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Facilitating Collaborations to Develop Combination Investigational Cancer Therapies Workshop Summary (2012) / Chapter Skim
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2 Why Combinations and Collaborations Are Necessary
Pages 3-10

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From page 3...
... Dr. Rachel Sherman, associate director for Medical Policy at the 3
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From page 4...
... , and a kinase called MET.2 In some cases, when these receptors are blocked with targeted therapies, tumor cells die and patients go into remission. Two major downstream signaling pathways emanate from these receptor tyrosine kinases -- the PI3K (phosphatidylinositol 3-kinase)
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From page 5...
... Two downstream signaling pathways of EGFR, the PI3K and MAPK pathways, can foster tumor growth by inhibiting cell death and promoting cell division. Thus, targeted therapies blocking receptor tyrosine kinases can block the downstream effects of these signaling pathways.
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From page 6...
... These bypasses activate the same key downstream tumor growthpromoting signaling pathways so that the tumor no longer needs the kinase the drug inhibits in order to grow. Research suggests that most cancers have multiple drivers -- multiple inputs into the PI3K-AKT and MAPK pathways that can serve as bypasses, according to Dr.
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From page 7...
... T cells or tumor infiltrating lymphocytes are removed from a cancer patient and activated and expanded. These activated T cells and tumor infiltrating lymphocytes are then returned to the patient after patient treatment withimage, text replaced and now editable FIGURE 2, fixed chemotherapy, and in some cases radiotherapy, and/or hematopoietic stem cell transplantation.
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From page 8...
... Another reason combination cancer therapies are needed is because of the heterogeneity of the cancer cells within individual patients, particularly in advanced tumors, in which the genetic instability of tumor cells fosters the emergence of multiple metastatic clones, each with a different genetic profile and varying sensitivity to specific treatments.
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From page 9...
... As Dr. David Stern, professor of pathology at Yale Medical School and associate director of the Shared Resources for the Yale Comprehen sive Cancer Center, summarized, "There are rapid routes through genetic and epigenetic plasticity, through on-target and bypass mutations, and through tumor cell population heterogeneity.
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Key Terms

  • cancer therapies
  • targeted therapies
  • tumor growth
  • tumor cells
  • combination cancer

  • cancer cells
  • receptor tyrosine
  • epidermal growth
  • factor receptor
  • tumor cell

  • tumor infiltrating
  • cancer center
  • cell division
  • signaling pathways
  • tyrosine kinases

  • infiltrating lymphocytes
  • foster tumor
  • cancer patients
  • tumor vaccine
  • promoting cell

  • inhibiting cell
  • normal cell
  • cell death
  • mapk kinase
  • tyrosine kinase

  • protein kinase
  • combination therapy
  • activated protein
  • vaccine combined
  • mammalian target


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