home.
Correlative nanomechanical profiling
with super-resolution F - actin imaging reveals novel insights into mechanisms of cisplatin resistance in
ovarian cancer cells Sharma S, Santiskulvong C, Bentolila, L A, Rao J, Dorigo O and Gimzewski J K 2012 Nanomedicine: Nanotechnology, Biology, and Medicine 8 757 - 766
A phase II study of allogeneic natural killer
cell therapy to treat patients
with recurrent
ovarian and breast
cancer.
Dr. Matsuzaki has accumulated extensive expertise in T -
cell biology and mechanisms of immune suppression in periphery and tumor microenvironments in patients
with ovarian cancer.
Odunsi K, Qian F, Matsuzaki J, Mhawech - Fauceglia P, Andrews C, Hoffman EW, Pan L. Ritter G, Villella J, Thomas B, Rodabaugh K, Lele S, Shrikant P, Old LJ, Gnjatic S. (2007) Vaccination
with an NY - ESO - 1 peptide of HLA class I / II specificities induces integrated humoral and T
cell responses in
ovarian cancer.
The approach developed by the MGH team starts
with the engineered protein, which in this case fuses an antibody fragment targeting a protein called mesothelin — expressed on the surface of such tumors as mesothelioma,
ovarian cancer and pancreatic
cancer — to a protein from the tuberculosis bacteria that stimulates the activity of dendritic and other immune
cells.
«Visualizing how
cancer cells interact
with a tumor microenvironment that accurately reflects the complex biology of
ovarian cancer should help us understand the mechanisms underlying metastatic progression as well as identify new therapeutics that can inhibit this process,» said clinical gynecologic oncologist Ernst Lengyel, MD, PhD, senior author of the study and a professor of obstetrics and gynecology at the University of Chicago.
Using state - of - the - art proteomics and associated computational methods, the Speicher laboratory is investigating protein changes associated
with ovarian cancer, melanoma, cardiac injury resulting from breast
cancer therapies, ectopic pregnancy, red
cell diseases, and other clinical disorders.
And the whole benefit that is when your blood sugar's not spiking like that, you're not over secreting insulin; when you're not over secreting insulin, you're not gonna develop insulin resistance and all of the effects of that may have
with ovarian cyst or
cancer cells or inflammation and our blood pressure.