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MontréalDetailed Forecast Subscribe Subscriber Services ePaper canada. Photograph by: Alex Brandon , THE ASSOCIATED PRESSMONT­REAL — If Jon Coop­er didn’t exist, John Grish­am would have to in­vent him. Maybe he did. The for­mer law­yer has an easy man­ner, a fresh face, the abil­ity to talk with ease and pur­pose and a lit­tle good hu­mour. His Tampa Bay Light­ning are down 2-0 to the Mont­real Cana­diens in their first-round play­off ser­ies, with Game 3 Sun­day night in Mont­real. And the first-year NHL head coach is treat­ing it like a pleas­ant day in court, with a jury that can yet be swayed. “Every­one thinks we’re sup­pos­ed to lose,” said Coop­er after Tampa’s mor­ning skate. “Now I’m hear­ing done, be on the golf course by Wed­nes­day, I’ve heard it all. “But at some point they’re go­ing to have to do that in front of their fans, try and knock us out. I’m sure they’ve never had a 2-0 lead on the road and come back and blown it. Mont­real did just that in 2011 against Bos­ton, of course, and against Carolina in 2006. It was a love­ly dig, breez­i­ly de­liv­ered, with a bit of a wink. This wasn’t Raptors gen­er­al man­ager Masai Ujiri tell­ing an ador­ing crowd in To­ron­to, “F--- Brook­lyn,” be­fore Game 1 of their play­off ser­ies. But it was a coach who wasn’t afraid to be a lit­tle play­ful, which hock­ey could use more of. “If you real­ly look at the whole sea­son of what’s gone on here, I don’t think there’s one per­son in this room if they were picking who would make the play­offs this year in our div­ision was picking the Tampa Bay Light­ning to go any­where,” said Coop­er, a 46-year-old, who was born in Prince George, B.C., and played some high school hock­ey in Sas­katch­ewan. “We were like a hot pick for num­ber six, maybe a lit­tle bit num­ber sev­en in our div­ision. Those guys in there ended up com­ing se­cond. Then we get to the play­offs and every­body picked — I think we had 40 poll­sters we went through, and I think 35 of the 40 picked the Mont­real Cana­diens to beat us. So it doesn’t mat­ter how well we play, we were still not picked to do any­thing. “I’m sure in­jur­ies prob­ably helped struc­ture why people chose us to not win the ser­ies. We get home ice and don’t de­liv­er the way clear­ly we want­ed to. Coop­er is a great ex­plain­er, and it’s one of his strengths as a coach. He got here by coach­ing kids while he was practicing law in Lan­sing, Mich. He even­tu­al­ly quit law to coach in Tex­ar­kana, Texas, and worked his way to the NHL. Tampa sur­vived Ste­ven Stamkos’s bro­ken leg and Martin St. Louis’s thun­der­ous mood to post a 101-point sea­son, and Coop­er has been their steady man at the helm, with rook­ies every­where and con­stant tur­bu­lence. The in­jur­ies have con­tinued, with starting goal­tend­er Ben Bish­op and super-rook­ie Ondrej Palat hurt. Palat, in­jured in Game 1, was a game-time de­ci­sion for Game 3. When Mont­real counter­part Mi­chel Therrien speaks, you can al­most see him forming the sen­ten­ces in his head, and eras­ing any­thing that could be too in­ter­est­ing, in either lan­guage. He is under pres­sure be­cause he is Mont­real’s head coach. Some­times he lets some­thing slip — like Sun­day, when he told re­por­ters, “We know where Palat is hurt. We have to play phys­ic­al against him, and take away his time and space.” It wasn’t quite mena­cing, but Therrien’s been a bully for a long time. Coop­er, mean­while, is still at ease, and pretty hon­est for both a law­yer and a hock­ey coach. He was pressed, a lit­tle later, on wheth­er the pres­sure was real­ly on Mont­real. He smiled.“Well, there’s only pres­sure be­cause two games doesn’t win you a ser­ies,” Coop­er said. “But let’s be a real­ist here. They’re up two games to zero. I would like to be up two games to zero. I think in that situ­a­tion, they’re in a bet­ter spot than we are. I’d rath­er be up 2-0 than down 2-0.”He may be booed Sun­day night, but it’s not like Coop­er doesn’t like Mont­real, for the re­cord. It’s all an op­por­tun­ity.“I’ll tell you one thing about be­ing in Mont­real, and I think I said this in Tampa, as a fan and as a coach in the league, there’s some­thing about com­ing to Mont­real and be­ing in this arena — from the pres­en­ta­tion be­fore the game to when you’re on the ice to the atmos­phere, they hit a home run,” Coop­er said.“I’m sure it’s a treas­ure to play here be­cause the fans are ex­treme­ly pas­sion­ate: they cheer, they have chants, they under­stand the game, and as a vis­itor it’s real­ly cool to be a part of that.“I’ve real­ly enjoyed it. We played an Amer­ican League game here dur­ing the lock­out and there was 18,000 fans here and it was just a ton of fun. I’ve been for­tun­ate to play a few regu­lar-sea­son games here and we’ve just real­ly have enjoyed it. I per­son­al­ly have real­ly enjoyed the atmos­phere. You try to sit here and say, `Is this a hos­tile en­viron­ment?’ I’m sure it is, but I don’t like to look at it that way.