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2012 | 10 | 1 | 10-24

Article title

Leczenie systemowe chorych na raka piersi z nadekspresją HER2. Część II

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EN
Systemic treatment of HER2-positive breast cancer. Part II

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Abstracts

EN
HER2-positive breast cancer is associated with an aggressive clinical course and poor prognosis. At present, these patients may be offered targeted therapies directed against a specific molecular target, i.e. HER2 receptor. Standard agents of this class include trastuzumab (monoclonal antibody) and lapatinib (small-molecule inhibitor of HER2- receptor-associated tyrosine kinase). As estimated, about 25% of breast tumors are HER2-positive, and these patients are candidates for trastuzumab therapy. A precondition for initiation of the treatment is confirmation of overexpression of HER2 protein or amplification of HER2 gene in tumor cells. Trastuzumab administered as adjuvant treatment improves recurrence-free survival by 7% and overall survival by 3%. On the other hand, the same drug combined with chemotherapy in patients with disseminated breast cancer increases objective response rate, improves progression-free survival and overall survival as compared with chemotherapy alone. As estimated, only about 50% of HER2-positive patients obtained a clinical benefit following trastuzumab-based palliative treatment. There are several theories explaining the phenomenon of primary and secondary resistance to antibody-treatment. Patients previously undergoing with anthracycline- and taxoid-based chemotherapy, who experience recurrence or progression after trastuzumab, may benefit from administration of lapatinib, a HER1/HER2-associated small-molecule tyrosine kinase inhibitor, combined with capecitabine. Studies of novel therapeutic strategies in patients with HER2-positive breast cancer are underway, testing both new anti-HER2 antibodies (T-DM1, pertuzumab) and other small-molecule tyrosine kinase inhibitors (neratinib).
PL
HER2-dodatni rak piersi charakteryzuje się bardziej agresywnym przebiegiem i gorszym rokowaniem. W chwili obecnej istnieje możliwość zastosowania u tych chorych terapii ukierunkowanych na cel molekularny, jakim jest receptor HER2. Standardowo stosowanymi lekami tej grupy są przeciwciało monoklonalne trastuzumab i drobnocząsteczkowy inhibitor kinazy tyrozynowej receptorów HER2 i HER1 – lapatynib. Szacuje się, że około 25% guzów piersi jest HER2-pozytywnych – u tych chorych należy rozważyć wdrożenie terapii trastuzumabem. Warunkiem koniecznym rozpoczęcia leczenia jest wykazanie nadekspresji białka HER2 lub amplifikacji genu HER2 w komórkach nowotworowych. Trastuzumab stosowany w ramach leczenia uzupełniającego zwiększa przeżycie wolne od nawrotu o 7%, a przeżycie całkowite o 3%. Z kolei lek stosowany w skojarzeniu z chemioterapią u chorych z rozsianym rakiem piersi zwiększa odsetek obiektywnych odpowiedzi, wydłuża czas przeżycia wolny od progresji oraz czas przeżycia całkowitego w porównaniu z samą chemioterapią. Szacuje się, że tylko połowa chorych HER2-pozytywnych odnosi korzyść kliniczną z terapii paliatywnej opartej na trastuzumabie. Istnieje kilka teorii tłumaczących zjawisko pierwotnej i wtórnej oporności na leczenie przeciwciałem. U chorych leczonych wcześniej chemioterapią opartą na antracyklinach i taksoidach, u których dochodzi do nawrotu lub progresji po leczeniu trastuzumabem, można zastosować drobnocząsteczkowy inhibitor kinaz tyrozynowych HER1/HER2 – lapatynib w skojarzeniu z kapecytabiną. Obecnie trwają badania nad nowymi strategiami terapeutycznymi u chorych z HER2-pozytywnym rakiem piersi. Są to zarówno nowe przeciwciała „anty-HER2” (T-DM1, pertuzumab), jak i kolejne drobnocząsteczkowe inhibitory kinaz tyrozynowych (neratynib).

Discipline

Year

Volume

10

Issue

1

Pages

10-24

Physical description

Contributors

  • Klinika Chemioterapii Nowotworów Katedry Onkologii Uniwersytetu Medycznego w Łodzi. Kierownik Kliniki: dr hab. n. med. Piotr Potemski, prof. UM Correspondence to: Szpital Specjalistyczny im. M. Kopernika w Łodzi, ul. Paderewskiego 4, 93-509 Łódź, tel.: 42 689 54 31, faks: 42 689 54 32

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article

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bwmeta1.element.psjd-d9aaf545-9795-49e2-adf4-3670f029cb85
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