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Onkologinės ligos - 37

QUOTE(willow @ 2012 08 31, 18:13)
Oi, merginos, seniau maniau, kad sapnų išpranašavimas tik egzotiškas laisvalaikio praleidimas. Kai keletas sapnų išsipildė - pradėjau tikėti. Aš ir savąją ligą išsapnavau: įtraukė mane purvino vandens sūkurys ir skęsti pradejau... Kažkas pastatė ant pačio duobės kraštelio, kur apačioj šniokščia tamsus vanduo.... atgal neįkritau, bet taip ir atsibudau su paskutiniu epizodu ant to duobės krašto.... Šiandien irgi nekokį sapną sapnavau: pamečiau pasą, banko korteles, pinigus, visokius dokumentus.... Vargai, nemalonumai darbe.... bet išsipildo ne visi. Kokie pildosi,kokie - ne, dėsningumo dar neišsiaiškinau  smile.gif

http://www.up.lt/str...article_id=2679 wilow radau toki straipsni kur her2--- gydomas bevacizumabu.ar zinojai?
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QUOTE(dina1 @ 2012 09 01, 18:10)
http://www.up.lt/str...article_id=2679 wilow radau toki straipsni kur her2--- gydomas bevacizumabu.ar zinojai?

Taip, skaičiau, tačiau tik metastazavusiam....
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QUOTE(willow @ 2012 09 01, 20:05)
Taip, skaičiau, tačiau tik metastazavusiam....

bet tai nesamone laukia kol atsiras metastaziu. verysad.gif mano atveju tai anksciau herceptina skirdavo irgi mestazavusiam veziu,dabar tik kazkaip keli metai kai nelaukia kol prades plisti,aciu dievui
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Taip, Dina, pas mus daug tokių nesąmonių. Kaip ir biofosfonatai, kurie yra geras vaistas prieš metastazess kauluose, deja, juos skiria tik kai jau jos atsiranda....
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QUOTE(grazuoliukas @ 2012 09 01, 17:20)
Sveikutės 4u.gif Kokios Jūs visos stiprios bigsmile.gif Ir aš bandau tokia būti.
Man prie  puse metų diagnozavo smegenų naviką.Atlikus operaciją paaiškėjo,kad tai II astrocitoma. NOrs operavęs daktarasminėjo,kad nieko GREIČIAUSIAI nereikės,dėja...Nuvykus į onkologinį paskyrė radioterapiją (30 kartų). ANot gydančios daktarės- visa tai,kad inkubuoti tą vietą,kur buvo auglys,kaddaugiau jis nebeatsinaujintų.
Bandau neišskysti,nes turiu būti stipri dėl savo artmųjų ir mano mažųjų pipirų.
Kuriai buvo paskirtas svitinimas,kada mazdaug pasireiskia salutiniai poveikiai...?Jau buvau 7 kartus,pakolkas tfu tfu tfu,bet kiekvien1kart1 eidama vis bijau...uždedatą tą kaukę ir bijau, kad imsiu nebeatsikelsiu ar nuims ją,o aš nebematysiu... verysad.gif


Na, onkologai dar vis laikosi įprastos taktikos, o chirurgai yra linkę laikytis nuomonės, kad radioterapijos geriau nenaudoti. Po jos pakartotinai operuoti sunku. Kas teisus, sunku pasakyti.

Šalutinių poveikių gali išvis nebūti. Tik kad plaukai išslinks švitinimo taškuose. Po to viskas atauga, be jokios žymės. Būna, kad oda sureaguoja švitinimo taškuose, bet ne visiems.

Nesijaudink, astrocitoma nėra toks piktas navikas, auga lėtai, nebūna metastazių. Be to, kasdien atsiranda vis naujų gydymo būdų. Palyginus kas buvo prieš 10 metų, viskas labai keičiasi.
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QUOTE(willow @ 2012 09 01, 22:40)
Taip, Dina, pas mus daug tokių nesąmonių. Kaip ir biofosfonatai, kurie yra geras vaistas prieš metastazess kauluose, deja, juos skiria tik kai jau jos atsiranda....

