dijual nih... harga Rp. 4.300.000,- negoAcer Aspire One
Spek:
- Intel Atom 1.6Ghz
- DDR 1Gb
- HDD SATA 160GB
- wifi
- CardReader
- Modem
- Camera
- 10 inci
- Driver
- Colour Blue Black
- baru pakai 2 bulan
27 July 2009
laptop acer one
dijual nih... harga Rp. 4.300.000,- negoAcer Aspire One
Spek:
04 April 2009
Role of tumour-associated macrophages in tumour progression
Two different approaches – the use of various transgenic mouse models and the analysis of human tumours – have demonstrated a close link between the activity of tumour-associated macrophages (TAMs) and tumour progression. TAMs are abundant in most forms of solid tumour, where they often display a relatively immature phenotype and are positively correlated with tumour angiogenesis and/or progression .Pollard's group crossed PyMT-MMTV mice (which spontaneously develop mammary tumours) with the transgenic op/op mouse model lacking the gene for colony-stimulating factor-1, a crucial growth factor for macrophages and their precursors from the bone marrow, namely blood monocytes. The tumours that developed in these macrophage-depleted mice showed a slower rate of progression to malignancy and formed far fewer metastases in the lungs than those in non-macrophage-depleted mice. Moreover, Pollard's group recently characterised the development of the vasculature in PyMT-MMTV tumours during progression to malignancy and showed that the onset of the 'angiogenic switch' (the formation of the high-density vessel network associated with the transition to malignancy) was regulated by TAMs. Preinvasive mammary lesions in op/op mice exhibited both a delayed angiogenic switch and transition to malignancy, whereas genetic restoration of the macrophage population in tumours reversed this. Although these studies suggest that TAMs have a key role in promoting tumour angiogenesis, progression to malignancy and metastasis, they have yet to be confirmed in similar studies with other macrophage-depleted, transgenic mouse tumour models.
However, these data accord well with our finding that high numbers of TAMs correlate with increased tumour angiogenesis, lymph node status and reduced survival of breast cancer patients. Moreover, we showed that TAMs in breast carcinomas express numerous tumour-promoting factors such as the important mitogen epidermal growth factor and the pro-angiogenic cytokine vascular endothelial growth factor (VEGF). TAMs have also been shown to release a variety of other cytokines and enzymes known to promote tumour invasion, angiogenesis and metastasis. Recent studies indicate that when macrophages migrate into tumours they downregulate their expression of the potent anti-angiogenic cytokine IL-12 .
These findings have prompted investigations into how the tumour microenvironment 'educates' macrophages to perform these pro-tumour activities. Here we outline the important role of tumour hypoxia in this, both in the form of a direct effect on the expression of pro-tumour genes by TAMs, and indirectly by upregulating the pro-angiogenic cytokine angiopoietin-2 (Ang-2), which in turn has profound effects on TAM function.
dari bebagai sumber
However, these data accord well with our finding that high numbers of TAMs correlate with increased tumour angiogenesis, lymph node status and reduced survival of breast cancer patients. Moreover, we showed that TAMs in breast carcinomas express numerous tumour-promoting factors such as the important mitogen epidermal growth factor and the pro-angiogenic cytokine vascular endothelial growth factor (VEGF). TAMs have also been shown to release a variety of other cytokines and enzymes known to promote tumour invasion, angiogenesis and metastasis. Recent studies indicate that when macrophages migrate into tumours they downregulate their expression of the potent anti-angiogenic cytokine IL-12 .
These findings have prompted investigations into how the tumour microenvironment 'educates' macrophages to perform these pro-tumour activities. Here we outline the important role of tumour hypoxia in this, both in the form of a direct effect on the expression of pro-tumour genes by TAMs, and indirectly by upregulating the pro-angiogenic cytokine angiopoietin-2 (Ang-2), which in turn has profound effects on TAM function.
dari bebagai sumber
Cervical Cancer Overview
The uterine cervix is the lowest portion of a woman's uterus (womb). Most of the uterus lies in the pelvis, but part of the cervix is located in the vagina, where it connects the uterus with the vagina.
