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A recent discovery by stem cell scientists at Cedars-Sinai may help make cancer treatment more efficient and shorten the time it takes for people to recover from radiation and chemotherapy.
Published in the journal Nature Communications, the study by Dr. John Chute and his team (and co-funded by CIRM) revealed a mechanism through which the blood vessels in the bone marrow respond to injury, such as from chemotherapy or radiation.
Each year, about 650,000 cancer patients receive chemotherapy in an outpatient oncology clinic in the United States.
When people receive radiation or chemotherapy as part of their cancer treatment, their blood counts plummet. It typically takes several weeks for these counts to return to normal levels. During this period patients are at risk for developing infections that may lead to hospitalization, disruptions in chemotherapy schedules, and even death.
Chute and his colleagues found that when mice receive radiation treatment, the cells that line the inner walls of the blood vessels in the bone marrow produce a protein called semaphorin 3A. This protein tells another protein, called neuropilin 1, to kill damaged blood vessels in the bone marrow.
When the investigators blocked the ability of these blood vessel cells to produce neuropilin 1 or semaphorin 3A, or injected an antibody that blocks semaphorin 3A communication with neuropilin 1, the veins and arteries in the bone marrow regenerated faster following irradiation. In addition, blood counts increased dramatically after one week.
“We’ve discovered a mechanism that appears to control how blood vessels regenerate following injury,” said Chute, senior author of the paper. “Inhibiting this mechanism causes rapid recovery of the blood vessels and blood cells in bone marrow following chemotherapy or irradiation.”
In principle, Chute said, targeting this mechanism could allow patients to recover following chemotherapy in one to two weeks, instead of three or four weeks as currently experienced.
Christina M. Termini, a post-doctoral scientist at the David Geffen School of Medicine at UCLA, was the first author of this study. Read the source press release here.
The Stem Cellar 
Cancer patients undergoing radiation and chemotherapy are depleted of hematopoietic stem cells and damage most of the vascular niche of BM. Current investigation in mice showed that blocking the interaction between Neutropilin 1(NRP1)and Semaphorin 3A(SEMA3A) accelerates BM vascular regeneration and concordantly drives hematopoitic reconstitution in irradiated mice. The therapeutic of treatment may substantially improve health and efficiency of radiation and chemotherapy in cancer patients.
However, NRP1 has been implicated as a co-receptor for SMA3A. Both NRP1 and SMA3A are highly expressed in a wide spectrum of tumors and influence the progression and vascularization of tumors. NRP1 expression is elevated in a number of patients tumor samples, including brain, prostate, breast, colon and lung cancers. In addition, evidence proved that, NRP1 levels are positively correlated to tumor metastatic and invasiveveness. Previous finding suggested that NRP1 has both anti- and promigratory characteristic in different tumor types. For instance, NRP1 can downregulate B16(F10) melanoma cells migration. Silencing of NRP1 increased overall mobility and morphology changes of tumors. Tumors are heterogeneous and instability in genotype and phenotype. Both radiation and chemotherapy approaches do not completely eradicated the tumor in cancer patients. Thus, a small proportion of tumors escape from those treatments may develop resistance and becoming more aggressive phenotype. If NRP1 is a targeted entity of treatment, the nature of tumors to evade the new treatment may cause tumors to transform into more metastatic phenotype. This may further downregulate the efficiency of both radiation and chemotherapy in cancer patients.