Bifosfonatus reikia pirktis patiems. Turi pinigiukų - perki, neturi - neperki. verysad.gif O gal dabar jau skiria? g.gif Prieš pora ir daugiau metų mes pirkomės. Kainos kosminės. Seniau pusmečiui buvo kompensuojama, o paskui ministeris sveikatos (Padaiga) kompensaciją 'nuėmė', atseit ne pirmo būtinumo onkologinis vaistas, o kad labai daugeliui reikalingas - nė motais. verysad.gif
O tie vaistukai nepamainomi - mamytei visus nugaros skausmus nuėmė, galėjo pilnaverčiai (kiek įmanoma dėl chemijų) gyventi.

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Šį pranešimą redagavo rasų lanka: 02 rugsėjo 2012 - 19:22
QUOTE(rasų lanka @ 2012 09 02, 19:20)
Bifosfonatus reikia pirktis patiems. Turi pinigiukų - perki, neturi - neperki.  verysad.gif O gal dabar jau skiria?  g.gif Prieš pora ir daugiau metų mes  pirkomės. Kainos kosminės. Seniau pusmečiui buvo kompensuojama, o paskui ministeris sveikatos (Padaiga) kompensaciją 'nuėmė', atseit ne pirmo būtinumo onkologinis vaistas, o kad labai daugeliui reikalingas - nė motais.  verysad.gif
O tie vaistukai nepamainomi - mamytei visus nugaros skausmus nuėmė, galėjo pilnaverčiai (kiek įmanoma dėl chemijų) gyventi.


Kalbėjau su moterim, kuriai metastazavo į kaulus, jai skyrė kompensuojamus, tiesa, kiek, nepasiteiravau.

Gavau naujienų iš Cancernetwork apie hormonams teigiamą. Įmetu,kam įdomu.

