Roche recently announced encouraging preliminary combination data from a phase Ib study on cancer immunotherapy candidate MPDL3280A (anti-PDL1) in combination with Avastin.
The results from the study showed that the combination of MPDL3280A and Avastin was well tolerated and shrank tumors in approximately 40% of patients with previously untreated metastatic renal cell carcinoma (mRCC).
OCTOBER 14, 2014
Bristol-Myers Squibb, Pharmacyclics and Janssen are teaming up to test the power of a new potential cancer immunotherapy in treating patients with non-Hodgkin lymphoma.
The drugmakers have signed a clinical trials agreement under which they will assess B-MS’ investigational PD-1 immune checkpoint inhibitor Opdivo (nivolumab) in combination with Imbruvica (ibrutinib), an oral Bruton's tyrosine kinase inhibitor co-developed and co-marketed by Pharmacyclics and Janssen.
New immune treatments don’t just “boost” or “activate” the immune system. It’s not so simple. Our immune systems are highly complex, involving dozens of cells and chemicals that work in concert to first recognize the target (such as an infectious agent) and then attack and eliminate it. Once the target has been eliminated, the immune attack must stop or it would cause injury to the body. Think of an infection you may have had, on your skin or internally, such as a urinary tract or respiratory infection. You experience the symptoms of the infection, such as fever, malaise, burning urine or cough, and then as your immune system battles the infection successfully (often with the aid of antibiotics), you feel the healing of recovery. The attack is over and your immune system quiets down.
It is this process of “putting the brakes on” that the new immune therapies harness. The therapies target proteins on our immune cells: PD-1 and CTLA-4. Both PD-1 and CTLA-4 exist as antennae or receptors on the surfaces of immune cells to stop the immune attack once it has done its job. It turns out that cancer cells also employ PD-1 and CTLA-4 to prevent immune cells from recognizing them.
In 2011, ipilimumab (Yervoy), which blocks CTLA-4, was approved by the US Food and Drug Administration to treat metastatic melanoma. Recently, pembrolizumab (Keytruda), which blocks PD-1, was also approved to treat melanoma. Plus, drugs like Yervoy and Keytruda are being combined in some trials, perhaps to greater effect than when either drug is used alone.
Search: Genentech cozies up to Newlink in $1B+ cancer immunotherapy pact
By Marie Powers, Staff Writer
Newlink Genetics Corp., which has kept its head down and plowed forward in an approach reflective of its Ames, Iowa, setting, gained validation of those efforts in an exclusive global license with Genentech Inc., a unit Roche AG, potentially valued at more than $1 billion. The companies will develop NLG919, Newlink's indoleamine 2,3-dioxygenase (IDO) pathway inhibitor, and embark on a broader research collaboration to discover next-generation IDO/ tryptophan 2,3-dioxygenase (TDO) compounds.
IDO pathway inhibitors represent a class of immune checkpoint inhibitors akin to recently developed antibodies targeting CTLA-4, PD-1 and PD-L1, representing potential breakthrough approaches to cancer therapy. The IDO pathway regulates immune response by suppressing T-cell activation, which enables local tumor immune escape. Studies have shown that the IDO pathway is active in many cancers, both within tumor cells as a direct defense against T cell attack and also within antigen-presenting cells in tumor-draining lymph nodes, where the pathway promotes peripheral tolerance to tumor associated antigens (TAA). When hijacked by developing cancers in this manner, the IDO pathway may facilitate the survival, growth, invasion and metastasis of malignant cells whose expression of TAAs might otherwise be recognized and attacked by the immune system.
The next major catalyst for Newlink is the second interim readout from the phase III IMPRESS (Immunotherapy for Pancreatic Resectable Cancer Survival Study) data for hyperacute pancreas candidate, algenpantucel-L, expected in the next few months.
Search: Meet Unum, a new immunotherapy biotech with Fidelity, Atlas and Sanofi in its corner
October 21, 2014 | By Damian Garde
As the promise of harnessing the immune system to fight cancer grabs headlines around the industry, venture stalwarts Fidelity Biosciences and Atlas Venture have teamed up to launch Unum Therapeutics, a Cambridge, MA, startup with a hybrid approach to the field.
"We've created Unum to rapidly develop this universal cell therapy platform and to explore its potential in a number of different cancer types," Wilson said in a statement. "With our Series A funding from Fidelity Biosciences, Atlas Venture, and Sanofi-Genzyme BioVentures, we will drive our lead program into Phase I testing and aim to quickly validate the ACTR approach in the clinic."
Meanwhile, the promise of similar therapies has spurred billions in investment across the industry. Adaptimmune, at work on a TCR platform, raised $104 million in September, a few months removed from signing deal with GlaxoSmithKline ($GSK) worth up to $350 million. Juno, another private biotech, has raised more than $300 million in just over a year to support its CAR-T efforts, and Kite Pharma ($KITE) pulled off a $128 million IPO to fund R&D in the same field.
Only a week away for the NASDAQ noncompliance letter, then oncy announces their miniscule cash position a week or two later. oncy going down HARD.
Skeeta Bug Likes It.
Sentiment: Strong Sell
i remember fondly me telling d2fool that genieinthebottleman, matdum and the rest of the calgary cabal were frauds... in particular genie had d2fool wrapped around the fraudster scientist fingers and now genieisnotinthbottle genie has whooshed disappeared, him and his cabal of criminals on to the next mark
...hmmm with 100% certainty i link this collapse to the "deal" between ONCY and LPC..like i predicted the pressure on this stock is to the downside until say lets $0.10.. when an incompetent overcompensated CEO gives away the farm to some 3rd rate financier expect a price collapse. i guess all longs are praying for something positive but i have no idea what that may be
Same team my friend. I've always thought that. If d2 had 200k invested he would not have bashed ONCY all of these past 12 years. It's just not logical. Instead of vilifying the Big-Time clown he is trying to verify his team mate
On the bright side, the weather is fantastic here and all is good. How are you guys? All the critters doing well?