“I like to look at it like it’s a great hock­ey en­viron­ment and em­brace this be­cause there’s a lot of sto­ried hist­ory that’s been in this build­ing and we can ac­tual­ly be a part of this hist­ory. We are a part of this hist­ory. Now we can be a part of hist­ory that’s real­ly not talked about so much, or we can be a part of hist­ory that’s real­ly talked about. And let’s have fun with that. « Previous 1 2 View as one page Next »© Copyright (c) Postmedia Network Inc. 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ygalindo@ucsd. IMAGE: Some lung cancer cells become resistant to drugs. Researchers identified an existing drug that reverses stem cell-like properties of tumors, resensitizing them to drug. Click here for more information. Most drugs used to treat lung, breast and pancreatic cancers also promote drug-resistance and ultimately spur tumor growth. Researchers at the University of California, San Diego School of Medicine have discovered a molecule, or biomarker, called CD61 on the surface of drug-resistant tumors that appears responsible for inducing tumor metastasis by enhancing the stem cell-like properties of cancer cells. The findings, published in the April 20, 2014 online issue of Nature Cell Biology, may point to new therapeutic opportunities for reversing drug resistance in a range of cancers, including those in the lung, pancreas and breast. "There are a number of drugs that patients respond to during their initial cancer treatment, but relapse occurs when cancer cells become drug-resistant," said David Cheresh, PhD, Distinguished Professor of Pathology and UC San Diego Moores Cancer Center associate director for Innovation and Industry Alliances. IMAGE: When lung cancer cells become drug resistant, tumor cells return as shown in brown. Click here for more information. Cheresh and colleagues investigated how tumor cells become resistant to drugs like erlotinib or lapatinib, known as receptor tyrosine kinase inhibitors and commonly used in standard cancer therapies. They found that as drug resistance occurs, tumor cells acquire stem cell-like properties that give them the capacity to survive throughout the body and essentially ignore the drugs. Specifically, the scientists delineated the molecular pathway that facilitates both cancer stemness and drug resistance, and were able to identify existing drugs that exploit this pathway. These drugs not only reverse stem cell-like properties of tumors, but also appear to re-sensitize tumors to drugs that the cancer cells had developed resistance to. "The good news is that we've uncovered a previously undefined pathway that the tumor cells use to transform into cancer stem cells and that enable tumors to become resistant to commonly used cancer drugs," said Cheresh. IMAGE: Researchers identified an existing drug, bortezomib, that reverses stem cell-like properties of tumors, resensitizing them to drugs as shown in this photo of lung cancer cells. Click here for more information. Based on these findings, Hatim Husain, MD, an assistant professor who treats lung and brain cancer patients at Moores Cancer Center, has designed a clinical trial to attack this pathway in patients whose tumors are drug-resistant. The trial will be open to patients with lung cancer who have experienced cancer progression and drug resistance to erlotinib. It is expected to begin in the next year. "Resistance builds to targeted therapies against cancer, and we have furthered our understanding of the mechanisms by which that happens," said Husain. "Based on these research findings we now better understand how to exploit the 'Achilles heel' of these drug-resistant tumors. Treatments will evolve into combinational therapies where one may keep the disease under control and delay resistance mechanisms from occurring for extended periods of time. Although the trial is expected to begin with patients who have already experienced drug resistance, Husain hopes to extend the study to reach patients in earlier stages to prevent initial resistance. Co-authors include Laetitia Seguin, Aleksandra Franovic, M. Fernanda Camargo, Jacqueline Lesperance, Kathryn C. Elliott, Mayra Yebra, Ainhoa Mielgo, Jay S. Desgrosellier, Sudarshan Anand and Sara M. Weis, UCSD Department of Pathology and UC San Diego Moores Cancer Center; Shumei Kato, UCSD Division of Hematology/Oncology; Andrew Lowy, UCSD Department of Surgery, Division of Surgical Oncology; Tina Cascone, Lixia Diao, Jing Wang, Ignacio I. Wistuba and John V. Heymach, University of Texas, MD Anderson Cancer Center; and Scott M. Lippman, UC San Diego Moores Cancer Center. Funding for this research came, in part, from National Institutes of Health grants CA45726, CA168692, HL57900, R37-50286 and CA155620, National Cancer Institute grant T32CA121938, the Association pour la Recherche contre le Cancer ARC and La Fondation Philippe. AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system. Copyright ©2014 by AAAS, the science society. 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