Hormone Receptor–Positive Breast Cancer: The Known and the Unknown
By Shaheenah Dawood, MBBCh, MPH, MRCP (UK)1, Ana M. Gonzalez-Angulo, MD2 | Penktadienis, 2012, Rugpjūčio 10
1Department of Medical Oncology, Dubai Hospital, United Arab Emirates, 2Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas
________________________________________
Over the last decade, retrospective and prospective studies, as well as multiple editorials expressing various expert opinions, have been published that explore different aspects of the subtypes of breast cancer that we know to exist. Interestingly, with each piece of data and viewpoint published, we acknowledge the fact that breast cancer is a heterogeneous disease, comprising multiple subtypes about which there are myriad questions. The review by Lim and colleagues, on the natural history of hormone receptor–positive breast cancer, is timely as it gives us a comprehensive overview of the most important data on the subject published to date. It takes us through a proposed natural history of this disease derived from the existing data, and examines some of the interesting questions that have arisen.
What do we know about hormone receptor–positive disease? We know it has a known target for treatment with endocrine therapy; it is more chemotherapy-resistant compared with human epidermal growth factor receptor 2 (HER2)-positive and triple-negative breast cancer; it tends to recur late, possibly after completion of endocrine therapy; and like every other subtype identified, it, too, is heterogeneous. Yet has any of this knowledge changed the way we treat a woman with hormone receptor–positive cancer today, compared with a decade ago? The answer is probably both yes and no.
Consider a typical case of a postmenopausal woman with a T2N1M0 hormone receptor–positive HER2-negative breast cancer. The question that frequently arises is: Does this type of patient require chemotherapy? Berry et al[1] showed in a retrospective analysis of three prospective trials that the addition of chemotherapy resulted in an absolute improvement in 5-year disease-free survival of 22.8% and 7% in women with estrogen receptor–negative and estrogen receptor–positive disease, respectively. This indicates that a benefit exists, but not as much as that for women with hormone receptor–negative disease. How can we truly know the benefit of subjecting a patient to the potential toxicities of chemotherapy? The answer may come from genomic risk assessments of breast tumor tissues.
The recurrence score derived from Oncotype DX (Genomic Health, Inc) is able to categorize hormone receptor–positive, node-negative tumors into high and low risk groups that do and do not benefit from the addition of chemotherapy, respectively. Oncotype DX has been validated in multiple datasets, leading to its incorporation into practice guidelines. Its role in patients with node-positive disease is currently being investigated. Albain et al[2] used the recurrence score to determine the benefit of the addition of chemotherapy in patients with node-positive disease who were enrolled in the Southwest Oncology Group (SWOG) 8814 trial (which randomized women to endocrine therapy alone or to endocrine therapy and chemotherapy), demonstrating no benefit for the addition of chemotherapy in women with a recurrence score of less than 18 and a significant benefit in those with a recurrence score greater than or equal to 31. RxPONDER is a large prospective planned trial whose objective is to determine the benefit of chemotherapy among women with hormone receptor–positive breast cancer, one to three positive nodes, and a recurrence score less than or equal to 25. Thus, until the results are available, the standard would be to add chemotherapy to this patient’s treatment regimen.
Despite having mechanisms in place to determine chemotherapy benefit in this cohort, unfortunately there is no precise way at prsent to determine the degree of benefit and resistance to endocrine therapy at the individual level of the patient with hormone receptor–positive breast cancer. Lim et al describe various mechanisms that could be potentially responsible for de novo and acquired endocrine resistance. The most studied of these mechanisms is the activated PI3 kinase pathway that confers resistance to endocrine therapy. One way to overcome this resistance is to combine endocrine therapy with an mTOR inhibitor such as everolimus (Afinitor), the benefit of which has been demonstrated in patients with hormone receptor–positive breast cancer who have progressed on endocrine therapy. Whether we can use this upfront in the adjuvant setting is a question that is being studied. Such agents are not without toxicity, however, and this warrants the development of methods that would allow up-front determination of specific tumors inherently resistant to endocrine therapy. Tumors that co-express HER2 are also known to be less responsive to endocrine therapy in the absence of an anti-HER2 agent, which raises the question of whether 1 year of adjuvant trastuzumab(Drug information on trastuzumab) (Herceptin) is enough in women whose tumors co-express both receptors. The arm of the HERA (Herceptin Adjuvant) trial that is investigating 2 years of trastuzumab may shed some light on this issue. Another explanation for lack of response to endocrine therapy may simply be the inaccurate measurement of estrogen and progesterone(Drug information on progesterone) receptor levels using immunohistochemistry, with studies indicating that the inaccuracy rate could be as high as 20%.[3] Although the multitude of resistance mechanisms appears daunting, the ability to accurately determine up-front resistance to endocrine therapy is an active area of research. Recent and interesting work comes from Symmans e al,[4] who developed the sensitivity to endocrine therapy (SET) index that assesses the expression of genes correlated with estrogen to better predict outcome in response to endocrine therapy.
The questions of how long to give adjuvant endocrine therapy, and how much of a role resistance mechanisms play in women with hormone receptor–positive breast cancer who recur upon completion of 5 years of adjuvant endocrine therapy are currently the focus of multiple clinical trials. Prospective studies have demonstrated the continued benefit of endocrine therapy, in postmenopausal women, in the form of an aromatase inhibitor following completion of 5 years of tamoxifen(Drug information on tamoxifen). Whether postmenopausal women who get up-front aromatase inhibitors will benefit from more than 5 years of endocrine therapy is a question currently under investigation. Such strategies are designed to reduce the late recurrence known to be associated with hormone receptor–positive disease. Accurately identifying women at risk for a late recurrence (who will specifically require continued suppression of the estrogen receptor pathway) will be important if we are to spare those who do not need it from the long-term effects of estrogen-deprivation therapy.
Three decades ago, data from prospective clinical trials revealed the benefit of endocrine therapy among women with hormone receptor–positive breast cancer. Three decades later, we have come a long way in understanding the biology of this disease and developing strategies to improve outcomes. No doubt molecular profiling will continue to play a crucial role in allowing individualization of treatment strategies. We still have a long way to go, however. The time ahead is an exciting one, with results of a number of clinical trials eagerly anticipated. Given the current rate of progress in this field, it may not be completely unlikely that women with hormone receptor–positive breast cancer will be cured of this disease in the foreseeable future.

Financial Disclosure: Dr. Dawood has received an honorarium in the past year from GlaxoSmithKline. Dr. Gonzalez-Angulo has no significant financial interest or other relationship with the manufacturers of any products or providers of any service mentioned in this article.

TP yra dar vienas didelis straipsnis apie hormoninį gydymą. Įmetu nuorodą, nes str labai ilgas. Primenu, jog reikia prisiregistruoti.
http://www.cancernet...e/10165/2077056
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Šį pranešimą redagavo willow: 02 rugsėjo 2012 - 19:31
QUOTE(willow @ 2012 09 02, 21:26)
Kalbėjau su moterim, kuriai metastazavo į kaulus, jai skyrė kompensuojamus, tiesa, kiek, nepasiteiravau.