Ha ha ha, the notion of Brad and all of his little Brads taking a paycut is hillarious! After milking their retail investors for over $250,000,000 over the past 15 years, obviously, the Calgary-Keystone Cops know exactly what they are doing. The fact that after the last 2 months, the usual shills here STILL are defending him/them is just stupifying. Yeah, sure, they all loaded up at .41....
Anyone still long this trainwreck should just mail their cash into Kensington Crescent NW directly and cut the MMs out of the transaction. Bailey, IlliterateLunatic, Kenny, you are all painfully stupid to observe. You fools should have listened to the wisdom of Parcels.
Clin Chim Acta. 2014 Apr 20;431:211-20. doi: 10.1016/j.cca.2014.01.049. Epub 2014 Feb 15.
KRAS mutations: analytical considerations.
Herreros-Villanueva M1, Chen CC2, Yuan SS3, Liu TC4, Er TK5.
Colorectal cancer (CRC) is the third most common cancer and the second most common cause of cancer death globally. Significant improvements in survival have been made in patients with metastasis by new therapies. For example, Cetuximab and Panitumumab are monoclonal antibodies that inhibit the epidermal growth receptor (EGFR). KRAS mutations in codon 12 and 13 are the recognized biomarkers that are analyzed in clinics before the administration of anti-EGFR therapy. Genetic analyses have revealed that mutations in KRAS predict a lack of response to Panitumumab and Cetuximab in patients with metastatic CRC (mCRC). Notably, it is estimated that 35-45% of CRC patients harbor KRAS mutations. Therefore, KRAS mutation testing should be performed in all individuals with the advanced CRC in order to identify the patients who will not respond to the monoclonal EGFR antibody inhibitors.
"while i no nothing of LPC or the specifics of this deal,"
Would you put that on a piece of paper, put a bow on it and mail it to D2. And send me the bill. heeeeeeehe.
Sentiment: Strong Buy
share price of ONCY would move towards $1.00 and i was proven 100% correct...if the price floor on LPC2 is say $0.10 the price of ONCY will move continuously towards $0.10... understand this, while i no nothing of LPC or the specifics of this deal, IME firms like LPC risk $0 in these deals, they are structured in ways that EOD result in massive dilution (ps and the last person i would want calling the shots is BT he is so anti-retail shareholder it is alarming to me, he has as best i can tell a real disdain for retail shareholders)
Oncolytic reovirus preferentially induces apoptosis in KRAS mutant colorectal cancer cells, and synergizes with irinotecan.
Reovirus is a double stranded RNA virus, with an intrinsic preference for replication in KRAS mutant cells. As 45% of human colorectal cancers (CRC) harbor KRAS mutations, we sought to investigate its efficacy in KRAS mutant CRC cells, and examine its impact in combination with the topoisimerase-1 inhibitor, irinotecan. Reovirus efficacy was examined in the KRAS mutant HCT116, and the isogenic KRAS WT Hke3 cell line, and in the non-malignant rat intestinal epithelial cell line. Apoptosis was determined by flow cytometry and TUNEL staining. Combination treatment with reovirus and irintoecan was investigated in 15 CRC cell lines, including the HCT116 p21 isogenic cell lines. Reovirus preferentially induced apoptosis in KRAS mutant HCT116 cells compared to its isogenic KRAS WT derivative, and in KRAS mutant IEC cells. Reovirus showed a greater degree of caspase 3 activation with PARP 1 cleavage, and preferential inhibition of p21 protein expression in KRAS mutant cells. Reovirus synergistically induced growth inhibition when combined with irinotecan. This synergy was lost upon p21 gene knock out. Reovirus preferentially induces apoptosis in KRAS mutant colon cancer cells. Reovirus and irinotecan combination therapy is synergistic, p21 mediated, and represents a novel potential treatment for patients with CRC. PMID:24798549
Maitra, Radhashree; Seetharam, Raviraja; Tesfa, Lydia; Augustine, Titto A; Klampfer, Lidija; Coffey, Matthew C; Mariadason, John M; Goel, Sanjay
Search: Characterization of rare transforming KRAS mutations in sporadic colorectal cancer.
KRAS mutational status has been shown to be a predictive biomarker of resistance to anti-EGFR monoclonal antibody (mAb) therapy in patients with metastatic colorectal cancer. We report the spectrum of KRAS mutation in 1506 patients with colorectal cancer and the identification and characterization of rare insertion mutations within the functional domain of KRAS. KRAS mutations are found in 44.5% (670/1506) of the patients. Two cases are found to harbor double mutations involving both codons 12 and 13. The frequencies of KRAS mutations at its codons 12, 13, 61, and 146 are 75.1%, 19.3%, 2.5%, and 2.7%, respectively. The most abundant mutation of codon 12 is G12D, followed by G12V and G12C while G13D is the predominant mutation in codon 13. Mutations in other codons are rare. The KRAS mutation rate is significantly higher in women (48%, 296/617) than in men (42.1%, 374/889, P = 0.023). Tumors on the right colon have a higher frequency of KRAS mutations than those on the left (57.3% vs. 40.4%, P
mink. - you've averaged down to own beaucoup thousands of shares at no cost?. Sure you have. You're no smarter than you are honest. I don't remember a single time you suggested trading when the stock was up. Or trading at all. Now all of a sudden when we hit .$50 your gazillion shares are .$50 in the money. Yeah, right. What a pathetic joke.