Cancer of the cervix occurs when the cells of the cervix change in a way that leads to abnormal growth and invasion of other tissues or organs of the body.
Like all cancers, cancer of the cervix is much more likely to be cured if it is detected early and treated immediately.
One of the key features of cervical cancer is its slow progression from normal cervical tissue, to precancerous (or dysplastic) changes in the tissue, to invasive cancer.
The slow progression through numerous precancerous changes is very important because it provides opportunities for prevention and early detection and treatment.
These opportunities have caused the decline of cervical cancer over the past decades in the United States.
Invasive cancer means that the cancer affects the deeper tissues of the cervix and may have spread to other parts of the body. This spread is called metastasis. Cervical cancers don't always spread, but those that do most often spread to the lungs, the liver, the bladder, the vagina, and/or the rectum.
fr:many resources
Cancer of the cervix occurs when the cells of the cervix change in a way that leads to abnormal growth and invasion of other tissues or organs of the body.
Like all cancers, cancer of the cervix is much more likely to be cured if it is detected early and treated immediately.
One of the key features of cervical cancer is its slow progression from normal cervical tissue, to precancerous (or dysplastic) changes in the tissue, to invasive cancer.
The slow progression through numerous precancerous changes is very important because it provides opportunities for prevention and early detection and treatment.
These opportunities have caused the decline of cervical cancer over the past decades in the United States.
Invasive cancer means that the cancer affects the deeper tissues of the cervix and may have spread to other parts of the body. This spread is called metastasis. Cervical cancers don't always spread, but those that do most often spread to the lungs, the liver, the bladder, the vagina, and/or the rectum.
fr:many resources
Cervical Cancer Causes
Cervical cancer begins with abnormal changes in the cervical tissue. The risk of developing these abnormal changes has been associated with certain factors, including previous infection with human papillomavirus (HPV), early sexual contact, multiple sexual partners, cigarette smoking, and taking oral contraceptives (birth control pills).
Forms of HPV, a virus whose different types cause skin warts, genital warts, and other abnormal skin and body surface disorders, have been shown to lead to many of the changes in cervical cells that may eventually lead to cancer.
Genetic material that comes from certain forms of HPV has been found in cervical tissues that show cancerous or precancerous changes.
In addition, women who have been diagnosed with HPV are more likely to develop a cervical cancer that has genetic material matching the strain of virus that caused the infection.
These findings demonstrate a strong link between the virus and cervical cancer.
Because HPV can be transmitted by sexual contact, early sexual contact and having multiple sexual partners have been identified as strong risk factors for the development of cervical lesions that may progress to cancer.
Cigarette smoking is another risk factor for the development of cervical cancer. The chemicals in cigarette smoke interact with the cells of the cervix, causing precancerous changes that may over time progress to cancer.
Oral contraceptives ("the pill") may increase the risk for cervical cancer, especially in women who use oral contraceptives for longer than 5 years
fr: many sources
Forms of HPV, a virus whose different types cause skin warts, genital warts, and other abnormal skin and body surface disorders, have been shown to lead to many of the changes in cervical cells that may eventually lead to cancer.
Genetic material that comes from certain forms of HPV has been found in cervical tissues that show cancerous or precancerous changes.
In addition, women who have been diagnosed with HPV are more likely to develop a cervical cancer that has genetic material matching the strain of virus that caused the infection.
These findings demonstrate a strong link between the virus and cervical cancer.
Because HPV can be transmitted by sexual contact, early sexual contact and having multiple sexual partners have been identified as strong risk factors for the development of cervical lesions that may progress to cancer.
Cigarette smoking is another risk factor for the development of cervical cancer. The chemicals in cigarette smoke interact with the cells of the cervix, causing precancerous changes that may over time progress to cancer.
Oral contraceptives ("the pill") may increase the risk for cervical cancer, especially in women who use oral contraceptives for longer than 5 years
fr: many sources
Subscribe to:
Posts (Atom)