Na, tai tikrai labai jai pasisekė. thumbup.gif

Sveikatos visoms ir visiems. 4u.gif
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QUOTE(willow @ 2012 09 02, 19:26)
Kalbėjau su moterim, kuriai metastazavo į kaulus, jai skyrė kompensuojamus, tiesa, kiek, nepasiteiravau.

Gavau naujienų iš Cancernetwork apie hormonams teigiamą. Įmetu,kam įdomu.

Hormone Receptor–Positive Breast Cancer: The Known and the Unknown
By Shaheenah Dawood, MBBCh, MPH, MRCP (UK)1, Ana M. Gonzalez-Angulo, MD2 | Penktadienis, 2012, Rugpjūčio 10
1Department of Medical Oncology, Dubai Hospital, United Arab Emirates, 2Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas
________________________________________
Over the last decade, retrospective and prospective studies, as well as multiple editorials expressing various expert opinions, have been published that explore different aspects of the subtypes of breast cancer that we know to exist. Interestingly, with each piece of data and viewpoint published, we acknowledge the fact that breast cancer is a heterogeneous disease, comprising multiple subtypes about which there are myriad questions. The review by Lim and colleagues, on the natural history of hormone receptor–positive breast cancer, is timely as it gives us a comprehensive overview of the most important data on the subject published to date. It takes us through a proposed natural history of this disease derived from the existing data, and examines some of the interesting questions that have arisen.
What do we know about hormone receptor–positive disease? We know it has a known target for treatment with endocrine therapy; it is more chemotherapy-resistant compared with human epidermal growth factor receptor 2 (HER2)-positive and triple-negative breast cancer; it tends to recur late, possibly after completion of endocrine therapy; and like every other subtype identified, it, too, is heterogeneous. Yet has any of this knowledge changed the way we treat a woman with hormone receptor–positive cancer today, compared with a decade ago? The answer is probably both yes and no.
Consider a typical case of a postmenopausal woman with a T2N1M0 hormone receptor–positive HER2-negative breast cancer. The question that frequently arises is: Does this type of patient require chemotherapy? Berry et al[1] showed in a retrospective analysis of three prospective trials that the addition of chemotherapy resulted in an absolute improvement in 5-year disease-free survival of 22.8% and 7% in women with estrogen receptor–negative and estrogen receptor–positive disease, respectively. This indicates that a benefit exists, but not as much as that for women with hormone receptor–negative disease. How can we truly know the benefit of subjecting a patient to the potential toxicities of chemotherapy? The answer may come from genomic risk assessments of breast tumor tissues.
The recurrence score derived from Oncotype DX (Genomic Health, Inc) is able to categorize hormone receptor–positive, node-negative tumors into high and low risk groups that do and do not benefit from the addition of chemotherapy, respectively. Oncotype DX has been validated in multiple datasets, leading to its incorporation into practice guidelines. Its role in patients with node-positive disease is currently being investigated. Albain et al[2] used the recurrence score to determine the benefit of the addition of chemotherapy in patients with node-positive disease who were enrolled in the Southwest Oncology Group (SWOG) 8814 trial (which randomized women to endocrine therapy alone or to endocrine therapy and chemotherapy), demonstrating no benefit for the addition of chemotherapy in women with a recurrence score of less than 18 and a significant benefit in those with a recurrence score greater than or equal to 31. RxPONDER is a large prospective planned trial whose objective is to determine the benefit of chemotherapy among women with hormone receptor–positive breast cancer, one to three positive nodes, and a recurrence score less than or equal to 25. Thus, until the results are available, the standard would be to add chemotherapy to this patient’s treatment regimen.
Despite having mechanisms in place to determine chemotherapy benefit in this cohort, unfortunately there is no precise way at prsent to determine the degree of benefit and resistance to endocrine therapy at the individual level of the patient with hormone receptor–positive breast cancer. Lim et al describe various mechanisms that could be potentially responsible for de novo and acquired endocrine resistance. The most studied of these mechanisms is the activated PI3 kinase pathway that confers resistance to endocrine therapy. One way to overcome this resistance is to combine endocrine therapy with an mTOR inhibitor such as everolimus (Afinitor), the benefit of which has been demonstrated in patients with hormone receptor–positive breast cancer who have progressed on endocrine therapy. Whether we can use this upfront in the adjuvant setting is a question that is being studied. Such agents are not without toxicity, however, and this warrants the development of methods that would allow up-front determination of specific tumors inherently resistant to endocrine therapy. Tumors that co-express HER2 are also known to be less responsive to endocrine therapy in the absence of an anti-HER2 agent, which raises the question of whether 1 year of adjuvant trastuzumab(Drug information on trastuzumab) (Herceptin) is enough in women whose tumors co-express both receptors. The arm of the HERA (Herceptin Adjuvant) trial that is investigating 2 years of trastuzumab may shed some light on this issue. Another explanation for lack of response to endocrine therapy may simply be the inaccurate measurement of estrogen and progesterone(Drug information on progesterone) receptor levels using immunohistochemistry, with studies indicating that the inaccuracy rate could be as high as 20%.[3] Although the multitude of resistance mechanisms appears daunting, the ability to accurately determine up-front resistance to endocrine therapy is an active area of research. Recent and interesting work comes from Symmans e al,[4] who developed the sensitivity to endocrine therapy (SET) index that assesses the expression of genes correlated with estrogen to better predict outcome in response to endocrine therapy.
The questions of how long to give adjuvant endocrine therapy, and how much of a role resistance mechanisms play in women with hormone receptor–positive breast cancer who recur upon completion of 5 years of adjuvant endocrine therapy are currently the focus of multiple clinical trials. Prospective studies have demonstrated the continued benefit of endocrine therapy, in postmenopausal women, in the form of an aromatase inhibitor following completion of 5 years of tamoxifen(Drug information on tamoxifen). Whether postmenopausal women who get up-front aromatase inhibitors will benefit from more than 5 years of endocrine therapy is a question currently under investigation. Such strategies are designed to reduce the late recurrence known to be associated with hormone receptor–positive disease. Accurately identifying women at risk for a late recurrence (who will specifically require continued suppression of the estrogen receptor pathway) will be important if we are to spare those who do not need it from the long-term effects of estrogen-deprivation therapy.
Three decades ago, data from prospective clinical trials revealed the benefit of endocrine therapy among women with hormone receptor–positive breast cancer. Three decades later, we have come a long way in understanding the biology of this disease and developing strategies to improve outcomes. No doubt molecular profiling will continue to play a crucial role in allowing individualization of treatment strategies. We still have a long way to go, however. The time ahead is an exciting one, with results of a number of clinical trials eagerly anticipated. Given the current rate of progress in this field, it may not be completely unlikely that women with hormone receptor–positive breast cancer will be cured of this disease in the foreseeable future.

Financial Disclosure: Dr. Dawood has received an honorarium in the past year from GlaxoSmithKline. Dr. Gonzalez-Angulo has no significant financial interest or other relationship with the manufacturers of any products or providers of any service mentioned in this article.

TP yra dar vienas didelis straipsnis apie hormoninį gydymą. Įmetu nuorodą, nes str labai ilgas. Primenu, jog reikia prisiregistruoti.
http://www.cancernet...e/10165/2077056

labas.man labai idomu nes mano jautrus hormonams tik angliskai nemoku ax.gif gal galetum trmpai papasakot ka ten raso?
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Na, va. Ir netikėk tu žmogus sapnais! Šeštadienį paryčiais atsikėliau atsigerti vandens - tai taip skrandį sukabino, kad net nesupratau kaip ant grindų atsidūriau. g.gif Tik girdžiu, kad vyras šaukia, o pati visai atsijungus nuo skausmo guliu. Visgi daugiau, kaip vieno mažo obuoliuko į dieną man negalima. doh.gif Kepti tinka, o tie gražūs, kieti, sultingi, niam niam net seilės bėga pagalvojus, tokius fokusus mano pilvelyje išdarinėja! blush2.gif Laimė, kad angliukų po ranka turėjau. Jėga! Dvidešimt tablečikių su pertraukėle susigrūdau ir jau po penkiolikos minučių ramiausiai miegojau. O jau maniau šakės. schmoll.gif Viskas, reikia grįžti prie normalios mitybos. smile.gif Kai valgiau troškintas daržoves ir grikių košę tokių nemalonumų neturėdavau. ax.gif
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Tema uždaryta pasiekus maksimalų leidžiamą puslapių skaičių.
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